Thalamic control of human attention driven by memory and learning. - PDF Download Free (2023)

Current Biology 24, 993–999, May 5, 2014 ª2014 The Authors

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Report Thalamic Control of Human Attention Driven by Memory and Learning Jose´ de Bourbon-Teles,1 Paul Bentley,1 Saori Koshino,1 Kushal Shah,1 Agneish Dutta,1 Paresh Malhotra,1 Tobias Egner,2 Masud Husain,3 and David Soto1,* 1Division of Brain Sciences, Department of Medicine, Imperial College London, Charing Cross Campus, St. Dunstan’s Road, London W6 8RP, UK 2Center for Cognitive Neuroscience and Department of Psychology & Neuroscience, Duke University, Levine Science Research Building, Box 90999, 450 Research Drive, Durham, NC 27708, USA 3Department of Experimental Psychology, University of Oxford, South Parks Road, Oxford OX1 3UD, UK

Summary The role of the thalamus in high-level cognition—attention, working memory (WM), rule-based learning, and decision making—remains poorly understood, especially in comparison to that of cortical frontoparietal networks [1–3]. Studies of visual thalamus have revealed important roles for pulvinar and lateral geniculate nucleus in visuospatial perception and attention [4–10] and for mediodorsal thalamus in oculomotor control [11]. Ventrolateral thalamus contains subdivisions devoted to action control as part of a circuit involving the basal ganglia [12, 13] and motor, premotor, and prefrontal cortices [14], whereas anterior thalamus forms a memory network in connection with the hippocampus [15]. This connectivity profile suggests that ventrolateral and anterior thalamus may represent a nexus between mnemonic and control functions, such as action or attentional selection. Here, we characterize the role of thalamus in the interplay between memory and visual attention. We show that ventrolateral lesions impair the influence of WM representations on attentional deployment. A subsequent fMRI study in healthy volunteers demonstrates involvement of ventrolateral and, notably, anterior thalamus in biasing attention through WM contents. To further characterize the memory types used by the thalamus to bias attention, we performed a second fMRI study that involved learning of stimulus-stimulus associations and their retrieval from long-term memory to optimize attention in search. Responses in ventrolateral and anterior thalamic nuclei tracked learning of the predictiveness of these abstract associations and their use in directing attention. These findings demonstrate a key role for human thalamus in higher-level cognition, notably, in mnemonic biasing of attention. Results We assessed a group of thalamic patients in a task probing the interaction between working memory (WM) contents and visual attention [16, 17], and then we used fMRI in healthy

*Correspondence: [emailprotected] This is an open access article under the CC BY license (http://

volunteers to test predictions derived from the lesion data. The study was approved by the West London Research Ethics committee. Patient Study Lesion maps appear in Figure 1. Figures 2A–2C depict the experimental paradigm (see also Supplemental Experimental Procedures available online). Thalamic patients’ performances were compared to 18 stroke controls (see Figure S1 for lesions) and 22 subjects without stroke who were admitted to the hospital for neurological evaluation. Experiment 1 We tested whether thalamic lesions disrupt WM cueing effects on search. Analyses of cue validity effects (neutral reaction time [RT] – valid RT) showed that control groups used the cues strategically to boost search. Thalamic patients consistently failed to do so, showing reduced validity effects relative to controls (Figure 2D; for statistics, see figure legend). Results held when cueing effects were transformed in order to account for interindividual variation in reaction time (RT) (i.e., (neutral RT 2 valid RT)/(neutral RT + valid RT); see Supplemental Experimental Procedures). No effects of target visual field (i.e., contralesional versus ipsilesional) were found here or in subsequent experiments. Intriguingly, two ventrolateral (VL) patients displayed a ‘‘reversed’’ validity effect, with slower performance in valid versus neutral trials. Patient VL3 showed a validity effect in the ‘‘normal’’ direction; however, its size was reduced relative to controls. We confirmed that validity effects in the control groups were higher than they were in each individual thalamic patient (all one sample t > 4, p < 0.0001; see also Figure S2A for individual data). Notably, patients VL1 and VL2 were tested in the acute stroke phase in the present experiment and subsequently also in the chronic phase (up to 1 year later; see experiments 2–4). Testing in both acute and chronic phases mitigated the possibility that our findings relate to functional or maladaptive plasticity. Patient VL3, however, took part in the first experiment 5 years poststroke. Hence, due to this longer recovery period, it is likely that compensatory mechanisms may have operated to regain some of the functional loss in this patient. Importantly, delayed recognition performance was high in the thalamic group (94.6% correct) and in the two control groups (95.4% and 94.4% correct, respectively) with no difference among control groups (for all: p > 0.8). The inability of thalamic patients to use the cue to guide search could thus not be explained by inability to retain it. Experiment 2 Given the striking reversed validity effect in patients VL1 and VL2, we sought to replicate this in experiment 2. Patients were reexamined 6 months and 10 months after experiment 1, respectively (Figure 1; bottom row confirms the chronic stage of VL lesions). We also varied the delay (2 s versus 6 s) between cue and search displays to assess whether the absence of a cueing effect in experiment 1 could be improved by allowing the patients to have more time to use the cue. Again, VL patients showed a reversed validity effect, which was not modulated by the delay between cue and search

