Presynaptic histamine H1 and H3 receptors modulate sympathetic ganglionic synaptic transmission in the guinea‐pig.

Christian, Edward P.; Weinreich, Daniel

doi:10.1113/jphysiol.1992.sp019385

Cited by 23 publications

(17 citation statements)

References 30 publications

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“…It is established that functional histamine receptors (H 1 -H 3 ) are expressed in SCG neurons of many animals, based on electrophysiology studies (5,6,28,31,36). In our current study, histamine inhibits M current at a concentration of 1 M and the EC 50 is 3.3 M, which falls in the proposed physiological concentration range (4).…”

Section: Discussionmentioning

confidence: 76%

“…1, D and G). Histamine receptors have been demonstrated in SCG by electrophysiological studies (6,36). To determine which receptor subtype was responsible for histamine-induced M current inhibition, histamine was applied to neurons in either the presence of mepyramine (1 M) or cimetidine (10 M).…”

Section: Histamine Suppresses Kcnq/m Current In Hek293 Cells and Rat mentioning

confidence: 99%

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Phosphatidylinositol 4,5-bisphosphate hydrolysis mediates histamine-induced KCNQ/M current inhibition

Liu

Liang²,

Liu³

et al. 2008

American Journal of Physiology-Cell Physiology

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The M-type potassium channel, of which its molecular basis is constituted by KCNQ2-5 homo- or heteromultimers, plays a key role in regulating neuronal excitability and is modulated by many G protein-coupled receptors. In this study, we demonstrate that histamine inhibits KCNQ2/Q3 currents in human embryonic kidney (HEK)293 cells via phosphatidylinositol 4,5-bisphosphate (PIP(2)) hydrolysis mediated by stimulation of H(1) receptor and phospholipase C (PLC). Histamine inhibited KCNQ2/Q3 currents in HEK293 cells coexpressing H(1) receptor, and this effect was totally abolished by H(1) receptor antagonist mepyramine but not altered by H(2) receptor antagonist cimetidine. The inhibition of KCNQ currents was significantly attenuated by a PLC inhibitor U-73122 but not affected by depletion of internal Ca(2+) stores or intracellular Ca(2+) concentration ([Ca(2+)](i)) buffering via pipette dialyzing BAPTA. Moreover, histamine also concentration dependently inhibited M current in rat superior cervical ganglion (SCG) neurons by a similar mechanism. The inhibitory effect of histamine on KCNQ2/Q3 currents was entirely reversible but became irreversible when the resynthesis of PIP(2) was impaired with phosphatidylinsitol-4-kinase inhibitors. Histamine was capable of producing a reversible translocation of the PIP(2) fluorescence probe PLC(delta1)-PH-GFP from membrane to cytosol in HEK293 cells by activation of H(1) receptor and PLC. We concluded that the inhibition of KCNQ/M currents by histamine in HEK293 cells and SCG neurons is due to the consumption of membrane PIP(2) by PLC.

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Section: Discussionmentioning

confidence: 76%

Section: Histamine Suppresses Kcnq/m Current In Hek293 Cells and Rat mentioning

confidence: 99%

Phosphatidylinositol 4,5-bisphosphate hydrolysis mediates histamine-induced KCNQ/M current inhibition

Liu

Liang²,

Liu³

et al. 2008

American Journal of Physiology-Cell Physiology

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“…Records of MEPPs and evoked EPPs were analysed using CDR, WCP and SCAN programs (DOS versions, Strathclyde University Superior Software; John Dempster). The data were analysed using a modified version of a computer program for evoked release (Mark Longerbeam, BME Systems; see also Christian & Weinreich, 1992), Microsoft Excel, Corel Quattro Pro and Sigma Plot.…”

Section: Methodsmentioning

confidence: 99%

Phorbol esters and adenosine affect the readily releasable neurotransmitter pool by different mechanisms at amphibian motor nerve endings

