The thalamic reticular nucleus (TRN) is a GABAergic nucleus that encapsulates the entire thalamus and is the primary source of inhibition for the thalamus. The TRN’s extensive connection within the thalamocortical loop and physiological functions have led researchers to describe the TRN as a “guard” of the gateway for the flow of information. From attentional modulation to memory consolidation, the TRN has been demonstrated to play a central role in these cognitive functions. The disruption of these cognitive functions are commonly seen within neurodevelopmental disorders like schizophrenia with a growing amount of evidence linking the TRN as a potential candidate integral for the pathophysiology. Most studies focus on the physiological properties and functions of the TRN however, there are major gaps in our understanding of the organization and the connection between morphology, neurochemistry, and physiology within the TRN. In this study, we investigate the molecular composition and expression of calretinin and SMI-32 within the TRN in non-human primates, postmortem human controls, and postmortem schizophrenia patients. Calretinin and SMI-32 are both neuroproteins that have been identified in unique populations within the TRN however the neuronal characteristics of these subpopulations have yet to be explored. We conducted quantitative analysis to estimate the population, density, and distribution of these neurons as well as morphological characteristics in distinct TRN sectors. Additionally, we investigated whether the expression of calretinin and parvalbumin are found in isolated and/or overlapping populations and where those distributions are present. We observed that the TRN is a heterogenous structure with continuous variation in the distributions and densities of CR and SMI-32. The features between non-human primate and human TRN are generally consistent in distribution patterns however the human TRN was observed to have decreased neuronal density and increased neuron size. Additionally, we observed an increase in both neuronal size and density within schizophrenia potentially identifying a possible dysfunction within the thalamocortical loop. Together these results will help further our understanding and the distinction between normal and pathological physiology which is a prerequisite for building biologically plausible computational models of diseased brains. / 2025-05-30T00:00:00Z
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/46295 |
| Date | 30 May 2023 |
| Creators | Coughlin, Brandon |
| Contributors | Zikopoulos, Vasileios |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
| Rights | Attribution-NonCommercial-NoDerivatives 4.0 International, http://creativecommons.org/licenses/by-nc-nd/4.0/ |
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