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Figure 1. Lesion Maps of Thalamic Patients For the sake of simplicity, patients (n = 6) are labeled by the name of the thalamic lesion site showing overlap across them. Diffusion weighted imaging (DWI) scans (left column) illustrate the thalamic lesion site in the acute stage. Individual lesions were mapped onto a 3D, high-resolution, histology-based atlas of thalamic areas [18]. Axial slices to the right depict the thalamic nuclei in different colors, and the lesion area is highlighted in white. Table S1 depicts the percentage of damage of each thalamic nucleus and connectivity information from a diffusion tensor imaging atlas of probabilistic connections between thalamic nuclei and cortical regions [14]. The critical VL lesions included VLa, VApc, VLpv, and VLpd, which are densely connected with PFC [14]. The bottom row depicts high-resolution structural MRI of the VL patients acquired during the chronic stage following stroke. For patient VL1, we present the T2 brain scan rather than the T1 brain scan. Note that patient VL2 also had a small lesion in the left pallidum. Details: VL patients’ lesions involved VLa (green), VLpv (yellow), VLpd (violet), VApc (blue), VPla (light cyan), and VAmc (red). Note that only the VL3 lesion involved part of the anterior nuclei (AD and AV; dark cyan). The lesions in our MD patient mainly involved MDpc (green), CL (red), CM (blue), Pf (violet), VM (yellow), VPM (cyan), and VPLp (light green). The pulvinar patients’ lesions involved PuA (green), PuL (violet), PuM (yellow), CM (red), MDpc (blue), and VPLp (cyan). The following abbreviations are used: VAmc, ventral anterior magnocellular; VApc, ventral anterior parvocellular; VLa, VL anterior; VLpd, VL posterior dorsal; VLpv, VL posterior ventral; VPla, ventral posterolateral anterior; MDpc, mediodorsal parvocellular; Pf, parafascicular; CL, central lateral; CM, central medial; VM, ventral medial; VPM, ventral posteromedial; PuM, medial pulvinar; PuL, lateral pulvinar; PuA, anterior pulvinar.

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(see Figure 2E). Notably, memory of the cue was intact in the two VL patients (100% correct). Experiment 3 In experiments 1 and 2, memory was assessed separately from the search task. It is possible that thalamic patients did not strongly commit the cue to WM despite it being search relevant and despite encouragement to use it strategically. Note, however, that this account would have predicted mere attenuation or absence of the WM bias rather than the reversed validity effect displayed by VL patients. Here, we included a memory test following the response to the search display in order to ensure that cues were in WM throughout the trials. Although delayed recognition memory was at ceiling (VL1 = 100% correct; VL2 = 97% correct), the same reversed validity effect was found (Figure 2F; see also Supplemental Experimental Procedures for a replication experiment). This seemingly paradoxical effect is consonant with the view that thalamic insult triggers inhibition of any perceptual input that matches WM contents. We tested a crucial implication of this hypothesis in experiment 4. Experiment 4 In experiments 1–3, WM contents were search relevant. However, recent research indicates that WM can automatically bias

attention even when WM contents are irrelevant and detrimental in search [16, 17]: search is impaired when the WM content reappears as a search distracter as opposed to when it is absent [16]. This effect is contingent on participants holding the cue in WM because no attention bias is apparent when cues are merely attended (even in neurological populations [19, 20]; see [16, 17] for reviews). To test the hypothesis that VL lesions result in the inhibition of memory-matching items, experiment 4 employed cues that were consistently invalid in search (Figure 2G). If the hypothesis was correct, then the patients would display better search performance than healthy controls in this invalid cueing protocol because the patients’ attention would be repelled by rather than be attracted to the memory-matching distracters. We tested VL patients and healthy controls, along with patients Pulv2 and MD, who acted as a refined control for testing whether the VL patients specifically show a reversed invalidity effect. We analyzed the cue-invalidity effects (invalid RT 2 neutral RT). Whereas healthy controls (n = 11) displayed attentional capture by irrelevant WM contents (i.e., slower search on invalid versus neutral trials), thalamic patients did not exhibit attentional capture (see Figures 2G and S2B for individual data).

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Figure 2. Patient Study: Trial Examples and Behavioral Data (A) Memory-guided search task in experiments 1, 2, and 3. Participants were given either the name of a color cue, which always matched the search target (100% valid), or a neutral cue (‘‘no cue’’). This was followed by a search task that included finding the circle containing two gaps in the vertical plane and reporting whether it was located to the left or to the right of the central fixation. Participants responded via a button press. (B) Delayed recognition task. In experiments 1 and 2, the ability to maintain the memory cue was assessed in a separate recognition task. Participants were required to remember the color word, and, following a 2 s delay, they were required to respond whether the colored circle matched or did not match the verbal cue. Experiments 3 and 4 incorporated a memory test after the search to ensure that the cue was held in memory across the delay. (C) Invalid cueing in experiment 4. If the color word matched an item presented in the search display, this would never be the item surrounding the target (100% invalid trials). (D) Experiment 1: Cue-validity effects on search (median neutral RT 2 median valid RT) for the thalamic patients and for the control groups (error bars show SEM of the cue-validity effect). The size of the cue-validity effects was reduced in the thalamic group relative to age-matched patients with lesions outside the thalamus (n = 18; t(22) = 23.5; p = 0.002; independent sample two-tailed t test) and in the nonstroke group of age-matched controls (n = 22; t(26) = 23.4; p = 0.002). Individual median RT data and SEM across the different validity conditions are presented in Table S2. (E) Experiment 2: Search RTs as a function of cue-validity (Neu, neutral; Val, valid) and cue-search delay in patients VL1 and VL2. Note that performance of the patients in the short delay condition was compared with the performance of control groups from experiment 1, which had been tested with the same delay. Cueing effects differed significantly between the patients with lesions outside the thalamus and the two VL patients, and the same held for the comparison with the nonstroke group (t > 11, p < 0.0001). (F) Experiment 3: Search RTs as a function of cue validity in the version of the task that incorporated a memory test after the search. VL patients showed reversed validity effects relative to the nonstroke controls and the stroke control group (all one sample t > 10, p < 0.0001). (G) Experiment 4: Cue-invalidity effects (invalid RT 2 neutral RT) for the thalamic patients and the healthy controls. Importantly, we only analyzed search trials with correct recognition memory responses. Healthy controls (n = 11) displayed slower search in invalid trials relative to neutral trials (F(2,10) = 50.47; p = 0.0001). Invalidity effects were significantly lower in the thalamic patients than in the healthy controls (t(26) = 23.38; p = 0.002). This pattern of results held when the data were transformed to account for overall individual search latencies (Supplemental Experimental Procedures).

