scholarly journals Glutamate as a Stressoric Factor for the Ex Vivo Release of Catecholamines from the Rabbit Medial Prefrontal Cortex (mPFC)

Life ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1386
Author(s):  
Bogdan Feliks Kania ◽  
Danuta Wrońska ◽  
Izabela Szpręgiel ◽  
Urszula Bracha
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Ex Vivo ◽  
Inhibitory Effect ◽  
Nerve Fibers ◽  
Excitatory Neurotransmitter ◽  
Memory Processing ◽  
Sympathetic Nerve Fibers ◽  
The Central Nervous System ◽  
Emotion Memory

One of the major roles of glutamic acid (Glu) is to serve as an excitatory neurotransmitter within the central nervous system (CNS). This amino acid influences the activity of several brain areas, including the thalamus, brainstem, spinal cord, basal ganglia, and pons. Catecholamines (CAs) are synthesized in the brain and adrenal medulla and by some sympathetic nerve fibers. CAs, including dopamine (DA), norepinephrine (NE), and epinephrine (E), are the principal neurotransmitters that mediate a variety of CNS functions, such as motor control, cognition, emotion, memory processing, pain, stress, and endocrine modulation. This study aims to investigate the effects of the application of various Glu concentrates (5, 50, and 200 µM) on CAs release from rabbit medial prefrontal cortex (mPFC) slices and compare any resulting correlations with CAs released from the hypothalamus during 90 min of incubation. Medial prefrontal cortex samples were dissected from decapitated, twelve-week-old female rabbits. The results demonstrated that Glu differentially influences the direct release of CAs from the mPFC and the indirect release of CAs from the hypothalamus. When under stress, the hypothalamus, a central brain structure of the HPA axis, induces and adapts such processes. Generally, there was an inhibitory effect of Glu on CAs release from mPFC slices. Our findings show that the effect arises from Glu’s action on higher-order motivational structures, which may indicate its contribution to the stress response by modulating the amount of CAs released.

Medial prefrontal cortex oxytocin-opioid receptors interaction in spatial memory processing in rats

2019 ◽  
Vol 209 ◽  
pp. 112599 ◽  
Author(s):  
Reza Salighedar ◽  
Amir Erfanparast ◽  
Esmaeal Tamaddonfard ◽  
Farhad Soltanalinejad
Keyword(s):  
Prefrontal Cortex ◽  
Spatial Memory ◽  
Medial Prefrontal Cortex ◽  
Opioid Receptors ◽  
Memory Processing

scholarly journals Myocardial infarction sensitizes medial prefrontal cortex to inhibitory effect of locus coeruleus stimulation in rats

2016 ◽  
Vol 233 (13) ◽  
pp. 2581-2592 ◽  
Author(s):  
Jaimee Glasgow ◽  
Yevgeniya Koshman ◽  
Allen M. Samarel ◽  
Kuei Y. Tseng ◽  
Karie Scrogin
Keyword(s):  
Myocardial Infarction ◽  
Prefrontal Cortex ◽  
Locus Coeruleus ◽  
Medial Prefrontal Cortex ◽  
Inhibitory Effect

scholarly journals Rostral and caudal BLA engage distinct circuits in the prelimbic and infralimbic PFC

2021 ◽  
Author(s):  
Kasra Manoocheri ◽  
Adam G Carter
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Basolateral Amygdala ◽  
Pyramidal Tract ◽  
Ex Vivo ◽  
Layer 2 ◽  
Deep Layers ◽  
Local Circuits ◽  
Whole Cell Recordings

