scholarly journals Ethanol Potentiation of GABAergic Synaptic Transmission May Be Self-Limiting: Role of Presynaptic GABAB Receptors

2004 ◽  
Vol 24 (47) ◽  
pp. 10679-10686 ◽  
Author(s):  
O. J. Ariwodola
Keyword(s):  
Synaptic Transmission ◽  
Gabab Receptors ◽  
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

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.

scholarly journals Role of increased GABAergic synaptic transmission in morphine tolerance

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Erin N. Bobeck ◽  
Katherine L. Suchland ◽  
Rachel Haseman ◽  
Susan L. Ingram
Keyword(s):  
Synaptic Transmission ◽  
Morphine Tolerance ◽  
Gabaergic Synaptic Transmission

Role of GABA transporter 3 in GABAergic synaptic transmission at striatal output neurons

Synapse ◽  
2009 ◽  
Vol 63 (10) ◽  
pp. 921-929 ◽  
Author(s):  
Knut Kirmse ◽  
Sergei Kirischuk ◽  
Rosemarie Grantyn
Keyword(s):  
Synaptic Transmission ◽  
Gaba Transporter ◽  
Output Neurons ◽  
Gabaergic Synaptic Transmission
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