scholarly journals Mild Traumatic Brain Injury Reduces Spine Density of Projection Neurons in the Medial Prefrontal Cortex and Impairs Extinction of Contextual Fear Memory

2018 ◽  
Vol 35 (1) ◽  
pp. 149-156 ◽  
Author(s):  
Jing Zhao ◽  
Jonathan Huynh ◽  
Michael J. Hylin ◽  
John J. O'Malley ◽  
Alec Perez ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Brain Injury ◽  
Medial Prefrontal Cortex ◽  
Mild Traumatic Brain Injury ◽  
Fear Memory ◽  
Projection Neurons ◽  
Spine Density ◽  
Contextual Fear ◽  
Contextual Fear Memory

scholarly journals Parvalbumin-positive interneurons mediate neocortical-hippocampal interactions that are necessary for memory consolidation

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Frances Xia ◽  
Blake A Richards ◽  
Matthew M Tran ◽  
Sheena A Josselyn ◽  
Kaori Takehara-Nishiuchi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Fear Conditioning ◽  
Medial Prefrontal Cortex ◽  
Memory Consolidation ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Spiking Activity

Following learning, increased coupling between spindle oscillations in the medial prefrontal cortex (mPFC) and ripple oscillations in the hippocampus is thought to underlie memory consolidation. However, whether learning-induced increases in ripple-spindle coupling are necessary for successful memory consolidation has not been tested directly. In order to decouple ripple-spindle oscillations, here we chemogenetically inhibited parvalbumin-positive (PV+) interneurons, since their activity is important for regulating the timing of spiking activity during oscillations. We found that contextual fear conditioning increased ripple-spindle coupling in mice. However, inhibition of PV+ cells in either CA1 or mPFC eliminated this learning-induced increase in ripple-spindle coupling without affecting ripple or spindle incidence. Consistent with the hypothesized importance of ripple-spindle coupling in memory consolidation, post-training inhibition of PV+ cells disrupted contextual fear memory consolidation. These results indicate that successful memory consolidation requires coherent hippocampal-neocortical communication mediated by PV+ cells.

Hippocampus and Prefrontal Cortex Modulation of Contextual Fear Memory Is Dissociated by Inhibiting De Novo Transcription During Late Consolidation

2019 ◽  
Vol 56 (8) ◽  
pp. 5507-5519 ◽  
Author(s):  
Luciana M. Pereira ◽  
Caio M. de Castro ◽  
Lorena T. L. Guerra ◽  
Thaís M. Queiroz ◽  
João T. Marques ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
De Novo ◽  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory

scholarly journals Aggression, DRD1 polymorphism, and lesion location in penetrating traumatic brain injury

CNS Spectrums ◽  
2014 ◽  
Vol 19 (5) ◽  
pp. 382-390 ◽  
Author(s):  
Matteo Pardini ◽  
Frank Krueger ◽  
Colin A. Hodgkinson ◽  
Vanessa Raymont ◽  
Maren Strenziok ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Brain Injury ◽  
Dopamine Receptor ◽  
Medial Prefrontal Cortex ◽  
Dopaminergic System ◽  
Lateral Prefrontal Cortex ◽  
Lesion Location ◽  
Comt Val158met ◽  
The Relationship

ObjectiveThis study evaluated whether structural brain lesions modulate the relationship between pathological aggression and the dopaminergic system in traumatic brain injury (TBI). While converging evidence suggests that different areas of the prefrontal cortex modulate dopaminergic activity, to date no evidence exists of a modulation of endogenous dopaminergic tone by lesion localization in penetrating TBI (pTBI).MethodsThis study included 141 male Caucasian veterans who suffered penetrating pTBI during their service in Vietnam and 29 healthy male Caucasian Vietnam veterans. Participants were genotyped for 3 functional single nucleotide polymorphisms (SNPs): dopamine receptor D1 (DRD1) rs686, dopamine receptor D2 (DRD2) rs4648317, and catechol-O-methyltransferase (COMT) Val158Met. Patients underwent brain CT scans and were divided into medial prefrontal cortex, lateral prefrontal cortex, and posterior cortex lesion groups. Long-term aggression levels were evaluated with the agitation/aggression subscale of the Neuropsychiatric Inventory.ResultsOur data showed that carriers of more transcriptionally active DRD1 alleles compared to noncarriers demonstrated greater aggression levels due to medial prefrontal cortex lesions but reduced aggression levels due to lateral prefrontal cortex lesions independently of DRD2 rs4648317 or COMT Val158Met genotypes.ConclusionsOur results suggest that the relationship between pTBI-related aggression and the dopaminergic system is modulated by lesion location. Potentially lesion location could represent an easy-to-use, widely available, para-clinical marker to help in the development of an individualized therapeutic approach to pTBI-related pathological aggression.

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