scholarly journals G protein βγ subunits mediate presynaptic inhibition of transmitter release from rat superior cervical ganglion neurones in culture

2005 ◽  
Vol 563 (3) ◽  
pp. 765-776 ◽  
Author(s):  
Gary J. Stephens ◽  
Sumiko Mochida
Keyword(s):  
G Protein ◽  
Superior Cervical Ganglion ◽  
Transmitter Release ◽  
Presynaptic Inhibition ◽  
Cervical Ganglion

scholarly journals Desensitization-resistant and -sensitive GPCR-mediated inhibition of GABA release occurs by Ca2+-dependent and -independent mechanisms at a hypothalamic synapse

2016 ◽  
Vol 115 (5) ◽  
pp. 2376-2388 ◽  
Author(s):  
Reagan L. Pennock ◽  
Shane T. Hentges
Keyword(s):  
G Protein ◽  
Opioid Receptors ◽  
Transmitter Release ◽  
Presynaptic Inhibition ◽  
Calcium Influx ◽  
Gaba Release ◽  
Presynaptic Receptors ◽  
Postsynaptic Currents ◽  
Independent Mechanism ◽  
Μ Opioid Receptors

Whereas the activation of Gαi/o-coupled receptors commonly results in postsynaptic responses that show acute desensitization, the presynaptic inhibition of transmitter release caused by many Gαi/o-coupled receptors is maintained during agonist exposure. However, an exception has been noted where GABAB receptor (GABABR)-mediated inhibition of inhibitory postsynaptic currents (IPSCs) recorded in mouse proopiomelanocortin (POMC) neurons exhibit acute desensitization in ∼25% of experiments. To determine whether differential effector coupling confers sensitivity to desensitization, voltage-clamp recordings were made from POMC neurons to compare the mechanism by which μ-opioid receptors (MORs) and GABABRs inhibit transmitter release. Neither MOR- nor GABABR-mediated inhibition of release relied on the activation of presynaptic K+ channels. Both receptors maintained the ability to inhibit release in the absence of external Ca2+ or in the presence of ionomycin-induced Ca2+ influx, indicating that inhibition of release can occur through a Ca2+-independent mechanism. Replacing Ca2+ with Sr2+ to disrupt G-protein-mediated inhibition of release occurring directly at the release machinery did not alter MOR- or GABAB -mediated inhibition of IPSCs, suggesting that reductions in evoked release can occur through the inhibition of Ca2+ channels. Additionally, both receptors inhibited evoked IPSCs in the presence of selective blockers of N- or P/Q-type Ca2+ channels. Altogether, the results show that MORs and GABABRs can inhibit transmitter release through the inhibition of calcium influx and by direct actions at the release machinery. Furthermore, since both the desensitizing and nondesensitizing presynaptic receptors are similarly coupled, differential effector coupling is unlikely responsible for differential desensitization of the inhibition of release.

scholarly journals Facilitation, augmentation, and potentiation of synaptic transmission at the superior cervical ganglion of the rabbit.

1980 ◽  
Vol 76 (2) ◽  
pp. 213-231 ◽  
Author(s):  
J E Zengel ◽  
K L Magleby ◽  
J P Horn ◽  
D A McAfee ◽  
P J Yarowsky
Keyword(s):  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Time Constant ◽  
Superior Cervical Ganglion ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Gap Technique ◽  
Cervical Ganglion ◽  
Locke Solution ◽  
Underlying Mechanisms

The effect of repetitive stimulation on synaptic transmission was studied in the isolated superior cervical ganglion of the rabbit under conditions of reduced quantal content. Excitatory postsynaptic potentials (EPSP) were recorded with the sucrose gap technique to obtain estimates of transmitter release. Four components of increased transmitter release, with time constants of decay similar to those observed at the frog neuromuscular junction at 20 degrees C, were found in the ganglion at 34 degrees C: a first component of facilitation, which decayed with a time constant of 59 +/- 14 ms (mean +/- SD); a second component of facilitation, which decayed with a time constant of 388 +/- 97 ms; augmentation, which decayed with a time constant of 7.2 +/- 1 s; and potentiation, which decayed with a time constant of 88 +/- 25 s. The addition of 0.1-0.2 mM Ba2+ to the Locke solution increased the magnitude but not the time constant of decay of augmentation. Ba2+ had little effect on potentiation. The addition of 0.2-0.8 mM Sr2+ to the Locke solution appeared to increase the magnitude of the second component of facilitation. Sr2+ had little effect on augmentation or potentiation. These selective effects of Ba2+ and Sr2+ on the components of increased transmitter release in the rabbit ganglion are similar to the effects of these ions at the frog neuromuscular junction. Although the effects of Ba2+ and Sr2+ are similar in the two preparations, the magnitudes of augmentation and the second component of facilitation after a single impulse were about 6-10 times greater in the rabbit ganglion than at the frog neuromuscular junction. These results suggest that the underlying mechanisms in the nerve terminal that give rise to the components of increased transmitter release in the rabbit ganglion and frog neuromuscular junction are similar but not identical.

Evidence for a Blood Ganglion Barrier in the Superior Cervical Ganglion of the Rat

1982 ◽  
Vol 40 ◽  
pp. 204-204
Author(s):  
D. M. DePace
Keyword(s):  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Peripheral Nerves ◽  
Time Schedule ◽  
Transmission Electron ◽  
Cervical Ganglion ◽  
The Central Nervous System ◽  
Cervical Ganglia ◽  
Capillary Circulation ◽  
And Control

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.

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