Most importantly, the two VL patients now displayed a reversed invalidity effect and responded faster in invalid trials compared to neutral trials (see Figure 2G). Notably, memory performance in these patients was high (VL1: 98% correct; VL2: 97% correct; VL3: 97.3% correct; Pulv2: 90% correct; MD: 85% correct). Experiments 3 and 4 were conducted several months after stroke. We reiterate that patients VL1 and VL2 showed a similar reversed validity effect in the chronic and more acute stages, suggesting that the effect is unlikely to be the result of functional or maladaptive plasticity. Future research, however, ought to assess whether and how focal thalamic damage can trigger maladaptive functional reorganization changes in brain networks, which

may further account for the impaired WM biasing of attention reported here. fMRI Studies Experiment 1: Anterior Thalamus Is Involved in WM Biasing Given the limited sample size of our rare thalamic patients, we further probed the role of the VL and anterior thalamus in WM biasing of attention by using fMRI in healthy participants. Note that only one of the VL patients’ lesions (i.e., VL3) comprised the more anterior thalamic nuclei (i.e., anterior dorsal [AD] and anterior ventral [AV]; Figure 1 and Table S1), described as part of a memory network including the hippocampus [15]. We propose that anterior nuclei, along with VL thalamus’s contribution to action and oculomotor control [12, 13, 21, 22],

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Figure 3. fMRI Experiment 1 (A) Task: A visual cue to be held in memory is presented. Following a delay, the search display appears. The task is to discriminate the orientation of the tilted bar (i.e., \ or /). An example of invalid trial is presented. Invalid trials were compared to a neutral baseline in which the cue was absent from search. In memory catch trials (20%), the search array was replaced by a recognition memory test. (B) Search RTs across invalid and neutral trials (error bars show SEM). Search was impaired by the presence of an invalid WM distracter relative to the neutral baseline (t(38) = 7.08, p < 0.00001, two-tailed t test; Figure 3B), in keeping with an automatic bias of attention by WM contents. Memory accuracy was high (mean = 93% correct). Search accuracy was high (mean = 93.75% correct) and did not differ across the neutral and invalid trials (t(38) = 20.842; p > 0.4). (C) Thalamic responses were enhanced by the reappearance of the cue relative to the neutral baseline.

may represent a nexus between mnemonic and attention control functions. We tested this hypothesis further in an fMRI study of healthy volunteers (n = 39) by using a paradigm that assessed the automatic biases of attention through irrelevant WM content [23, 24] that was similar to experiment 4 except that (1) here, the cues were visual, (2) search displays were brief (0.1 s) to prevent saccades, and (3) the search target was a tilted line (/ or \) among vertical distracters (see Figure 3A and Supplemental Experimental Procedures). Behavioral results were consistent with automatic WM biasing of search (Figure 3B). Given our a priori interest in the thalamus, neuroimaging analyses used masks of the right and left thalami. Relative to the neutral baseline, there were increased responses to the reappearance of a WM distracter in bilateral pulvinar thalamus (medial pulvinar [PuM], lateral pulvinar [PuL], and inferior pulvinar [PuI]), mediodorsal thalamus (mediodorsal parvocellular [MDpc]), and, more critically, (1) VL regions overlapping with the patients’ lesion sites (ventrolateral anterior [VLa], ventrolateral posterior dorsal [VLpd], and ventral anterior parvocellular [VApc]) and (2) the more anterior thalamus bilaterally (including AV, anterior medial [AM], and AD) (see Figure 3C). These results survived correction for multiple comparisons within the thalamic regions of interest (ROIs) and across the whole brain. We also found activations in frontoparietal regions (Figure S3) and in the bilateral hippocampus (Montreal Neurological Institute [MNI]: 24, 220, 212 and 224, 226, 214). Given our a priori hypothesis concerning the thalamus, these activations are not discussed in great depth because they only provide correlational evidence, which, unlike our lesion evidence, precludes the formulation of causal inferences. We note that parietal and hippocampal responses have been recently associated with the strategic cognitive control over WM biases [25], and frontoparietal responses are classically involved in attention control [1]. Importantly, prior work has demonstrated that reappearance of WM contents is associated with increased neural responses relative to a nonrepetition baseline, whereas priming is associated with neural repetition suppression [26, 27]. Notably, we found no evidence for reduced responses to the reappearance of the memory cue in search. This is consistent with memory biases in this paradigm being contingent on WM [16, 17]. Experiment 2: Role of VL-Anterior Thalamus in Attention Biases Driven by Learning and Retrieval from Long-Term Memory So far, the findings indicate a thalamic role in WM-based attentional control. However, it remains possible that the thalamus’s role in attention may incorporate additional mnemonic

