scholarly journals The Janus face of GABAergic synaptic transmission during brain development

2020 ◽  
Vol 598 (10) ◽  
pp. 1801-1802
Author(s):  
Knut Holthoff
Keyword(s):  
Synaptic Transmission ◽  
Brain Development ◽  
Gabaergic Synaptic Transmission

Frequency-Dependent Modulation of Short-Term Plasticity of GABAergic Synaptic Transmission

2018 ◽  
Vol 9 (2) ◽  
pp. 119-126
Author(s):  
Oksana P. Kolesnyk ◽  
Svetlana A. Fedulova ◽  
Mycola S. Veselovsky
Keyword(s):  
Synaptic Transmission ◽  
Short Term ◽  
Frequency Dependent ◽  
Short Term Plasticity ◽  
Gabaergic Synaptic Transmission

Possible role of mitochondria in posttetanic potentiation of GABAergic synaptic transmission in rat neocortical cell cultures

Synapse ◽  
2005 ◽  
Vol 58 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Maksim V. Storozhuk ◽  
Svetlana Y. Ivanova ◽  
Pavel M. Balaban ◽  
Platon G. Kostyuk
Keyword(s):  
Synaptic Transmission ◽  
Cell Cultures ◽  
Posttetanic Potentiation ◽  
Gabaergic Synaptic Transmission

Postsynaptic mechanism may contribute to inhibitory acetylcholine effect on GABAergic synaptic transmission in hippocampal cell cultures

Synapse ◽  
2001 ◽  
Vol 41 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Maksim V. Storozhuk ◽  
Igor V. Melnick ◽  
Platon G. Kostyuk ◽  
Pavel V. Belan
Keyword(s):  
Synaptic Transmission ◽  
Cell Cultures ◽  
Hippocampal Cell ◽  
Postsynaptic Mechanism ◽  
Gabaergic Synaptic Transmission

scholarly journals Mu-opioids suppress GABAergic synaptic transmission onto orbitofrontal cortex pyramidal neurons with subregional selectivity

2020 ◽  
Author(s):  
Benjamin K. Lau ◽  
Brittany P. Ambrose ◽  
Catherine S. Thomas ◽  
Min Qiao ◽  
Stephanie L. Borgland
Keyword(s):  
Synaptic Transmission ◽  
Opioid Receptor ◽  
Orbitofrontal Cortex ◽  
Pyramidal Neurons ◽  
Mu Opioid Receptor ◽  
Mu Opioid ◽  
Inhibitory Synaptic Transmission ◽  
Receptor Coupling ◽  
Mu Opioids ◽  
Gabaergic Synaptic Transmission

AbstractThe orbitofrontal cortex (OFC) plays a critical role in evaluating outcomes in a changing environment. Administering opioids to the OFC can alter the hedonic reaction to food rewards and increase their consumption in a subregion specific manner. However, it is unknown how mu-opioid signalling influences synaptic transmission in the OFC. Thus, we investigated the cellular actions of mu-opioids within distinct subregions of the OFC. Using in-vitro patch clamp electrophysiology in brain slices containing the OFC, we found that the mu-opioid agonist, DAMGO produced a concentration-dependant inhibition of GABAergic synaptic transmission onto medial OFC (mOFC), but not lateral OFC (lOFC) neurons. This effect was mediated by presynaptic mu-opioid receptor activation of local parvalbumin (PV+)-expressing interneurons. The DAMGO-induced suppression of inhibition was long-lasting and not reversed upon washout of DAMGO, or by application of the mu-opioid receptor antagonist, CTAP, suggesting an inhibitory long-term depression (iLTD) induced by an exogenous mu-opioid. We show that LTD at inhibitory synapses is dependent on downstream cAMP/PKA signaling, which differs between the mOFC and lOFC. Finally, we demonstrate that endogenous opioid release triggered via moderate physiological stimulation can induce LTD. Taken together, these results suggest that presynaptic mu-opioid stimulation of local PV+ interneurons induces a long-lasting suppression of GABAergic synaptic transmission, which depends on subregional differences in mu-opioid receptor coupling to the downstream cAMP/PKA intracellular cascade. These findings provide mechanistic insight into the opposing functional effects produced by mu-opioids within the OFC.Significance StatementConsidering that both the OFC and the opioid system regulate reward, motivation, and food intake; understanding the role of opioid signaling within the OFC is fundamental for a mechanistic understanding of the sequelae for several psychiatric disorders. This study makes several novel observations. First, mu-opioids induce a long-lasting suppression of inhibitory synaptic transmission onto OFC pyramidal neurons in a regionally selective manner. Secondly, mu-opioids recruit PV+ inputs to suppress inhibitory synaptic transmission in the mOFC. Thirdly, the regional selectivity of mu-opioid action of endogenous opioids is due to the efficacy of mu-opioid receptor coupling to the downstream cAMP/PKA intracellular cascades. These experiments are the first to reveal a cellular mechanism of opioid action within the OFC.