Connections from the basolateral amygdala (BLA) to medial prefrontal cortex (PFC) regulate memory and emotion and become disrupted in neuropsychiatric disorders. We hypothesized that the diverse roles attributed to interactions between the BLA and PFC reflect multiple circuits nested within a wider network. To assess these circuits, we first used anatomy to show that the rostral BLA (rBLA) and caudal BLA (cBLA) differentially project to prelimbic (PL) and infralimbic (IL) subregions of the PFC, respectively. We then combined in vivo silicon probe recordings and optogenetics to show that rBLA primarily engages PL, whereas cBLA mainly influences IL. Using ex vivo whole-cell recordings and optogenetics, we then assessed which neuronal subtypes are targeted, showing that rBLA preferentially drives layer 2 (L2) cortico-amygdalar (CA) neurons in PL, whereas cBLA drives layer 5 (L5) pyramidal tract (PT) cells in IL. Lastly, we used soma-tagged optogenetics to explore the local circuits linking superficial and deep layers of PL, showing how rBLA can also impact L5 PT cells. Together, our findings delineate how subregions of the BLA target distinct networks within the PFC to have different influence on prefrontal output.

scholarly journals Inhibitory effect of clonidine on ketamine-induced norepinephrine release from the medial prefrontal cortex in rats

1999 ◽  
Vol 83 (6) ◽  
pp. 945-947 ◽  
Author(s):  
T. Kubota ◽  
K. Hirota ◽  
H. Yoshida ◽  
S. Takahashi ◽  
H. Ohkawa ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Inhibitory Effect ◽  
Norepinephrine Release

scholarly journals Corticotropin Releasing Factor Type 1 and 2 Receptor Signaling in the Medial Prefrontal Cortex Modulates Binge-Like Ethanol Consumption in C57BL/6J Mice

2019 ◽  
Vol 9 (7) ◽  
pp. 171 ◽  
Author(s):  
Stacey L. Robinson ◽  
Carlos A. Perez-Heydrich ◽  
Todd E. Thiele
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Ethanol Consumption ◽  
Inhibitory Effect ◽  
Ethanol Intake ◽  
Corticotropin Releasing Factor ◽  
Factor Type ◽  
Drinking In The Dark

Corticotropin releasing factor (CRF) signaling via limbic CRF1 and 2 receptors (CRF1R and CRF2R, respectively) is known to modulate binge-like ethanol consumption in rodents. Though CRF signaling in the medial prefrontal cortex (mPFC) has been shown to modulate anxiety-like behavior and ethanol seeking, its role in binge ethanol intake is unknown. Here, we used “drinking-in-the-dark” (DID) procedures in male and female C57BL/6J mice to address this gap in the literature. First, the role of CRF1R and CRF2R signaling in the mPFC on ethanol consumption was evaluated through site-directed pharmacology. Next, we evaluated if CRF1R antagonist reduction of binge-intake was modulated in part through CRF2R activation by co-administration of a CRF1R and CRF2R antagonist. Intra-mPFC inhibition of CRF1R and activation of CRF2R resulted in decreased binge-like ethanol intake. Further, the inhibitory effect of the CRF1R antagonist was attenuated by co-administration of a CRF2R antagonist. We provide novel evidence that (1) inhibition of CRF1R or activation of CRF2R in the mPFC reduces binge-like ethanol intake; and (2) the effect of CRF1R antagonism may be mediated via enhanced CRF2R activation. These observations provide the first direct behavioral pharmacological evidence that CRF receptor activity in the mPFC modulates binge-like ethanol consumption.

scholarly journals Presynaptic HCN channels constrain GABAergic synaptic transmission in pyramidal cells of the medial prefrontal cortex

2021 ◽  
Author(s):  
Wei Cai ◽  
Shu-Su Liu ◽  
Bao-Ming Li ◽  
Xue-Han Zhang
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Pyramidal Cells ◽  
Intrinsic Excitability ◽  
High Dose ◽  
Hcn Channels ◽  
Gabaergic Interneurons ◽  
Facilitation Effect ◽  
Basket Cells ◽  
The Central Nervous System