processes, such as when information from long-term memory is brought ‘‘online’’ to guide behavior. Here, we sought to further characterize the scope of memory types that may be involved in this thalamic control of attention. In the prior patient and fMRI study, the cueing of attention was accomplished via information in WM. We devised a new fMRI paradigm (n = 16) to assess whether the thalamus mediates attention guidance that relies on the learning of new stimulus-stimulus associations and their retrieval from long-term memory. Figures 4A and 4B illustrate the paradigm. Behavioral results were consistent with the acquisition of knowledge about cue predictiveness as training developed and its use in driving attention (Figure 4C). fMRI analyses tested for linear learning trends associated with the predictiveness of the cues (predictive > nonpredictive) across training blocks and also tested for exponential trends because the behavioral manifestation of learning had an abrupt onset in block 4 (Figure 4C). Given that we were only interested in thalamic responses, the analyses were based on anatomical ROIs comprising the entire left and entire right thalami. Responses in anterior (AV), ventrolateral (VLpd, VApc), and mediodorsal (MDpc) regions of the right thalamus (p < 0.05, corrected for multiple comparisons; Figure 4D) were consistent with both linear and exponential learning trends in the learning protocol. No clusters survived this threshold in the left thalamus. No cortical responses survived whole-brain correction. We then conducted additional unbiased ROI analyses based on the lesion evidence from our VL thalamus patients, and, accordingly, we used a 6-mm-radius spherical ROI that covered the anatomical lesion sites of our VL thalamus patients (centered at MNI 210, 210, 10, depicted in blue shading in Figure 4D). Voxels in left VApc and on the border of VLpd and MDpc thalamus tracked the predictiveness of the hiragana cues across training, consistent with an exponential learning trend (p < 0.05, voxel corrected for multiple comparisons across patient-based ROI; Figure 4D, voxels surrounded by white circles; these ROI results were corroborated by nonparametric permutation analyses). Although there were significant responses in the left VL thalamus, it appears that right thalamic responses were more prominent in this learning protocol relative to fMRI experiment 1. It is possible that involvement of the right thalamus is stronger when learning of stimulus-stimulus associations needs to take place to guide attention. Future studies ought to assess this possibility. Discussion The present studies characterized the functional contribution of the VL and anterior regions of the human thalamus in the

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Figure 4. fMRI Experiment 2 (A) Learning and search phases. Participants were encouraged to form associations between the Japanese hiragana cues (not drawn to scale in the figure) and the colors of the circles surrounding the search target in order to boost search performance. The top row depicts a predictive trial (the hiragana cue is predictive of a red circle containing the tilted target). The bottom row depicts a nonpredictive trial (here, the hiragana cue is not associated with any target feature). Predictive and nonpredictive cues were presented randomly across trials. Four hiragana cues were 100% predictive (each of them was associated with a particular color surrounding the search target). Four different hiragana cues were neutral (not associated with any target features). (B) Example of a recognition test trial. To further encourage learning, we presented recognition tests following each training block, which involved the presentation of hiragana probes, and participants were required to report whether or not the probes conferred predictive value for search and to rate how confident they were in their decisions on a confidence scale of 1–3. (C) RTs for predictive cues showed evidence of learning across blocks compared to nonpredictive cues (error bars show SEM of the difference between predictive and nonpredictive RTs). Due to a technical issue, behavioral data during scanning could not be recorded for one participant. Data from the remaining 15 participants were entered into a 5 (block) 3 2 (cue type: predictive and nonpredictive) repeated-measures ANOVA, which was performed over the median RTs of the correct search responses. There was a main effect of training (F(4,56) = 5.01; p = 0.006) such that search RTs became faster across the training blocks. Search performance was also faster following predictive rather than nonpredictive cues (F(1,14) = 8.77; p = 0.01). Importantly, these main effects were qualified by the presence of a significant interaction between cue type and block (F(4,56) = 4.33; p = 0.007). This interaction effect indicates that search performance became increasingly faster in predictive relative to nonpredictive trials as training developed. Search accuracy in the learning phase was very high (predictive trials = 92% correct; nonpredictive trials = 93% correct). There were no effects of block, cue, or interactions on search accuracy (for all: p > 0.45). Recognition data showed that learning of cue predictiveness improved with block (F(4,56) = 6.5; p = 0.001; Figure S4A; no other effects or interactions were evident; for all: p > 0.3). Likewise, memory confidence also increased with block (F(4,56) = 9.4; p = 0.001; Figure S4B). These results, along with the findings from the search latencies, are consistent with the acquisition of knowledge about cue predictiveness as training developed. (D) Thalamus responses followed linear and exponential trends to the predictiveness of the cues during the learning. The graph displays the percent signal change of the difference between the parameter estimate for predictive minus nonpredictive trials from all significant voxels in the right thalamus ROI across blocks.

