Impairment of gabaa receptor function byn-methyl-d-aspartate-mediated calcium influx in isolated ca1 pyramidal cells
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How chronic administration of benzodiazepines leads to unexplained chronic illnesses: A hypothesis
2018, Medical HypothesesCitation Excerpt :In addition to all the mechanics of the NO/ONOO(−) cycle that Pall has set forth, it is proposed here that an additional effect may be connected to the cycle: down-regulation or reduced GABAA receptor function. As previously discussed, research has demonstrated that GABAA receptor functioning may be dependent on proper calcium homeostasis and showed that elevated calcium influx through L-type VGCC’s [25] and elevated calcium influx through the NMDA pore [28] both led to lower GABAA receptor functioning. And although only larger rises of intracellular calcium lower GABAA receptor functioning, whereas smaller rises have the opposite effect by potentiating GABAA receptors [27], the NO/ONOO(−) cycle may result in levels of intracellular calcium sufficient to inhibit GABAA receptor functioning.
Additive effect of BLA GABA<inf>A</inf> receptor mechanism and (+)-MK-801 on memory retention deficit, an isobologram analysis
2016, Pharmacology Biochemistry and BehaviorCitation Excerpt :One possible interpretation is that the action of NMDA receptors on the GABAA response is long-term (Kim et al., 2000). Another possibility is that NMDA receptors may consecutively reduce GABAA conductivity via phosphatase activation and/or intracellular dephosphorylation of GABAA receptors (Stelzer and Shi, 1994). This assumption is reinforced by a study showing that NMDA regulates the structure of mRNA coding for the GABAA δ-subunit (Gault and Siegel, 1998).
Major dorsoventral differences in the modulation of the local CA1 hippocampal network by NMDA, mGlu5, adenosine A<inf>2A</inf> and cannabinoid CB<inf>1</inf> receptors
2016, NeuroscienceCitation Excerpt :We found that exogenous activation of NMDARs reduces synaptic transmission and paired-pulse inhibition and increases postsynaptic excitability. Qualitatively, these effects are in keeping with previous observations having shown that activation of NMDARs suppresses excitatory synaptic transmission (Chernevskaya et al., 1991; Manzoni et al., 1994; Tebano et al., 2005), enhances neuronal excitability (Sah et al., 1989; Mor and Grossman, 2007) and reduces GABAergic inhibition (Stelzer and Shi, 1994; Chisari et al., 2012) in the network of hippocampal pyramidal cells. In addition, we found that the action of NMDARs in reducing synaptic transmission was stronger in VH than DH while the effects on postsynaptic excitability and paired-pulse inhibition were much higher in DH than VH.
Network beyond IDO in psychiatric disorders: Revisiting neurodegeneration hypothesis
2014, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :While one study has demonstrated the excitotoxic effect of QUIN on GABAergic neurons (Perez-De La Cruz et al., 2012) another group has demonstrated the disturbance of high KYNA on GABAergic neurotransmission to the pyramidal neurons of hippocampus (Banerjee et al., 2012). According to the documented literature regarding cross-transmitter receptor plasticity mediated changes in GABA transmission following glutamate signaling, although either potentiation or suppression is possible, under many conditions Ca2 + influx through NMDA-R suppresses subsequent responsiveness of GABAA receptors (Stelzer and Shi, 1994). A recent study reported that in hippocampal neurons, conditioning with 20 μM NMDA for 20 s could suppress 50% of GABA responses (Chisari et al., 2012).
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2013, Identification of Neural Markers Accompanying Memory