Dissociation of Spatial-, Object-, and Sound-Coding Neurons in the Mediodorsal Nucleus of the Primate Thalamus

2003 ◽  
Vol 89 (2) ◽  
pp. 1067-1077 ◽  
Author(s):  
Ikuo Tanibuchi ◽  
Patricia S. Goldman-Rakic

The mediodorsal nucleus (MD) is the thalamic gateway to the prefrontal cortex, an area of the brain associated with spatial and object working memory functions. We have recorded single-neuron activities from the MD nucleus in monkeys trained to perform spatial tasks with peripheral visual stimuli and a nonspatial task with foveally presented pictures of objects and faces—tasks identical to those we have previously used to map regional specializations in the dorso- and ventro-lateral prefrontal cortex, respectively. We found that MD neurons exhibited categorical specificity—either responding selectively to locations in the spatial tasks or preferentially to specific representations of faces and objects in the nonspatial task. Spatially tuned neurons were located in parts of the MD connected with the dorsolateral prefrontal cortex while neurons responding to the identity of stimuli mainly occupied more ventral positions in the nucleus that has its connections with the inferior prefrontal convexity. Neuronal responses to auditory stimuli were also examined, and vocalization sensitive neurons were found in more posterior portions of the MD. We conclude that MD neurons are dissociable by their spatial and nonspatial coding properties in line with their cortical connections and that the principle of information segregation in cortico-cortical pathways extends to the “association” nuclei of the thalamus.

2016 ◽  
Vol 113 (52) ◽  
pp. E8492-E8501 ◽  
Author(s):  
Roland G. Benoit ◽  
Daniel J. Davies ◽  
Michael C. Anderson

Imagining future events conveys adaptive benefits, yet recurrent simulations of feared situations may help to maintain anxiety. In two studies, we tested the hypothesis that people can attenuate future fears by suppressing anticipatory simulations of dreaded events. Participants repeatedly imagined upsetting episodes that they feared might happen to them and suppressed imaginings of other such events. Suppressing imagination engaged the right dorsolateral prefrontal cortex, which modulated activation in the hippocampus and in the ventromedial prefrontal cortex (vmPFC). Consistent with the role of the vmPFC in providing access to details that are typical for an event, stronger inhibition of this region was associated with greater forgetting of such details. Suppression further hindered participants’ ability to later freely envision suppressed episodes. Critically, it also reduced feelings of apprehensiveness about the feared scenario, and individuals who were particularly successful at down-regulating fears were also less trait-anxious. Attenuating apprehensiveness by suppressing simulations of feared events may thus be an effective coping strategy, suggesting that a deficiency in this mechanism could contribute to the development of anxiety.


e-Neuroforum ◽  
2018 ◽  
Vol 24 (1) ◽  
pp. A11-A18
Author(s):  
Sabine Windmann ◽  
Grit Hein

Abstract Altruism is a puzzling phenomenon, especially for Biology and Economics. Why do individuals reduce their chances to provide some of the resources they own to others? The answer to this question can be sought at ultimate or proximate levels of explanation. The Social Neurosciences attempt to specify the brain mechanisms that drive humans to act altruistically, in assuming that overtly identical behaviours can be driven by different motives. The research has shown that activations and functional connectivities of the Anterior Insula and the Temporoparietal Junction play specific roles in empathetic versus strategic forms of altruism, whereas the dorsolateral prefrontal cortex, among other regions, is involved in norm-oriented punitive forms of altruism. Future research studies could focus on the processing of ambiguity and conflict in pursuit of altruistic intentions.


1997 ◽  
Vol 170 (2) ◽  
pp. 134-139 ◽  
Author(s):  
Ross M. G. Norman ◽  
A. K. Malla ◽  
S. L. Morrison-Stewart ◽  
E. Helmes ◽  
P. C. Williamson ◽  
...  