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interplay between memory and attention. The lesion evidence demonstrates that thalamic lesions lead to impaired guidance of visual attention by WM contents. Remarkably, VL patients displayed reversed effects of cue validity independent of the relevance of the memory contents for search, even when they knew that cues were consistently associated with the target (experiments 1–3) or with a distracter (experiment 4). Importantly, the inability of the thalamic patients to use the cue in order to drive attention cannot be accounted for by an inability to retain the cue information in memory. These results are in keeping with the view that thalamic lesions disrupt the obligatory WM bias of attention that is observed in the healthy brain. The VL thalamus, including VLa, VApc, and VLpd areas identified in our lesion and fMRI findings, is densely connected with cognitive control substrates in the prefrontal cortex (PFC) [14]. VL regions are also an integral part of the cortico-subcortical circuit comprising superior frontal regions and the superior colliculus for controlling eye movements [21, 22] and covert attention [28, 29]. This is one pathway through which the VL thalamus may be functionally relevant for the triggering of attention-biasing signals. Furthermore, the anterior thalamus and the mamillothalamic tract are critical for normal memory function [30, 31], and the

anterior nuclei also form part of a network comprising the hippocampus, mammillary bodies, and posterior cingulate cortex, which is relevant for recollective aspects of memory [15, 32]. Notably, recent research has demonstrated the role of the hippocampus in attentional guidance by WM and long-term memory [33, 34] as part of a network including the posterior cingulate and parietal cortex [34]. Based on the connectivity profile outlined above, it is possible that VL and anterior thalamus lesions lead to widespread damage of attention circuits—through connections with the superior frontal cortex and PFC [14]—and also memory circuits—via connections with hippocampus and posterior cingulate [15, 32]—which are key in controlling attention. Notably, whole-brain results from fMRI experiment 1 showed that the thalamus was coactivated along with frontoparietal areas and the hippocampus. Together, these findings help us understand the role of the thalamus in attention control by memory as part of a broader cortico-subcortical network. Thalamic damage may trigger disconnection between areas involved in perceptual selection and mnemonic control, leading to inhibition of memory-matching signals. Hence, the deployment of attention is directed away from those items.

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These findings therefore indicate that in the normal functioning brain, the VL and anterior thalamus are key parts of the neural circuit mediating the automatic capture of attention by stimuli-matching WM contents, a notion that we confirmed in the first fMRI experiment. Our lesion evidence enhances understanding of the nature of the functional role of the thalamus in memory and attention interactions beyond what could be anticipated from correlative fMRI findings alone. If the functional role of the thalamus was to regulate the activation state of memory representations based on their current relevance for task goals (e.g., downweighting representations associated with memory distracters for search), then we would have expected thalamic lesions to produce magnified attention biases by irrelevant contents held in memory (as previously found following PFC damage [20]). PFC lesions can lead to increased attentional capture by search distracters held in WM [20], suggesting that PFC mediates the capacity to shield irrelevant WM contents from the processes that guide search. Together, these findings indicate that the thalamus’s role in WM biases of attention is dissociable from that of the PFC. Memory biases of attention were attenuated in pulvinar patients. It has been debated whether the pulvinar’s role in attention is related to the orienting or filtering of distracters [4, 9, 35]. Our lesion evidence is consistent with a pulvinar role in the orientation of attention, namely from the contents of WM. A filtering account would have predicted exacerbated distraction by irrelevant WM contents in pulvinar patients. Finally, our second fMRI experiment showed that thalamic responses track the acquisition of stimulus-stimulus associations that are used to optimize attention in search. Hence, it demonstrates the flexible scope of memory types supported by the thalamus in the service of attention and how this can be shaped by experience and learning. Animal studies point to a role of the anterior thalamus in memory and learning [36–39], and human studies implicated the VL thalamus in memory and language [40–42]. These findings, together with the present work, indicate that the anterior and VL thalamus can mediate attention control driven by information held in WM that is already consolidated in the cognitive repertoire (e.g., color cues) in addition to mediating the role of experience, the learning of new regularities, and the retrieval of learned information from long-term memory to guide attention. Supplemental Information Supplemental Information includes Supplemental Experimental Procedures, four figures, and four tables and can be found with this article online at Acknowledgments This work was supported by grants from the MRC (UK, 89631) and the Bial Foundation. We thank Marty Sereno and the BUCNI staff for their kind support with the imaging protocol. Received: February 1, 2014 Revised: February 24, 2014 Accepted: March 7, 2014 Published: April 17, 2014 References 1. Corbetta, M., and Shulman, G.L. (2002). Control of goal-directed and stimulus-driven attention in the brain. Nat. Rev. Neurosci. 3, 201–215.

