NMDARs in prefrontal cortex – Regulation of synaptic transmission and plasticity

Banks, Paul J; Bashir, Zafar I.

doi:10.1016/j.neuropharm.2021.108614

Cited by 5 publications

(2 citation statements)

References 78 publications

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“…Thus, changes of activity within the hippocampus are implicated in a number of neurological and neuropsychiatric disorders, ranging from Alzheimer's disease and schizophrenia to addiction and seizures (Duman, 2014; Gondard et al, 2019; Olsen & Sheng, 2012; Small et al, 2011). Based on both clinical and animal studies, dysfunctions of the hippocampus can arise from an imbalance of the excitatory and inhibitory neuronal activities, which can ultimately cause diseases through deficits in hippocampal neurotransmission and plasticity, as well as altered local and long‐distance communications to other regions of the brain (Banks & Bashir, 2021; Belujon & Grace, 2017; Jacobson & Sapolsky, 1991; Li et al, 2015; Sigurdsson et al, 2010). Specifically, deviations from normal hippocampal neural activities represent misattribution of context and emotional valence, leading to symptoms typically associated with emotional disturbances, memory deficits and psychosis.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of 14‐3‐3 proteins increases the intrinsic excitability of mouse hippocampal CA1 pyramidal neurons

Logue,

Vilmont,

Zhang

et al. 2024

Eur J of Neuroscience

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Abstract14‐3‐3 proteins are a family of regulatory proteins that are abundantly expressed in the brain and enriched at the synapse. Dysfunctions of these proteins have been linked to neurodevelopmental and neuropsychiatric disorders. Our group has previously shown that functional inhibition of these proteins by a peptide inhibitor, difopein, in the mouse brain causes behavioural alterations and synaptic plasticity impairment in the hippocampus. Recently, we found an increased cFOS expression in difopein‐expressing dorsal CA1 pyramidal neurons, indicating enhanced neuronal activity by 14‐3‐3 inhibition in these cells. In this study, we used slice electrophysiology to determine the effects of 14‐3‐3 inhibition on the intrinsic excitability of CA1 pyramidal neurons from a transgenic 14‐3‐3 functional knockout (FKO) mouse line. Our data demonstrate an increase in intrinsic excitability associated with 14‐3‐3 inhibition, as well as reveal action potential firing pattern shifts after novelty‐induced hyperlocomotion in the 14‐3‐3 FKO mice. These results provide novel information on the role 14‐3‐3 proteins play in regulating intrinsic and activity‐dependent neuronal excitability in the hippocampus.

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Section: Introductionmentioning

confidence: 99%

Inhibition of 14‐3‐3 proteins increases the intrinsic excitability of mouse hippocampal CA1 pyramidal neurons

Logue,

Vilmont,

Zhang

et al. 2024

Eur J of Neuroscience

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show abstract

“…Although aging is a multifactorial process, several lines of evidence indicate that a hypofunction of NMDA receptors (NMDARs) contributes to age-related cognitive decline ( Clayton et al, 2002 ; Foster, 2007 ; Mostany et al, 2013 ; Kumar and Foster, 2019 ). NMDARs are critical in regulating activity-dependent synaptic plasticity and are involved in many cognitive functions ( Kuehl-Kovarik et al, 2000 ; Paoletti and Neyton, 2007 ; Forsyth et al, 2015 ; Bye and McDonald, 2019 ; Banks and Bashir, 2021 ). In addition to glutamate, NMDAR activation requires the binding of a co-agonist: glycine or D-serine ( Schell et al, 1995 ; Bergeron et al, 1998 ; Pollegioni and Sacchi, 2010 ; Cummings and Popescu, 2015 ; Guo et al, 2017 ; Bodner et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Aging-Associated Cognitive Decline is Reversed by D-Serine Supplementation

Nava-Gomez

Calero-Vargas

Higinio-Rodríguez

et al. 2022

eNeuro

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Brain aging is a natural process that involves structural and functional changes that lead to cognitive decline, even in healthy subjects. This detriment has been associated with NMDA receptor (NMDAR) hypofunction because of a reduction in the brain levels of D-serine, the endogenous NMDAR co-agonist. However, it is not clear whether D-serine supplementation could be used as an intervention to reduce or reverse age-related brain alterations. In the present work, we aimed to analyze the D-serine effect on aging-associated alterations in cellular and large-scale brain systems that could support cognitive flexibility in rats. We found that D-serine supplementation reverts the age-related decline in cognitive flexibility, frontal dendritic spine density, and partially restored large-scale functional connectivity without inducing nephrotoxicity; instead, D-serine restored the thickness of the renal epithelial cells that were affected by age. Our results suggest that D-serine could be used as a therapeutic target to reverse age-related brain alterations.

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Activation of mediodorsal thalamic dopamine receptors inhibited nicotine-induced anxiety in rats: A possible role of corticolimbic NMDA neurotransmission and BDNF expression

Mousavi,

Rezayof,

Alijanpour

et al. 2023

Pharmacology Biochemistry and Behavior

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NMDARs in prefrontal cortex – Regulation of synaptic transmission and plasticity

Cited by 5 publications

References 78 publications

Inhibition of 14‐3‐3 proteins increases the intrinsic excitability of mouse hippocampal CA1 pyramidal neurons

Inhibition of 14‐3‐3 proteins increases the intrinsic excitability of mouse hippocampal CA1 pyramidal neurons

Aging-Associated Cognitive Decline is Reversed by D-Serine Supplementation

Activation of mediodorsal thalamic dopamine receptors inhibited nicotine-induced anxiety in rats: A possible role of corticolimbic NMDA neurotransmission and BDNF expression

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