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PubMed2002

Repolarization of the presynaptic action potential and short-term synaptic plasticity in the chick ciliary ganglion.

Stimulation-induced increases in synaptic efficacy have been described as being composed of multiple independent processes that arise from the activation of distinct mechanisms at the presynaptic terminal. In the chick ciliary ganglion, four components of short-term synaptic plasticity have been described: F1 and F2 components of facilitation, augmentation, and potentiation. In the present study, intracellular recording from the presynaptic calyciform nerve terminal of the chick ciliary ganglion revealed that the late repolarization and afterhypolarization (AHP) phases of the presynaptic action potential are affected by repetitive stimulation and that the time course of these effects parallel that of facilitation. The effects of these changes in the presynaptic action potential time course on calcium influx were tested by using the recorded action potential waveforms as voltage command stimuli during whole-cell patch-clamp recordings from acutely isolated chick ciliary ganglion neurons. The "facilitated" action potential waveform (slowed repolarization, decreased AHP amplitude) evoked calcium current with slightly but significantly greater total calcium influx. Taken together, these results are consistent with the hypothesis that activity-dependent changes in the presynaptic action potential are one of several mechanisms contributing to the facilitation phase of stimulation-induced increases in transmitter release in this preparation.

Action Potentials↗
PubMed1993

[Responses of toad spinal ganglion neurons to repetitive stimulation of their central and peripheral processes].

Intracellular recordings were made from 48 toad dorsal root ganglion neurons in vitro while electrical stimulation was delivered respectively to their dorsal root or sciatic nerve input. The average conduction velocities were respectively 12 m/s and 15 m/s. With progressively increasing frequency of stimulation, 30% of the recorded cells showed simultaneous decrease of amplitude, wave decomposition and dropping of propagated response to both inputs while 70% of the cells showed more or less different patterns of degradation of the various parameters. Complete failure of neurons to follow the inputs occurred respectively at 126 and 323 Hz. Evidently the dorsal root ganglion neurons reported in the present work pertain to type A neuron with central processes smaller in diameter than peripheral ones A possible mechanism underlying the different changes is discussed.

Animals↗
PubMed1995

Electrical stimulation of the Gasserian ganglion induces structural alterations of calcitonin gene-related peptide-immunoreactive perivascular sensory nerve terminals in the rat cerebral dura mater: a possible model of migraine headache.

Calcitonin gene-related peptide (CGRP)-positive sensory nerve fibers in the rat supratentorial dura mater are equipped with varicosities and club-like nerve terminals, often attached to the walls of blood vessels. Brief electrical stimulation of the Gasserian ganglion results in significant swelling and increased immunohistochemical staining of ipsilateral perivascular club-like terminals, while long-lasting electrical stimulation induces their disintegration or bursting, resulting in irregular, corroded outlines of terminals and en passant beads. Stimulation-induced morphological alterations of perivascular terminals may represent a structural basis of increased CGRP content in jugular blood which follows electrical stimulation of the Gasserian ganglion and accompanies migraine attacks.

Animals↗
PubMed1999

Alterations in neurokinin A-, substance P- and calcitonin gene-related peptide immunoreactivities in the caudal trigeminal nucleus of the rat following electrical stimulation of the trigeminal ganglion.

We have carried out an immunohistochemical study on the presence of neurokinin A (NKA) and substance P (SP) in the rat caudal trigeminal nucleus (CTN) after electrical stimulation of the trigeminal ganglion (TG), used as an experimental model to induce alterations, some of which may occur during migraine attacks (release of vasoactive peptides from perivascular trigeminal axons and neurogenic inflammation). Both unilateral, 30 min electrical stimulation (5 Hz, 5 ms, 0.1-1 mA) of the TG and 5 min stimulation with a slight increase in the stimulating parameters (7.5 Hz, 5 ms, 1.4 mA) caused a significant depletion of the NKA and SP immunoreactivities (-IR) of the TG nerve central terminals in the ipsilateral CTN. Calcitonin gene-related peptide (CGRP)-IR of the ipsilateral CTN was also studied in the CTN using the increased stimulating parameters and a marked depletion of CGRP-IR was also observed following TG stimulation. Such depletion may be due to the release of neuropeptides from the trigeminal central terminals. These findings suggest that NKA, SP and CGRP could act as neurotransmitters at the first central synapses of the trigeminal nociceptive pathway to transmit the sensory stimuli to the higher brain centers.

