Prostaglandin E2 depresses GABA release onto parvocellular neuroendocrine neurones in the paraventricular nucleus of the hypothalamus via presynaptic receptors

2018 ◽  
Vol 30 (11) ◽  
pp. e12638 ◽  
Author(s):  
Zahra Khazaeipool ◽  
Meagan Wiederman ◽  
Wataru Inoue
Keyword(s):  
Prostaglandin E2 ◽  
Paraventricular Nucleus ◽  
Gaba Release ◽  
Presynaptic Receptors

scholarly journals 5-HT1B Receptor-Mediated Presynaptic Inhibition of GABA Release in the Suprachiasmatic Nucleus

2005 ◽  
Vol 93 (6) ◽  
pp. 3157-3164 ◽  
Author(s):  
Jayne R. Bramley ◽  
Patricia J. Sollars ◽  
Gary E. Pickard ◽  
F. Edward Dudek
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Receptor Agonist ◽  
Gaba Release ◽  
Presynaptic Receptors ◽  
Clear Effect ◽  
Whole Cell Patch Clamp ◽  
Bath Application ◽  
Hypothalamic Slices ◽  
Photic Input ◽  
Serotonergic Innervation

The suprachiasmatic nucleus (SCN) receives a dense serotonergic innervation that modulates photic input to the SCN via serotonin 1B (5-HT1B) presynaptic receptors on retinal glutamatergic terminals. However, the majority of 5-HT1B binding sites in the SCN are located on nonretinal terminals and most axonal terminals in the SCN are GABAergic. We therefore tested the hypothesis that 5-HT1B receptors might also be located on SCN GABAergic terminals by examining the effects of the highly selective 5-HT1B receptor agonist CP-93,129 on SCN miniature inhibitory postsynaptic currents (mIPSCs). Whole cell patch-clamp recordings of mIPSCs were obtained from rat and mouse SCN neurons in hypothalamic slices. Using CsCl-containing microelectrodes with QX314, we isolated mPSCs that were sensitive to the GABAA receptor antagonist, bicuculline. Bath application of CP-93,129 (1 μM) decreased the frequency of mIPSCs by an average of 22% ( n = 7) in rat SCN neurons and by an average of 30% ( n = 8) in mouse SCN neurons with no clear effect on mIPSC amplitude. In mice lacking functional 5-HT1B receptors, CP-93,129 (1 μM) had no clear effect on the frequency or the amplitude of mIPSCs recorded in any of the cells tested ( n = 4). The decrease in the frequency of mIPSCs of SCN neurons produced by the selective 5-HT1B receptor agonist CP-93,129 is consistent with the interpretation that 5-HT1B receptors are located on GABA terminals in the SCN and that 5-HT inhibits GABA release via a 5-HT1B presynaptic receptor-mediated mechanism.

Is GABA release modulated by presynaptic receptors?

Nature ◽  
1978 ◽  
Vol 274 (5674) ◽  
pp. 904-905 ◽  
Author(s):  
P. R. MITCHELL ◽  
I. L. MARTIN
Keyword(s):  
Gaba Release ◽  
Presynaptic Receptors

scholarly journals Adrenocorticotropin Response and Nicotine-Induced Norepinephrine Secretion in the Rat Paraventricular Nucleus Are Mediated through Brainstem Receptors*

Endocrinology ◽  
1997 ◽  
Vol 138 (5) ◽  
pp. 1935-1943 ◽  
Author(s):  
Yitong Fu ◽  
Shannon G. Matta ◽  
James D. Valentine ◽  
Burt M. Sharp
Keyword(s):  
Paraventricular Nucleus ◽  
Fourth Ventricle ◽  
Presynaptic Receptors ◽  
In Vivo Microdialysis ◽  
Dark Phase ◽  
Acth Secretion ◽  
Nicotinic Cholinergic Receptors ◽  
Dose Dependent ◽  
Made In