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26. Soto, D., Humphreys, G.W., and Rotshtein, P. (2007). Dissociating the neural mechanisms of memory-based guidance of visual selection. Proc. Natl. Acad. Sci. USA 104, 17186–17191. 27. Miller, E.K., and Desimone, R. (1994). Parallel neuronal mechanisms for short-term memory. Science 263, 520–522. 28. Cavanaugh, J., and Wurtz, R.H. (2004). Subcortical modulation of attention counters change blindness. J. Neurosci. 24, 11236–11243. 29. Thompson, K.G., Biscoe, K.L., and Sato, T.R. (2005). Neuronal basis of covert spatial attention in the frontal eye field. J. Neurosci. 25, 9479– 9487. 30. Van der Werf, Y.D., Scheltens, P., Lindeboom, J., Witter, M.P., Uylings, H.B., and Jolles, J. (2003). Deficits of memory, executive functioning and attention following infarction in the thalamus; a study of 22 cases with localised lesions. Neuropsychologia 41, 1330–1344. 31. von Cramon, D.Y., Hebel, N., and Schuri, U. (1985). A contribution to the anatomical basis of thalamic amnesia. Brain 108, 993–1008. 32. Vann, S.D., and Albasser, M.M. (2009). Hippocampal, retrosplenial, and prefrontal hypoactivity in a model of diencephalic amnesia: Evidence towards an interdependent subcortical-cortical memory network. Hippocampus 19, 1090–1102. 33. Stokes, M.G., Atherton, K., Patai, E.Z., and Nobre, A.C. (2012). Longterm memory prepares neural activity for perception. Proc. Natl. Acad. Sci. USA 109, E360–E367. 34. Soto, D., Greene, C.M., Kiyonaga, A., Rosenthal, C.R., and Egner, T. (2012). A parieto-medial temporal pathway for the strategic control over working memory biases in human visual attention. J. Neurosci. 32, 17563–17571. 35. Snow, J.C., Allen, H.A., Rafal, R.D., and Humphreys, G.W. (2009). Impaired attentional selection following lesions to human pulvinar: evidence for homology between human and monkey. Proc. Natl. Acad. Sci. USA 106, 4054–4059. 36. Byatt, G., and Dalrymple-Alford, J.C. (1996). Both anteromedial and anteroventral thalamic lesions impair radial-maze learning in rats. Behav. Neurosci. 110, 1335–1348. 37. Vann, S.D., and Aggleton, J.P. (2003). Evidence of a spatial encoding deficit in rats with lesions of the mammillary bodies or mammillothalamic tract. J. Neurosci. 23, 3506–3514. 38. Aggleton, J.P., Neave, N., Nagle, S., and Hunt, P.R. (1995). A comparison of the effects of anterior thalamic, mamillary body and fornix lesions on reinforced spatial alternation. Behav. Brain Res. 68, 91–101. 39. Parker, A., and Gaffan, D. (1997). The effect of anterior thalamic and cingulate cortex lesions on object-in-place memory in monkeys. Neuropsychologia 35, 1093–1102. 40. Vilkki, J. (1978). Effects of thalamic lesions on complex perception and memory. Neuropsychologia 16, 427–437. 41. Ojemann, G.A., Blick, K.I., and Ward, A.A., Jr. (1971). Improvement and disturbance of short-term verbal memory with human ventrolateral thalamic stimulation. Brain 94, 225–240. 42. Ojemann, G.A. (1977). Asymmetric function of the thalamus in man. Ann. N Y Acad. Sci. 299, 380–396.


What is the role of thalamus in learning and memory? ›

Your thalamus plays a role in keeping you awake and alert. Role in thinking (cognition) and memory. Your thalamus is connected with structures of your limbic system, which is involved in processing and regulating emotions, formation and storage of memories, sexual arousal and learning.

Does the thalamus control attention? ›

Abstract. Attention is the process by which information and selection occurs, the thalamus plays an important role in the selective attention of visual and auditory information. Selective attention is a conscious effort; however, it occurs subconsciously, as well.

Does the thalamus control memory? ›

The thalamus, with its cortical, subcortical, and cerebellar connections, is a critical node in networks supporting cognitive functions known to decline in normal aging, including component processes of memory and executive functions of attention and information processing.

Does Alzheimer's affect the thalamus? ›

Acta Neuropathol.

Which part of thalamus is related to memory? ›

Two subregions of the human thalamus most often implicated in long-term memory are the anterior thalamic nucleus (AT) and mediodorsal nucleus (MD) [1].

What part of the brain controls learning and memory? ›

Hippocampus. A curved seahorse-shaped organ on the underside of each temporal lobe, the hippocampus is part of a larger structure called the hippocampal formation. It supports memory, learning, navigation and perception of space.

What part of the brain is responsible for control of attention? ›

Brain Structure

The front of the brain behind the forehead is the frontal lobe. The frontal lobe is the part of the brain that helps people to organize, plan, pay attention, and make decisions.

What emotions does the thalamus control? ›

The thalamus is another region of the brain implicated in the limbic system; this structure is found at the heart of the forebrain and is responsible for emotion processing, such as fear, sadness, disgust, happiness, and pleasure.

Does the thalamus control decision-making? ›

Task selectivity was more strongly dependent on thalamic inputs than cortico-cortical inputs. Our results suggest that the thalamus drives subnetworks within frontal cortex coding distinct features of decision-making.

Does the thalamus control alertness? ›

The thalamus is composed of different nuclei that each serve a unique role, ranging from relaying sensory and motor signals, as well as regulation of consciousness and alertness.

What thalamic nucleus is involved in memory processes? ›

The region in the thalamus that contributes to declarative memory is the anterior and medial division, containing the anterior nuclei, the medial dorsal nucleus and the intralaminar and midline nuclei.

What are the symptoms of thalamic dementia? ›

Bilateral lesions of the thalamus may yield severe neuropsychological disturbances, including memory, speech, and visuospatial dysfunction; furthermore, in some instances, a condition known as thalamic dementia may develop [3,6,8,11,19], in which amnesia, speech disturbances, and confusion may be associated with apathy ...

What is thalamic dementia? ›

Thalamic dementia is an uncommon type of stroke that presents with disorientation, behavioral changes, and impairment of executive functions, with relative preservation of motor functions.