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are widely expressed in neurons in the central nervous system. It has been documented that HCN channels regulate the intrinsic excitability of pyramidal cells in the medial prefrontal cortex (mPFC) of rats. Here, we report that HCN channels limited GABAergic transmission onto pyramidal cells in the mPFC. Pharmacological block of HCN channels resulted in a significant increase in the frequency of both spontaneous and miniature inhibitory postsynaptic currents (IPSCs) in mPFC pyramidal cells. Such facilitation effect on mIPSCs required presynaptic Ca2+ influx and reversed by high-dose cAMP. Such facilitation did not exist in the presence of the T-type Ca2+ channel selective blockers. Immunofluorescence staining revealed that HCN channels expressed in presynaptic GABAergic terminals, as well as in both soma and neurite of parvalbumin-expressing (PV-expressing) basket cells in the mPFC. The present results indicate that HCN channels in GABAergic interneurons, most likely PV-expressing basket cells, constrain inhibitory control over layer 5-6 pyramidal cells through restricting presynaptic Ca2+ entry.

scholarly journals Input-specific regulation of glutamatergic synaptic transmission in the medial prefrontal cortex by mGlu2/mGlu4 receptor heterodimers

2021 ◽  
Vol 14 (677) ◽  
pp. eabd2319
Author(s):  
Zixiu Xiang ◽  
Xiaohui Lv ◽  
Xin Lin ◽  
Daniel E. O’Brien ◽  
Molly K. Altman ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Metabotropic Glutamate Receptors ◽  
Ex Vivo ◽  
Metabotropic Glutamate ◽  
Excitatory Transmission ◽  
Glutamatergic Synaptic Transmission ◽  
Glutamatergic Signaling ◽  
Specific Regulation ◽  
G Protein Coupled

Metabotropic glutamate receptors (mGluRs) are G protein–coupled receptors that regulate various aspects of central nervous system processing in normal physiology and in disease. They are thought to function as disulfide-linked homodimers, but studies have suggested that mGluRs can form functional heterodimers in cell lines. Using selective allosteric ligands, ex vivo brain slice electrophysiology, and optogenetic approaches, we found that two mGluR subtypes—mGluR2 and mGluR4 (or mGlu2 and mGlu4)—exist as functional heterodimers that regulate excitatory transmission in a synapse-specific manner within the rodent medial prefrontal cortex (mPFC). Activation of mGlu2/mGlu4 heterodimers inhibited glutamatergic signaling at thalamo-mPFC synapses but not at hippocampus-mPFC or amygdala-mPFC synapses. These findings raise the possibility that selectively targeting these heterodimers could be a therapeutic strategy for some neurologic and neuropsychiatric disorders involving specific brain circuits.

scholarly journals Presynaptic HCN channels constrain GABAergic synaptic transmission in pyramidal cells of the medial prefrontal cortex

Biology Open ◽  
2021 ◽  
Author(s):  
Wei Cai ◽  
Shu-Su Liu ◽  
Bao-Ming Li ◽  
Xue-Han Zhang
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Pyramidal Cells ◽  
Intrinsic Excitability ◽  
Hcn Channels ◽  
Gabaergic Interneurons ◽  
Facilitation Effect ◽  
Basket Cells ◽  
The Central Nervous System ◽  
Pharmacological Blockade

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are widely expressed in neurons in the central nervous system. It has been documented that HCN channels regulate the intrinsic excitability of pyramidal cells in the medial prefrontal cortex (mPFC) of rodents. Here, we report that HCN channels limited GABAergic transmission onto pyramidal cells in rat mPFC. The pharmacological blockade of HCN channels resulted in a significant increase in the frequency of both spontaneous and miniature inhibitory postsynaptic currents (IPSCs) in mPFC pyramidal cells, whereas potentiation of HCN channels reversely decreases the frequency of mIPSCs. Furthermore, such facilitation effect on mIPSC frequency required presynaptic Ca2+ influx. Immunofluorescence staining showed that HCN channels expressed in presynaptic GABAergic terminals, as well as in both soma and neurite of parvalbumin-expressing (PV-expressing) basket cells in mPFC. The present results indicate that HCN channels in GABAergic interneurons, most likely PV-expressing basket cells, constrain inhibitory control over layer 5-6 pyramidal cells by restricting presynaptic Ca2+ entry.

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