Animals↗
PubMed1985

The effect of nicotine and cytisine on 3H-acetylcholine release from cortical slices of guinea-pig brain.

Nicotine 1.8 X 10(-5)-1.8 X 10(-4) mol/l enhanced the spontaneous 3H-efflux from guinea-pig cortical slices preloaded with 3H-choline and perfused in the presence of hemicholinium (HC-3). The facilitation of tritium outflow was prevented by tetrodotoxin 5 X 10(-7) mol/l and by D-tubocurarine 4.5 X 10(-6) mol/l. Nicotine 1.8 X 10(-6)-1.8 X 10(-4) mol/l, and the agonist cytisine 5 X 10(-7)-5 X 10(-5) mol/l increased, in a concentration-dependent way, 3H-efflux from electrically-stimulated slices (0.2 Hz). The concentration-response curves of both drugs were parallelly shifted to the right by D-tubocurarine 4.5 X 10(-6) mol/l. The EC50 values (i.e. the concentrations required to cause a 50% increase in the S2/S1 ratio) changed for nicotine from 5.58 X 10(-5) to 4.34 X 10(-4) and for cytisine from 6.3 X 10(-6) to 2.75 X 10(-4) mol/l in the absence and in the presence of the antagonist, respectively. In the range of 0.2-2 Hz the magnitude of the effect of nicotine was inversely related to the rate of stimulation. The response to nicotine was subject to rapidly developing tachyphylaxis; it was resistant to atropine. It is concluded that nicotine and cytisine facilitate 3H-efflux from the cholinergic nerve endings of guinea-pig cerebral cortex. This effect involves sodium-dependent mechanisms and is due to an interaction of the drugs with receptors showing affinity for D-tubocurarine.

Acetylcholine↗
PubMed1992

The nature of the acetylcholine receptor in a Buccinum proboscis muscle examined by the sucrose-gap voltage clamp technique.

1. ACh dose-response curves for the radicular retractor muscle of Buccinum showed maximum force and membrane depolarisation of 3.3 mV at 50 mumol l-1 ACh. 2. PCh was found to be almost a full agonist for force and induced higher membrane depolarisations than ACh while BCh was only a partial agonist of very low potency. This suggests an AChR neither muscarinic nor nicotinic in mammalian terminology. 3. Neither muscarine nor nicotine had any direct agonistic effects on the muscle but pre-exposure to nicotine inhibited both force and membrane depolarisation induced by a subsequent dose of ACh. 4. The specific muscarinic and nicotinic antagonists atropine, d-tubocurarine and gallamine all inhibited ACh responses in a dose-dependent manner. 5. Single sucrose-gap recording showed that ACh induced a depolarisation resulting in a contracture. Double sucrose-gap voltage clamp recording showed that 10 mumol l-1 ACh induced an inward transmembrane current of ca 2 microA. Both ACh-induced depolarisation and inward current were abolished in Na-free media. 6. When clamped at a series of membrane voltages between natural Em and positive potentials the ACh-induced Na-dependent inward current declined as Em was reduced and was abolished at -10 mV. This current showed no reversal even at strong positive membrane voltages. 7. The AChR of this muscle appears to be neither exclusively nicotinic nor muscarinic but a hybrid and shows characteristics of voltage inactivation.

Animals↗
PubMed1998

Mechanisms underlying constrictor and dilator responses to perivascular nerve stimulation in canine lingual arteries.