Abstract Nicotine is a potent stimulus for the secretion of ACTH, and norepinephrinergic neurons originating in the brainstem are involved. Prior reports using in vivo microdialysis in alert rats have shown that nicotine, administered ip or into the fourth ventricle, stimulated the release of norepinephrine (NE) into the hypothalamic paraventricular nucleus (PVN), the site of neurons containing CRH. In the present studies, rats received an iv infusion of nicotine into the jugular vein on alternate days during their active (dark) phase; therefore, direct correlations between the levels of NE microdialyzed from the PVN and plasma ACTH could be made in each animal. Nicotine administered iv (0.045–0.135 mg/kg) elicited dose-dependent increases in both NE and ACTH (P < 0.01). A significant correlation was found between nicotine-stimulated NE release in the PVN and ACTH secretion (r = 0.91, P < 0.01). To address whether the site(s) of action of nicotine was on presynaptic receptors on NE terminals in the PVN or on receptors on neurons in brainstem regions accessible from the fourth ventricle, the nicotinic cholinergic antagonist, mecamylamine (0.1–4.8 μg), was microinjected directly into the PVN or into the fourth ventricle before nicotine infusion. Fourth-ventricular administration of mecamylamine (1.6 μg) or higher, before iv nicotine (0.09 mg/kg), completely blocked both NE release in the PVN (IC50 = 0.64 μg) and ACTH secretion (IC50 = 0.40 μg) (P < 0.01, compared with vehicle before nicotine), whereas it was ineffective when injected directly into the PVN. The results demonstrate that the nicotinic cholinergic receptors in the brainstem, rather than presynaptic receptors within the PVN itself, mediate nicotine-stimulated PVN NE release and ACTH secretion.

scholarly journals Signalling pathway of nitric oxide in synaptic GABA release in the rat paraventricular nucleus

2003 ◽  
Vol 554 (1) ◽  
pp. 100-110 ◽  
Author(s):  
De-Pei Li ◽  
Shao-Rui Chen ◽  
Thomas F. Finnegan ◽  
Hui-Lin Pan
Keyword(s):  
Nitric Oxide ◽  
Paraventricular Nucleus ◽  
Gaba Release ◽  
Signalling Pathway

Effects of VPAC2 Receptor Activation on Membrane Excitability and GABAergic Transmission in Subparaventricular Zone Neurons Targeted by Suprachiasmatic Nucleus

2009 ◽  
Vol 102 (3) ◽  
pp. 1834-1842 ◽  
Author(s):  
M.L.H.J. Hermes ◽  
M. Kolaj ◽  
P. Doroshenko ◽  
E. Coderre ◽  
L. P. Renaud
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Gaba Release ◽  
Receptor Activation ◽  
Presynaptic Receptors ◽  
Circadian Pacemaker ◽  
Membrane Excitability ◽  
Patch Clamp Recording ◽  
Subparaventricular Zone ◽  
Rat Brain Slice ◽  
Vip Receptor

The hypothalamic suprachiasmatic nucleus (SCN) harbors the master circadian pacemaker. SCN neurons produce the amino acid γ-aminobutyric acid (GABA) and several peptide molecules for coordination and communication of their circadian rhythms. A subpopulation of SCN cells synthesizes vasoactive intestinal polypeptide (VIP) and provides a dense innervation of the subparaventricular zone (SPZ), an important CNS target of the circadian pacemaker. In this study, using patch-clamp recording techniques and rat brain slice preparations, the contribution of VIP to SCN efferent signaling to SPZ was evaluated by examining membrane responses of SPZ neurons to exogenous VIP receptor ligands. In ∼50% of the SPZ neurons receiving monosynaptic GABAA receptor–mediated inputs from SCN, bath-applied VIP (0.5–1 μM) resulted in a membrane depolarization caused by tetrodotoxin-resistant inward currents reversing at ∼−23 mV. These data suggest the existence of postsynaptic receptors that activate a nonselective cationic conductance. In addition, a subset of SPZ neurons showed an increase in the amplitude of SCN-evoked GABAergic inhibitory postsynaptic currents (IPSCs) and a decrease in their paired-pulse ratios. This, together with an increase in frequency of spontaneous and miniature IPSCs, implies the presence of presynaptic receptors that facilitate GABA release from SCN and possibly other synaptic terminals. The effects occurred in separate neurons and could be mimicked by the selective VPAC2 receptor agonist BAY 55-9837 (0.2–0.5 μM) and partially blocked by the VIP receptor antagonist VIP(6-28) (5 μM). The results indicate that VIP acts via both post- and presynaptic VPAC2 receptors to differentially modulate SCN GABAergic signaling to distinct subpopulations of SPZ neurons.

Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and alpha-latrotoxin in the hippocampus

1996 ◽  
Vol 75 (5) ◽  
pp. 2017-2028 ◽  
Author(s):  
M. Capogna ◽  
B. H. Gahwiler ◽  
S. M. Thompson
Keyword(s):  
Synaptic Transmission ◽  
Presynaptic Inhibition ◽  
Receptor Agonist ◽  
Gabab Receptor ◽  
Gaba Release ◽  
Presynaptic Receptors ◽  
Gamma Aminobutyric Acid ◽  
Calcium Dependent ◽  
Opioid Receptor Agonist ◽  
Voltage Dependent

1. Presynaptic inhibition of synaptic transmission in the hippocampus was investigated by comparing the effects of several agonists on miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs). 2. The Ca2+ ionophore ionomycin increased the frequency of mEPSCs and mIPSCs but did not affect their amplitude. Ionomycin-induced release required extracellular Ca2+ and was prevented by pretreatment with botulinum neurotoxin serotype F, like evoked synaptic transmission. Unlike evoked transmission, however, this increase did not involve activation of voltage-dependent Ca2+ channels because it was insensitive to Cd2+. 3. Both the lanthanide gadolinium and alpha-latrotoxin produced increases in the frequency of mEPSCs and mIPSCs, but their actions were independent of extracellular Ca2+. 4. Adenosine, the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen, and a mu-opioid receptor agonist strongly reduced the frequency of synaptic currents triggered by all three secretagogues. 5. We conclude that activation of these presynaptic receptors can reduce high frequencies of vesicular glutamate and GABA release by directly impairing transmitter exocytosis. Presynaptic inhibition of gadolinium- and alpha-latrotoxin-induced release indicates that this impairment occurs without changes in intraterminal Ca2+ homeostasis and when vesicle fusion is rendered Ca2+ independent, respectively. 6. The inhibition of ionomycin-induced release provides additional evidence for a direct, neurotransmitter receptor-mediated modulation of the proteins underlying vesicular docking or fusion as an important component of presynaptic inhibition of evoked synaptic transmission.

Interleukin-1 beta acts at hypothalamic sites to inhibit gastric acid secretion in rats

1992 ◽  
Vol 263 (3) ◽  
pp. G414-G418 ◽  
Author(s):  
E. Saperas ◽  
H. Yang ◽  
Y. Tache
Keyword(s):  
Prostaglandin E2 ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Paraventricular Nucleus ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Medial Preoptic Area ◽  
Anterior Hypothalamus ◽  
Interleukin 1 Beta

It has been established that interleukin-1 beta (IL-1 beta) injected into the cerebrospinal fluid inhibits gastric acid secretion in rats. Brain sites of action of IL-1 beta were investigated in conscious rats implanted unilaterally with chronic hypothalamic cannula. Gastric acid secretion was monitored 2 h after pylorus ligation. Human recombinant IL-1 beta (10 ng) microinjected into the medial preoptic area, anterior hypothalamus, and paraventricular nucleus inhibited gastric acid secretion by 76-83%. IL-1 beta microinjected into the ventromedial hypothalamus and other hypothalamic sites outside of responsive sites had no effect. IL-1 beta inhibitory action in the medial preoptic area was dose related (0.1-10 ng), prevented by indomethacin (5 mg/kg ip), and mimicked by prostaglandin E2. These results show that IL-1 beta acts in the medial preoptic area/anterior hypothalamus and paraventricular nucleus to inhibit acid secretion in pylorus-ligated rats and that IL-1 beta action is likely to involve prostaglandin E2.

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.

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