What are the cognitive effects of thalamic stroke? ›

In cognitive aspects of thalamic function, damage to the anterior portions of the thalamus results in memory loss [2],[3], and damage to midline thalamic nuclei that may develop into inattention and executive dysfunction, such as deficits of impulse control and decision-making [4],[5].

What are some interesting facts about the thalamus? ›

The thalamus is a large, symmetrical (meaning there is one in each cerebral hemisphere) structure that makes up most of the mass of the diencephalon. A large number of pathways travel through the thalamus, including all of the sensory pathways other than those devoted to olfaction (smell).

Are long term memories stored in the thalamus? ›

Memories may be sorted by the thalamus before being stored long term. The thalamus – a structure in the centre of the brain that relays information from the senses – may be responsible for sorting memories before they are stored long term, a study in mice suggests.

Where does the thalamus get information from? ›

In the visual system, the thalamus receives input from the retina, which is relayed to the brain via the optic nerve. Signals are sent to the lateral geniculate nucleus of the thalamus which then forwards them onto the primary visual cortex (area V1) in the occipital lobe.

Where is trauma stored in the brain? ›

When a person experiences a traumatic event, adrenaline rushes through the body and the memory is imprinted into the amygdala, which is part of the limbic system. The amygdala holds the emotional significance of the event, including the intensity and impulse of emotion.

Which part of the brain is linked to memory intelligence and learning power? ›

Hippocampus. The hippocampus, located in the brain's temporal lobe, is where episodic memories are formed and indexed for later access.

What part of the brain controls memory loss? ›

At first, Alzheimer's disease typically destroys neurons and their connections in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex responsible for language, reasoning, and social behavior.

What part of the brain regulates levels of awareness attention and motivation? ›

Frontal lobe: Responsible for motor function, language, and cognitive processes, such as executive function, attention, memory, affect, mood, personality, self-awareness, and social and moral reasoning.

Which brain part is responsible for paying attention to important changes in stimuli or information? ›

In both cases, the prefrontal cortex — the control center for most cognitive functions — appears to take charge of the brain's attention and control relevant parts of the visual cortex, which receives sensory input.

What part of the brain is responsible for keeping your attention on what you doing and for helping you sort out important and unimportant information? ›

[1] The frontal lobe, located anteriorly to the central sulcus, is responsible for voluntary motor function, problem-solving, attention, memory, and language. Located in the frontal lobe are the motor cortex and the Broca area.

What sense does the thalamus not control? ›

In all senses except for the olfactory sense, the thalamus is known to be involved in various functions ranging from basic sensory information to attention modulation.

Does the thalamus control imagination? ›

The neocortex and thalamus are responsible for controlling the brain's imagination, along with many of the brain's other functions such as consciousness and abstract thought.

Does thalamus control voluntary actions? ›

Thalamus functions to relay sensory and motor signals to the cerebral cortex besides regulation of sleep and alertness. The cerebral cortex is the outer covering of grey matter over the hemispheres and includes areas or cortices responsible for receiving sensory input and production of voluntary limb or eye movements.

Does thalamus control anxiety? ›

The thalamus has reciprocal connections with the amygdala and medial prefrontal cortex, and is thus believed to be involved in the production and regulation of anxiety and fear.

What happens if you stimulate the thalamus? ›

Taken together, these studies indicate that electrical stimulation of the central thalamus may enhance cognitive performance through neocortical and hippocampal neuronal activation and specific regulation of gene expression.

Does the thalamus control fear? ›

Nucleus reuniens of the thalamus controls fear memory intensity, specificity and long-term maintenance during consolidation.

What vitamins help thalamus? ›

Researchers suggest that some nutrients may help the hypothalamus and pituitary glands to function. These include polyphenols, omega-3, and vitamins C, B1, and B12.

What activities use the thalamus? ›

While the thalamus is classically known for its roles as a sensory relay in visual, auditory, somatosensory, and gustatory systems, it also has significant roles in motor activity, emotion, memory, arousal, and other sensorimotor association functions.

What is a healthy lifestyle for the thalamus? ›

Some things you can do to support the hypothalamus, and the health of your endocrine and nervous systems, include exercising regularly, eating foods rich in chromium and healthy fats, getting enough sleep, and reducing stress.

What controls level of alertness? ›

The reticular activating system is found in the midbrain, pons, medulla and part of the thalamus. It controls levels of wakefulness, enables people to pay attention to their environments and is involved in sleep patterns.

Does the thalamus control coordination? ›

Motor thalamus (Mthal) is implicated in the control of movement because it is strategically located between motor areas of the cerebral cortex and motor-related subcortical structures, such as the cerebellum and basal ganglia (BG).

What controls alertness and arousal? ›

Norepinephrine. Norepinephrine (also called noradrenaline) increases blood pressure and heart rate. It's most widely known for its effects on alertness, arousal, decision-making, attention and focus.

What are the 3 main categories of thalamic nuclei? ›

The thalamus is a paired structure located in the center of the brain. Each side can divide into three groups of thalamic nuclei: a lateral nuclear group, a medial nuclear group, and an anterior nuclear group.

Which of the following thalamic nuclei is involved in conscious awareness? ›

Anterior nuclei of thalamus

These nuclei receive information from the limbic system, thus having important functions and influence upon emotional states, such as attention and alertness and memory acquisition.

Which nucleus is responsible for memory? ›

The caudate nucleus functions not only in planning the execution of movement, but also in learning, memory, reward, motivation, emotion, and romantic interaction.