In isolated canine lingual arteries denuded of the endothelium, transmural electrical stimulation (2-20 Hz) produced a frequency-related contraction which was not significantly influenced by prazosin but which was reversed to a relaxation by alpha,beta-methylene ATP. The responses were abolished by tetrodotoxin. The stimulation-induced relaxation was abolished by treatment with NG-nitro-L-arginine (L-NA, 10(-6) M) and restored by the addition of L-arginine. Neurogenic relaxation resistant to L-NA was not observed after electrical stimulation, even though the pulse width and stimulus intensity were raised. Under treatment with prazosin, alpha,beta-methylene ATP and indomethacin, the arterial strips responded to nicotine (10(-4) M) with a marked relaxation that was abolished by hexamethonium. The relaxation was significantly inhibited but not abolished by L-NA (10(-5) M), and raising the concentration of the inhibitor to 10(-4) M, did not produce additional inhibition. In the strips treated with L-NA, the nicotine-induced relaxation was abolished or markedly reduced under desensitization with vasoactive intestinal peptide (VIP) or calcitonin gene-related peptide (CGRP) and by treatment with high concentrations of beraprost, a stable analog of prostaglandin I2, but was unaffected by CGRP or VIP receptor antagonists. Relaxant responses to a low concentration of nicotine (5 x 10(-6) M) were abolished by L-NA and restored by L-arginine. Histochemical study demonstrated many nerve fibers and bundles containing NADPH diaphorase in the adventitia of the arteries. It is concluded that the neurogenic arterial contraction is induced mainly by ATP via stimulation of P2X purinoceptors, and that the relaxation induced by electrical stimulation or a low concentration of nicotine is mediated by nitric oxide (NO) released from perivascular nerves. In high concentrations, nicotine elicits marked relaxations possibly due to the liberation of NO from the nerve and also vasodilator substances that increase the content of cyclic AMP in the tissue. CGRP and VIP are unlikely to be involved.

Adenosine Triphosphate↗
PubMed1999

Neurogenic vasodilation mediated by nitric oxide in porcine cerebral arteries.

Mechanisms of neurogenic vasodilatation and its modification by superoxide, acetylcholine, and vasoactive intestinal peptide (VIP) in porcine cerebral arteries were investigated. Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips without endothelium were abolished by tetrodotoxin and hexamethonium, respectively. N(G)-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor, abolished or markedly reduced the neurogenic response but did not affect the relaxation by exogenous NO. The inhibitory effect was reversed by L-arginine. Duroquinone, a superoxide-generating agent, did not alter the relaxations induced by electrical stimulation and nicotine. However, in the strips treated with diethyldithiocarbamate, an inhibitor of copper/zinc superoxide dismutase (SOD), the responses were significantly inhibited by duroquinone. The inhibition was partially reversed by SOD. Physostigmine inhibited, but atropine potentiated, the neurogenic response. The relaxation was attenuated by acetylcholine but not by VIP. There were nerve fibers and bundles containing NADPH diaphorase in the adventitia of cerebral arteries. It appears that porcine cerebral arteries are innervated by NO synthase-containing nerves that liberate NO on excitation as a neurotransmitter to produce muscular relaxation, and the nerve function is protected by endogenous SOD from degradation of NO by superoxide anions. The neurogenic relaxation is inhibited by acetylcholine released from cholinergic nerves, possibly because of an impaired production or release of NO.

Acetylcholine↗
PubMed2000

A brainstem area mediating cerebrovascular and EEG responses to hypoxic excitation of rostral ventrolateral medulla in rat.