BackgroundOn the basis of Liddle's three-syndrome model of schizophrenia, it was predicted that: (1) symptoms of psychomotor poverty would be particularly correlated with impaired performance on neuropsychological tests likely to reflect functioning of the dorsolateral prefrontal cortex; (2) disorganisation would be particularly correlated with impaired performance on tests sensitive to medio-basal prefrontal functioning; and (3) reality distortion would be particularly correlated with measures sensitive to temporal lobe functioning.MethodThe above hypotheses were tested on 87 subjects with a confirmed diagnosis of schizophrenia. Patients' symptoms were scored for each of the three syndromes. Patients completed six neuropsychological tests designed to measure impairment in specific areas of the brain.ResultsThere was no support for the first two hypotheses. There was, however, evidence of a specific relationship between reality distortion and neuropsychological performance usually considered to be related to left temporal lobe functioning.ConclusionsAlthough not directly supporting the first two hypotheses; the results are, in general, consistent with there being different cortical-subcortical circuits associated with each of psychomotor poverty and disorganisation. Temporal lobe functioning appears to have particular significance for the reality distortion syndrome.


2021 ◽  
Vol 10 ◽  
pp. 2016
Author(s):  
Ali Zare ◽  
Alireza Ghanbari ◽  
Mohammad Javad Hoseinpour ◽  
Mahdi Eskandarian Boroujeni ◽  
Alimohammad Alimohammadi ◽  
...  

Background: Methamphetamine (MA), is an extremely addictive stimulant that adversely affects the central nervous system. Accumulating evidence indicates that molecular mechanisms such as oxidative stress, apoptosis, and autophagy are involved in the toxicity of MA. Considering experimental animal studies exhibiting MA-induced neurotoxicity, the relevance of these findings needs to be evidently elucidated in human MA users. It is generally assumed that multiple chemical substances released in the brain following MA-induced metabolic activation are primary factors underlying damage of neural cells. Hence, this study aimed to investigate the role of autophagy and apoptosis as well as oxidative stress in the brain of postmortem MA-induced toxicity. Materials and Methods: In this study, we determine the gene expression of autophagy and apoptosis, including BECN1, MAP1ALC3, CASP8, TP53, and BAX genes in ten healthy controls and ten chronic users of MA postmortem dorsolateral prefrontal cortex (DLPFC) by real-time polymerase chain reaction. Also, we applied immunohistochemistry in formalin-fixed and paraffin-embedded human brain samples to analyze brain-derived neurotrophic factor (BDNF). Also, spectrophotometry was performed to measure glutathione (GSH) content. Results: The expression level of apoptotic and autophagic genes (BECN1, MAP1ALC3, CASP8, TP53, and BAX) were significantly elevated, while GSH content and BDNF showed substantial reductions in DLPFC of chronic MA users. Discussion: Our data showed that MA addiction provokes transduction pathways, namely apoptosis and autophagy, along with oxidative mechanisms in DLPFC. Also, MA induces multiple functional and structural perturbations in the brain, determining its toxicity and possibly contributing to neurotoxicity. [GMJ.2021;10:e2016]


2020 ◽  
Author(s):  
Shahan Mamoor

We used public and published microarray data (1, 2) to identify the most significant gene expression changes in the brains of patients with psychotic disorders. We identified the 𝛄-aminobutyric acid receptor-associated protein-like 1 GABARAPL13 as differentially expressed in the dorsolateral prefrontal cortex of patients with schizophrenia as well as in the parvalbumin-positive layer 3 neurons of the dorsolateral prefrontal cortex of patients with schizophrenia and schizoaffective disorder. The brain tissues of patients with psychotic disorders expressed significantly lower levels of GABARAPL1 than that of non-affected control subjects. GABARAPL1 may be relevant to the biology of schizophrenia and related psychotic disorders.


