Morphological, structural, and functional alterations of the prefrontal cortex and the basolateral amygdala after early lesion of the rat mediodorsal thalamus

Ouhaz, Zakaria; Ba‐M’hamed, Saadia; Bennis, Mohamed

doi:10.1007/s00429-016-1354-2

Cited by 19 publications

(22 citation statements)

References 111 publications

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“…Our results clearly demonstrated that early TRN lesions induce a decrease in the number of C‐Fos positive neurons in all PFC subregions. These results are in accordance with our previous study showing a significant decrease in the basal levels of C‐Fos expression in the PFC after early MD lesions performed at P4 (Ouhaz, Ba‐M'hamed, & Bennis, ).…”

Section: Discussionsupporting

confidence: 93%

“…The present results show for the first time that early postnatal TRN lesions in Sprague Dawley rats reduce the performance of the animals during the object recognition test. These findings mimic the effect of early lesions of MD reported by Ouhaz et al (). We suggest that the deficit reported in our TRN lesion rats is induced by the early damage of TRN, conducting to the disruption of thalamocortical–corticothalamic projections during this critical phase of brain maturation.…”

Section: Discussionsupporting

confidence: 90%

“…They showed that dopaminergic deafferentation of the TRN using 6‐OHDA in adult rats had anxiolytic‐like effects in the plus maze (Pellow, Chopin, File, & Briley, ; Pellow & File, ) and burying behavior tests (Treit, ; TreitTerlecki & Pinel, ). However, these results seem to echo those obtained following early MD lesions performed at P4 (Ouhaz et al, , ). Since TRN and MD are reciprocally connected (Cornwall & Phillipson, ), TRN is in a key position to modulate the interaction between MD and the PFC, a circuit critically involved in fear‐related behavior (Chauveau, Celerier, Ognard, Pierard, & Beracochea, ).…”

Section: Discussionsupporting

confidence: 84%

“…Previous studies from our group have shed light on the importance of early MD‐PFC reciprocal connections in the post‐natal development, maturation, and functioning of the PFC (Ouhaz et al, , ). Interestingly, Mitrofanis and Guillery () suggested that TRN has a major developmental function by providing pioneering axons to the thalamus to guide later developing corticothalamic and thalamocortical axons to the targets.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, Ouhaz, Ba‐M'hamed, Mitchell, Elidrissi, and Bennis (, ) devised an animal model to test the long‐term effects of early developmental insult to MD on the onset of changes in behavior and in some domains of cognition. MD lesions were conducted on the day P4, which coincides with the time window when afferent and efferent connections are forming between the MD and PFC (van Eden, ).…”

Section: Introductionmentioning

confidence: 99%

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Early lesion of the reticular thalamic nucleus disrupts the structure and function of the mediodorsal thalamus and prefrontal cortex

Boukhari

Ouhaz

Ba‐M’hamed

et al. 2019

Developmental Neurobiology

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The thalamic reticular nucleus (TRN), part of the thalamus, is a thin GABAergic cell layer adjacent to the relay nuclei of the dorsal thalamus. It receives input from the cortex and other thalamic nuclei and provides major inhibitory input to each thalamic nucleus, particularly the mediodorsal nucleus (MD). As the MD is important for supporting optimal cortico-thalamo-cortical interactions during brain maturation, we hypothesized that that early damage to the TRN will cause major disturbances to the development and the functioning of the prefrontal cortex (PFC) and the MD. Rat pups at P4 were randomized in three groups: electrolytic lesion of TRN, TRN-shamlesion group, and the classical control group. Seven weeks later, all rats were tested with several behavioral and cognitive paradigms, and then perfused for histological and immunohistochemical studies. Results showed that TRN lesion rats exhibited reduced spontaneous activity, high level of anxiety, learning and recognition memory impairments. Besides the behavioral effects observed after early TRN lesions, our study showed significant cytoarchitectural and functional changes in the cingulate cortex, the dorsolateral and prelimbic subdivisions of the PFC, as well as in the MD.The assessment of the basal levels of neuronal activity revealed a significant reduction of the basal expression of C-Fos levels in the PFC. These experiments, which are the first to highlight the effects of early TRN lesions, provided evidence that early damage of the anterior part of the TRN leads to alterations that may control the development of the thalamocortical-corticothalamic pathways. K E Y W O R D S behavior, lesion, mediodorsal thalamus, prefrontal cortex, thalamic reticular nucleus 914 | EL BOUKHARI Et AL. | 915 EL BOUKHARI Et AL. How to cite this article: El Boukhari H, Ouhaz Z, Ba-M'hamed S, Bennis M. Early lesion of the reticular thalamic nucleus disrupts the structure and function of the mediodorsal thalamus and prefrontal cortex. Develop Neurobiol. 2019;79:913-933. https ://doi.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Early lesion of the reticular thalamic nucleus disrupts the structure and function of the mediodorsal thalamus and prefrontal cortex

Boukhari

Ouhaz

Ba‐M’hamed

et al. 2019

Developmental Neurobiology

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The Role of miR-150 in Stress-Induced Anxiety-Like Behavior in Mice

et al. 2018

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Stress plays a crucial role in several psychiatric disorders, including anxiety. However, the underlying mechanisms remain poorly understood. Here, we used acute stress (AS) and chronic restraint stress (CRS) models to develop anxiety-like behavior and investigate the role of miR-150 in the hippocampi of mice. Corticosterone levels as well as glutamate receptors in the hippocampus were evaluated. We found that anxiety-like behavior was induced after either AS or CRS, as determined by the open-field test (OFT) and elevated plus-maze test (EPM). Increased corticosterone levels were observed in the blood of AS and CRS groups, while the expression of miR-150 mRNA in the hippocampus was significantly decreased. The expressions of GluN2A, GluR1, GluR2, and V-Glut2 in the hippocampus were decreased after either AS or CRS. Hippocampal GAD67 expression was increased by AS but not CRS, and GluN2B expression was decreased by CRS but not AS. Adult miR-150 knockout mice showed anxiety-like behavior, as assessed by the OFT and EPM. The expressions of GluN2A, GluN2B, GluR1, and GluR2 were also downregulated, but the expression of V-Glut2 was upregulated in the hippocampi of miR-150 knockout mice compared with wild-type mice. Interestingly, we found that the miR-150 knockout mice showed decreased dendrite lengths, dendrite branchings, and numbers of dendrite spines in the hippocampus compared with wild-type mice. These results suggest that miR-150 may influence the synaptic plasticity of the hippocampus and play a significant role in stress-induced anxiety-like behavior in adult mice.

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