We sought to identify the medullary relay area mediating the elevations of regional cerebral blood flow (rCBF) and synchronization of the electroencephalogram (EEG) in the rat cerebral cortex elicited by hypoxic excitation of reticulospinal sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM ). In anaesthetized spinalized rats electrical stimulation of RVLM elevated rCBF (laser-Doppler flowmetry) by 31 +/- 6 %, reduced cerebrovascular resistance (CVR) by 26 +/- 8 %, and synchronized the EEG, increasing the power of the 5-6 Hz band by 98 +/- 25 %. Stimulation of a contiguous caudal region, the medullary cerebral vasodilator area (MCVA), had comparable effects which, like responses of RVLM, were replicated by microinjection of L-glutamate (5 nmol, 20 nl). Microinjection of NaCN (300 pmol in 20 nl) elevated rCBF (17 +/- 5 %) and synchronized the EEG from RVLM, but not MCVA, while nicotine (1.2 nmol in 40 nl) increased rCBF by 13 +/- 5 % and synchronized the EEG from MCVA. In intact rats nicotine lowered arterial pressure only from MCVA (101 +/- 3 to 52 +/- 9 mmHg). Bilateral electrolytic lesions of MCVA significantly reduced, by over 59 %, elevations in rCBF and, by 78 %, changes in EEG evoked from RVLM. Bilateral electrolytic lesions of RVLM did not affect responses from MCVA. Anterograde tracing with BDA demonstrated that RVLM and MCVA are interconnected. The MCVA is a nicotine-sensitive region of the medulla that relays signals elicited by excitation of oxygen-sensitive reticulospinal neurons in RVLM to reflexively elevate rCBF and slow the EEG as part of the oxygen-conserving (diving) reflex initiated in these neurons by hypoxia or ischaemia.

Animals↗
PubMed1994

Potentiation by tonic A2a-adenosine receptor activation of CGRP-facilitated [3H]-ACh release from rat motor nerve endings.

1. The effect of calcitonin gene-related peptide (CGRP) on [3H]-acetylcholine ([3H]-ACh) release from motor nerve endings and its interaction with presynaptic facilitatory A2a-adenosine and nicotinic acetylcholine receptors was studied on rat phrenic nerve-hemidiaphragm preparations loaded with [3H]-choline. 2. CGRP (100-400 nM) increased electrically evoked [3H]-ACh release from phrenic nerve endings in a concentration-dependent manner. 3. The magnitude of CGRP excitation increased with the increase of the stimulation pulse duration from 40 microseconds to 1 ms, keeping the frequency, the amplitude and the train length constants. With 1 ms pulses, the evoked [3H]-ACh release was more intense than with 40 microseconds pulse duration. 4. Both the nicotinic acetylcholine receptor agonist, 1,1-dimethyl-4-phenylpiperazinium, and the A2a adenosine receptor agonist, CGS 21680C, increased evoked [3H]-ACh release, but only CGS 21680C potentiated the facilitatory effect of CGRP. This potentiation was prevented by the A2a adenosine receptor antagonist, PD 115,199. 5. Adenosine deaminase prevented the excitatory effect of CGRP (400 nM) on [3H]-ACh release. This effect was reversed by the non-hydrolysable A2a-adenosine receptor agonist, CGS 21680C. 6. The nicotinic antagonist, tubocurarine, did not significantly change, whereas the A2-adenosine receptor antagonist, PD 115,199, blocked the CGRP facilitation. The A1-adenosine receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine, potentiated the CGRP excitatory effect. 7. The results suggest that the facilitatory effect of CGRP on evoked [3H]-ACh release from rat phrenic motor nerve endings depends on the presence of endogenous adenosine which tonically activates A2a-adenosine receptors. Since both CGRP and A2a-adenosine receptors are positively coupled to the adenylate cyclase/cyclic AMP system, cooperation between these receptors might occur at the second messenger transduction system level.

Acetylcholine↗
PubMed1995

Calcium channel subtypes for the sympathetic and parasympathetic nerves of guinea-pig atria.