2018 ◽  
Vol 29 (10) ◽  
pp. 4154-4168 ◽  
Author(s):  
Lisa Marieke Kluen ◽  
Lisa Catherine Dandolo ◽  
Gerhard Jocham ◽  
Lars Schwabe

Abstract Updating established memories in light of new information is fundamental for memory to guide future behavior. However, little is known about the brain mechanisms by which existing memories can be updated. Here, we combined functional magnetic resonance imaging and multivariate representational similarity analysis to elucidate the neural mechanisms underlying the updating of consolidated memories. To this end, participants first learned face–city name pairs. Twenty-four hours later, while lying in the MRI scanner, participants were required to update some of these associations, but not others, and to encode entirely new pairs. Updating success was tested again 24 h later. Our results showed increased activity of the dorsolateral prefrontal cortex (dlPFC) specifically during the updating of existing associations that was significantly stronger than when simple retrieval or new encoding was required. The updating-related activity of the dlPFC and its functional connectivity with the hippocampus were directly linked to updating success. Furthermore, neural similarity for updated items was markedly higher in the dlPFC and this increase in dlPFC neural similarity distinguished individuals with high updating performance from those with low updating performance. Together, these findings suggest a key role of the dlPFC, presumably in interaction with the hippocampus, in the updating of established memories.


2020 ◽  
Author(s):  
Shahan Mamoor

We used public and published microarray data (1, 2) to identify the most significant gene expression changes in the brains of patients with psychotic disorders. We identified PRDX53 as differentially expressed in the dorsolateral prefrontal cortex of patients with schizophrenia as well as in the parvalbumin-positive layer 3 neurons of the dorsolateral prefrontal cortex of patients with schizophrenia and schizoaffective disorder. The brain tissues of patients with psychotic disorders expressed significantly lower levels of PRDX5 than that of non-affected control subjects. PRDX5 may be relevant to the biology of schizophrenia and related psychotic disorders.


2021 ◽  
Vol 6 (6) ◽  

Although we have established effective treatments for anxiety disorders,the problem is on the rise worldwide, and the effect sizesfor treatments suggest that advancements are needed. Part of the reason for the limitations in our treatments may be because they are designed to address the disorder’s symptoms rather than its underlying cause. This paper is geared toward presenting a likely neurobiological cause and a proposed treatment. There is significant evidence that the basis for anxiety is a combination of stress, especially interpersonal stress, and an inability to find solutions to resolve it. Anxiety is the result of this lack of coping ability. The part of the brain involved in designing these coping strategies, especially when the stressor is complex and emotion-based, is the dorsolateral prefrontal cortex. That is because it is the brain’s “sketch pad,” in that it allows us to think of solutions on a “symbolic” rather than a concrete basis.Anxiety arises when the person is unable to use this brain region effectively in formulating solutions, and instead designs ineffective solutions. The reason for that deficit may stem from early childhood, during a phase of attachment in which parents do not engage spontaneously in child-induced play. The mother is unable to be spontaneous in sharing the child’s play,which is needed for the child to generate his or her own solutions to problems. This leads to an inability of the child’s dorsolateral prefrontal cortex structure to properly develop. This will manifest as a lack of “insight,” or ability to generate spontaneous solutions to problems instead focusing on routinized solutions to emotion-based problems later in life that often do not work. Evidence is provided in a case report of a patient with an anxiety disorder who could not solve his interpersonal problems because he lacked the necessary insight. This deficit was so profound that he could not use insight-based psychotherapy and found use of medication too sedating. By modelling a more spontaneous give and take between the therapist and the patient’s wife, who served as a “co-therapist,”the patient was able to learn to develop his own insight. His wife would tell the therapist the problems the patient was unable to tell him and would help the patient to learn to respond to the interpretations offered by the therapist. The patient learned how to imitate his wife and describe his problems, and then to imitate the therapist and generate his own insight. As this occurred, his anxiety was resolved. The basis of the attachment that developed with his therapists was based on the use of spontaneity, from which the patient learned his own insights resolving his anxiety.


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