What is the 5 word memory test? ›

Administration: The examiner reads a list of 5 words at a rate of one per second, giving the following instructions: “This is a memory test. I am going to read a list of words that you will have to remember now and later on. Listen carefully. When I am through, tell me as many words as you can remember.

What are the 10 warning signs of dementia? ›

10 Early Signs and Symptoms of Alzheimer's
  • Memory loss that disrupts daily life. ...
  • Challenges in planning or solving problems. ...
  • Difficulty completing familiar tasks. ...
  • Confusion with time or place. ...
  • Trouble understanding visual images and spatial relationships. ...
  • New problems with words in speaking or writing.

How is thalamic stroke diagnosed? ›

How is it diagnosed? If your doctor thinks you may have had a thalamic stroke, they'll likely start by taking an MRI or CT scan of your brain to determine the extent of the damage. They may also take a blood sample for further testing to check for blood glucose levels, platelet counts, and other information.

What happens to memory if thalamus is damaged? ›

Symptoms of damage to your thalamus include: Memory loss (amnesia). Lack of interest or enthusiasm (apathy). Loss of ability to understand language or speak (aphasia).

What psychological disorders are in the thalamus? ›

In addition to schizophrenia, the thalamus has also been implicated in other psychiatric illnesses including post-traumatic stress disorder (PTSD) and major depressive disorder (MDD).

Does Alzheimer's affect thalamus? ›

Acta Neuropathol.

What are the long term effects of a thalamic stroke? ›

A thalamic stroke occurs when a small blood vessel serving the thalamus becomes blocked. A blood clot or atherosclerotic plaque may cause the blockage. Tissue begins to die, which may lead to long-term brain damage, disability, or death.

How does the thalamus affect vision? ›

In the visual system, the lateral geniculate nucleus (LGN) of the dorsal thalamus is the gateway through which visual information reaches the cerebral cortex.

What functions are affected if the thalamus is damaged? ›

While thalamus damage primarily causes sensory problems, it can also lead to behavioral and cognitive changes. For example, many patients with a thalamus injury have incorrect speech patterns and can struggle to find the right words. Others display apathy and memory problems.

Is the thalamus involved in learning? ›

The Thalamus Helps the Cerebrum With Learning.

Is the hypothalamus involved in learning and memory? ›

Overall, these results suggest that hypothalamus or hypothalamus-like regions play critical roles in regulating diverse types of learning and memory, both related and unrelated to food.

What is the important function of thalamus? ›

The thalamus is a mostly gray matter structure of the diencephalon that has many essential roles in human physiology. The thalamus is composed of different nuclei that each serve a unique role, ranging from relaying sensory and motor signals, as well as regulation of consciousness and alertness.

What is the role of the hypothalamus in learning? ›

Such hypothalamic control of memory-related synaptic machinery may enable gating/thresholding/permissive/tagging operations within yet poorly defined logic gates for memory updating. Hypothalamic signals may thus facilitate cost-benefit analysis of learning and memory in real-world settings.

Does the thalamus control motivation? ›

Growing evidence from both human and rodent studies has implicated distinct thalamic nuclei in mediating motivated behaviors.

What is the role of the thalamus in awareness and perception? ›

The thalamus relays sensory impulses from receptors in various parts of the body to the cerebral cortex. A sensory impulse travels from the body surface towards the thalamus, which receives it as a sensation. This sensation is then passed onto the cerebral cortex for interpretation as touch, pain or temperature.

Which hormone is important in learning and memory? ›

Hormonal Influences on Memory

For example, several studies indicate that the major neuromodulation systems in the brain (such as those which use dopamine or serotonin) also greatly influence synaptic plasticity.

Which hormone is involved in our memories? ›

The adrenal stress hormones epinephrine and corticosterone released by emotional arousal regulate the consolidation of long-term memory. The amygdala plays a critical role in mediating these stress hormone influences.

What part of the brain controls emotions? ›

Three brain structures appear most closely linked with emotions: the amygdala, the insula or insular cortex, and a structure in the midbrain called the periaqueductal gray. A paired, almond-shaped structure deep within the brain, the amygdala integrates emotions, emotional behavior, and motivation.

Can you live without a thalamus? ›

1 The precise functions of these nuclei have been elusive, although it is clear that they must be very important given the dire consequences of damage to them. To destroy the thalamus is to kill; a person cannot live without a thalamus although people and other animals can do quite well without major chunks of cortex.

What are the 7 functions of the hypothalamus? ›

While it's very small, the hypothalamus plays a crucial role in many important functions, including:
  • releasing hormones.
  • maintaining daily physiological cycles.
  • controlling appetite.
  • managing sexual behavior.
  • regulating emotional responses.
  • regulating body temperature.
Mar 21, 2018

Which hypothalamic nuclei is related to memory? ›

The mamillary nucleus contributes to the limbic system as part of the Papez circuit. It is also involved in memory formation and controls exploratory behavior.

How do you reset your hypothalamus naturally? ›

Natural Ways to Boost Hypothalamus Function
  1. Increase Chromium Intake. Chromium is a trace mineral needed by the body in small amounts for healthy functioning. ...
  2. Use Essential Oils. ...
  3. Try Vitex (Especially If You're a Woman) ...
  4. Eat Healthy Fats. ...
  5. Get Enough Sleep and Reduce Stress. ...
  6. Exercise Regularly.
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