Searl

Silinsky

2003

The Journal of Physiology

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Phorbol esters and adenosine have been proposed to interact at common sites downstream of calcium entry at amphibian motor nerve endings. We thus studied the actions and interactions of phorbol esters and adenosine using electrophysiological recording techniques in conjunction with both binomial statistical analysis and high‐frequency stimulation at the amphibian neuromuscular junction. To begin this study, we confirmed previous observations that synchronous evoked acetylcholine (ACh) release (reflected as endplate potentials, EPPs) is well described by a simple binomial distribution. We then used binomial analysis to study the effects of the phorbol ester phorbol dibutyrate (PDBu, 100 nm) and adenosine (50 µm) on the binomial parameters n (the number of calcium charged ACh quanta available for release) and p (the average probability of release), where the mean level of evoked ACh release (m) =np. We found that PDBu increased m by increasing the parameter n whilst adenosine reduced m by reducing n; neither agent affected the parameter p. PDBu had no effect on either the potency or efficacy of the inhibition produced by adenosine. Subtle differences between these two agents were revealed by the patterns of EPPs evoked by high‐frequency trains of stimuli. Phorbol esters increased ACh release during the early phase of stimulation but not during the subsequent plateau phase. The inhibitory effect of adenosine was maximal at the beginning of the train and was still present with reduced efficacy during the plateau phase. When taken together with previous findings, these present results suggest that phorbol esters increase the immediately available store of synaptic vesicles by increasing the number of primed vesicles whilst adenosine acts at a later stage of the secretory process to decrease the number of calcium‐charged primed vesicles.

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“…If this is the case, H1 receptor-mediated inhibition of the PSC in response to the second pulse might be reversed by the first pulse, leading to an increase in the PPR. In the superior cervical ganglion, the activation of presynaptic H1 receptors is thought to modulate and potentiate sympathetic ganglionic synaptic transmission although the effects of H1 receptor activation are opposite to those in MMNs (Christian and Weinreich 1992). Those authors showed that histamine increases the mean amplitude of excitatory postsynaptic potentials (EPSPs) evoked by stimulation of the cervical sympathetic trunk without changing the amplitude of miniature EPSPs.…”

Section: Discussionmentioning

confidence: 98%

Involvement of histaminergic inputs in the jaw-closing reflex arc

Gemba

Nakayama

Nakamura

et al. 2015

Journal of Neurophysiology

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Histamine receptors are densely expressed in the mesencephalic trigeminal nucleus (MesV) and trigeminal motor nucleus. However, little is known about the functional roles of neuronal histamine in controlling oral-motor activity. Thus, using the whole-cell recording technique in brainstem slice preparations from Wistar rats aged between postnatal days 7 and 13, we investigated the effects of histamine on the MesV neurons innervating the masseter muscle spindles and masseter motoneurons (MMNs) that form a reflex arc for the jaw-closing reflex. Bath application of histamine (100 μM) induced membrane depolarization in both MesV neurons and MMNs in the presence of tetrodotoxin, whereas histamine decreased and increased the input resistance in MesV neurons and MMNs, respectively. The effects of histamine on MesV neurons and MMNs were mimicked by an H1 receptor agonist, 2-pyridylethylamine (100 μM). The effects of an H2 receptor agonist, dimaprit (100 μM), on MesV neurons were inconsistent, whereas MMNs were depolarized without changes in the input resistance. An H3 receptor agonist, immethridine (100 μM), also depolarized both MesV neurons and MMNs without changing the input resistance. Histamine reduced the peak amplitude of postsynaptic currents (PSCs) in MMNs evoked by stimulation of the trigeminal motor nerve (5N), which was mimicked by 2-pyridylethylamine but not by dimaprit or immethridine. Moreover, 2-pyridylethylamine increased the failure rate of PSCs evoked by minimal stimulation and the paired-pulse ratio. These results suggest that histaminergic inputs to MesV neurons through H1 receptors are involved in the suppression of the jaw-closing reflex although histamine depolarizes MesV neurons and/or MMNs.

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Presynaptic histamine H1 and H3 receptors modulate sympathetic ganglionic synaptic transmission in the guinea‐pig.

Cited by 23 publications

References 30 publications

Phosphatidylinositol 4,5-bisphosphate hydrolysis mediates histamine-induced KCNQ/M current inhibition

Phosphatidylinositol 4,5-bisphosphate hydrolysis mediates histamine-induced KCNQ/M current inhibition

Phorbol esters and adenosine affect the readily releasable neurotransmitter pool by different mechanisms at amphibian motor nerve endings

Involvement of histaminergic inputs in the jaw-closing reflex arc

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