Role of the medial prefrontal cortex in N-methyl-d-aspartate receptor antagonist induced sensorimotor gating deficit in rats

2004 ◽  
Vol 355 (1-2) ◽  
pp. 5-8 ◽  
Author(s):  
K. Schwabe ◽  
M. Koch
Keyword(s):  
Prefrontal Cortex ◽  
Receptor Antagonist ◽  
Medial Prefrontal Cortex ◽  
Sensorimotor Gating ◽  
Aspartate Receptor

scholarly journals Activation of GABAA receptors in the medial prefrontal cortex produces an anxiolytic-like response

2013 ◽  
Vol 25 (4) ◽  
pp. 221-226 ◽  
Author(s):  
Jalal Solati ◽  
Ramin Hajikhani ◽  
Yulia Golub
Keyword(s):  
Prefrontal Cortex ◽  
Receptor Antagonist ◽  
Medial Prefrontal Cortex ◽  
Gabaa Receptors ◽  
Receptor Agonist ◽  
Elevated Plus Maze ◽  
Elevated Plus Maze Test ◽  
Maze Test ◽  
Plus Maze

ObjectivesThere has been increasing evidence that the γ-aminobutyric acid (GABA)ergic system is involved in the neurobiology of anxiety. The present study aimed to investigate the role of GABAergic systems in the modulation of anxiety in the medial prefrontal cortex (mPFC) of rats using the elevated plus maze test.MethodsRats were anaesthetised with a mixture of ketamine and xylazine, and then special cannulae were inserted stereotaxically into the mPFC. After 5–7 days of recovery, the effects of intra-mPFC administration of GABAergic agents were studied.ResultsBilateral injection of the GABAA receptor agonist muscimol (0.25, 0.5 and 1 μg/rat) produces an anxiolytic-like effect, shown by significant increases in the percentage of open-arm time (%OAT) and percentage of open-arm entries (%OAE). Intra-mPFC administration of the GABAA receptor antagonist bicuculline (0.25, 0.5 and 1 μg/rat) produces significant anxiogenic-like behaviour. However, intra-mPFC injection of the GABAB receptor agonist baclofen (0.05, 0.1 and 0.2 μg/rat) and the GABAB receptor antagonist CGP35348 (5, 10 and 15 μg/rat) did not alter %OAT and %OAE significantly.ConclusionThe results of the present study demonstrate that the GABAergic system of the mPFC modulates anxiety-related behaviours of rats through GABAA receptors.

P3-411: THE 5-HT6 RECEPTOR ANTAGONIST LU AE58054 ALONE AND IN COMBINATION WITH DONEPEZIL POTENTIATES GAMMA OSCILLATIONS IN RAT MEDIAL PREFRONTAL CORTEX

2014 ◽  
Vol 10 ◽  
pp. P780-P781 ◽  
Author(s):  
Maria Amat Foraster ◽  
Kjartan Frisch Herrik ◽  
Nelly Richard ◽  
Jesper Frank Bastlund ◽  
Inge E.M. de Jong ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Receptor Antagonist ◽  
Medial Prefrontal Cortex ◽  
Gamma Oscillations

Amyloid-β Protein Precursor Deficiency Changes Neuronal Electrical Activity and Levels of Mitochondrial Proteins in the Medial Prefrontal Cortex

2021 ◽  
pp. 1-14
Author(s):  
Qingwei Huo ◽  
Sidra Tabassum ◽  
Ming Chen ◽  
Mengyao Sun ◽  
Yueming Deng ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Amyloid Β ◽  
Neuronal Firing ◽  
Mitochondrial Proteins ◽  
Amyloid Β Protein ◽  
Protein Precursor ◽  
Β Protein ◽  
Neuronal Electrical Activity

Background: Neuropathological features of Alzheimer’s disease are characterized by the deposition of amyloid-β (Aβ) plaques and impairments in synaptic activity and memory. However, we know little about the physiological role of amyloid-β protein precursor (AβPP) from which Aβ derives. Objective: Evaluate APP deficiency induced alterations in neuronal electrical activity and mitochondrial protein expression. Methods: Utilizing electrophysiological, biochemical, pharmacological, and behavioral tests, we revealed aberrant local field potential (LFP), extracellular neuronal firing and levels of mitochondrial proteins. Result: We show that APP knockout (APP -/- ) leads to increased gamma oscillations in the medial prefrontal cortex (mPFC) at 1-2 months old, which can be restored by baclofen (Bac), a γ-aminobutyric acid type B receptor (GABABR) agonist. A higher dose and longer exposure time is required for Bac to suppress neuronal firing in APP -/-  mice than in wild type animals, indicating enhanced GABABR mediated activity in the mPFC of APP -/-  mice. In line with increased GABABR function, the glutamine synthetase inhibitor, L-methionine sulfonate, significantly increases GABABR levels in the mPFC of APP -/-  mice and this is associated with a significantly lower incidence of death. The results suggest that APP -/-  mice developed stronger GABABR mediated inhibition. Using HEK 293 as an expression system, we uncover that AβPP functions to suppress GABABR expression. Furthermore, APP -/-  mice show abnormal expression of several mitochondrial proteins. Conclusion: APP deficiency leads to both abnormal network activity involving defected GABABR and mitochondrial dysfunction, suggesting critical role of AβPP in synaptic and network function.

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