scholarly journals The C-terminal of CASY-1/Calsyntenin regulates GABAergic synaptic transmission at the Caenorhabditis elegans neuromuscular junction

PLoS Genetics ◽  
2018 ◽  
Vol 14 (3) ◽  
pp. e1007263 ◽  
Author(s):  
Shruti Thapliyal ◽  
Amruta Vasudevan ◽  
Yongming Dong ◽  
Jihong Bai ◽  
Sandhya P. Koushika ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Gabaergic Synaptic Transmission ◽  
Casy 1

Role of Presynaptic L-Type Ca2+ Channels in GABAergic Synaptic Transmission in Cultured Hippocampal Neurons

1999 ◽  
Vol 81 (3) ◽  
pp. 1225-1230 ◽  
Author(s):  
Kimmo Jensen ◽  
Morten Skovgaard Jensen ◽  
John D. C. Lambert
Keyword(s):  
Synaptic Transmission ◽  
Transmitter Release ◽  
Hippocampal Neurons ◽  
Low Frequency ◽  
Tetanic Stimulation ◽  
Vesicle Release ◽  
Gabaergic Synaptic Transmission ◽  
Cultured Hippocampal Neurons ◽  
40 Hz

Role of presynaptic L-type Ca2+ channels in GABAergic synaptic transmission in cultured hippocampal neurons. Using dual whole cell patch-clamp recordings of monosynaptic GABAergic inhibitory postsynaptic currents (IPSCs) in cultured rat hippocampal neurons, we have previously demonstrated posttetanic potentiation (PTP) of IPSCs. Tetanic stimulation of the GABAergic neuron leads to accumulation of Ca2+ in the presynaptic terminals. This enhances the probability of GABA-vesicle release for up to 1 min, which underlies PTP. In the present study, we have examined the effect of altering the probability of release on PTP of IPSCs. Baclofen (10 μM), which depresses presynaptic Ca2+ entry through N- and P/Q-type voltage-dependent Ca2+ channels (VDCCs), caused a threefold greater enhancement of PTP than did reducing [Ca2+]o to 1.2 mM, which causes a nonspecific reduction in Ca2+ entry. This finding prompted us to investigate whether presynaptic L-type VDCCs contribute to the Ca2+ accumulation in the boutons during spike activity. The L-type VDCC antagonist, nifedipine (10 μM), had no effect on single IPSCs evoked at 0.2 Hz but reduced the PTP evoked by a train of 40 Hz for 2 s by 60%. Another L-type VDCC antagonist, isradipine (5 μM), similarly inhibited PTP by 65%. Both L-type VDCC blockers also depressed IPSCs during the stimulation (i.e., they increased tetanic depression). The L-type VDCC “agonist” (−)BayK 8644 (4 μM) had no effect on PTP evoked by a train of 40 Hz for 2 s, which probably saturated the PTP process, but enhanced PTP evoked by a train of 1 s by 91%. In conclusion, the results indicate that L-type VDCCs do not participate in low-frequency synchronous transmitter release, but contribute to presynaptic Ca2+ accumulation during high-frequency activity. This helps maintain vesicle release during tetanic stimulation and also enhances the probability of transmitter release during the posttetanic period, which is manifest as PTP. Involvement of L-type channels in these processes represents a novel presynaptic regulatory mechanism at fast CNS synapses.

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