1. The Ca2+ channel subtypes of the autonomic nerves of guinea-pig atria were elucidated by monitoring the effects of specific Ca2+ channel blockers on the negative and positive inotropic responses associated respectively, with stimulation of the parasympathetic and sympathetic nerves. 2. In left atria paced at 2-4 Hz, the negative inotropic effect induced by field stimulation of parasympathetic nerves (in the presence of propranolol) was abolished by omega-conotoxin MVIIC, a blocker of N-type and OPQ subfamily Ca2+ channels. omega-Conotoxin GVIA (an N-type blocker), omega-agatoxin IVA (a P-type blocker), nifedipine (an L-type blocker) and Ni2+ (a T- and R-type blocker) were much less effective. 3. The positive inotropic response resulting from field stimulation of the sympathetic nerves (in the presence of atropine) was abolished by both omega-conotoxins, while omega-agatoxin IVA, nifedipine and Ni2+ were ineffective. 4. In the spontaneously beating right atria, the early negative inotropic effect produced by 1,1-dimethyl-4-phenylpiperazinium was abolished by omega-conotoxin MVIIC, whereas the late positive inotropic effect was partially reduced, but not abolished, by a high concentration of omega-conotoxin GVIA. 5. None of the peptide toxins affected the chronotropic and the inotropic responses evoked by carbachol and isoprenaline. 6. These results suggested that, under physiological conditions, the release of acetylcholine from parasympathetic nerves is dominated by an OPQ subfamily Ca2+ channel while that of noradrenaline from sympathetic nerves is controlled by an N-type Ca2+ channel. Ligand-induced noradrenaline release appeared to recruit additional type(s) of Ca2+ channel.

Animals↗
PubMed1979

Characteristics of the internal anal sphincter and the rectum of the vervet monkey.

1. The physiology of the internal anal sphincter of the vervet monkey was investigated. 2. Strips of sphincter in vitro contracted to noradrenaline and adrenaline; adrenoceptors were mainly alpha-excitatory. Strips of rectal circular muscle relaxed to noradrenaline and contained both inhibitory alpha- and beta-adrenoceptors. 3. All strips contracted to acetylcholine. After hyoscine or atropine, high doses of acetylcholine relaxed all strips by stimulating intramural inhibitory neurones as relaxations were blocked by tetrodotoxin and hexamethonium. Nicotine and DMPP gave relaxations with similar characteristics. 4. It was concluded that relaxations to acetylcholine, nicotine and DMPP were not adrenergic as relaxations still occurred in strips from sympathetically denervated or reserpinized animals. The block of these relaxations by propranolol and guanethidine was considered to be unrelated to their actions as adrenergic blocking drugs. 5. All strips relaxed to field electrical stimulation (1--5 Hz) through stimulation of intramural inhibitory neurones as tetrodotoxin blocked these relaxations. Adrenergic blocking drugs, prior reserpinization or prior section of the hypogastric nerves did not block these responses. The relaxations were not therefore adrenergic. 6. 5-Hydroxytryptamine relaxed all strips but was not the transmitter in relaxations to acetylcholine, DMPP or nicotine, nor to field electrical stimulation, as desensitization of strips of 5-HT did not alter these responses. 7. The circular smooth muscle of the internal anal sphincter had a dense terminal adrenergic innervation which rapidly decreased orad. 8. In vivo, hypogastric nerve stimulation relaxed the rectum but contracted the sphincter. Sacral nerve root stimulation caused an after-contraction in both rectum and sphincter. In vivo, a close arterial injection of adrenaline or noradrenaline inhibited the spontaneous contraction waves of the rectum, but contracted the sphincter. Both these responses were blocked by phentolamine. 9. It was concluded that the internal anal sphincter is a discrete high pressure zone which was excitatory cholinergic and adrenergic innervations and an inhibitory non-adrenergic innervation.

Adrenergic Fibers↗
PubMed1993

Cholinergic and noradrenergic modulation of the slow (approximately 0.3 Hz) oscillation in neocortical cells.

1. The pedunculopontine tegmental (PPT) cholinergic nucleus and the locus coeruleus (LC) noradrenergic nucleus were electrically stimulated to investigate their effects on the recently described slow oscillation (approximately 0.3 Hz) of neocortical neurons. Intracellular recordings of slowly oscillating, regular-spiking and intrinsically bursting neurons from cortical association areas 5 and 7 (n = 140) were performed in anesthetized cats. 2. Pulse trains to the PPT nucleus produced the blockage of rhythmic (approximately 0.3 Hz) depolarizing-hyperpolarizing sequences in 79% of tested cortical neurons and transformed this slow cellular rhythm into tonic firing. The latency of the cortical cellular response to PPT stimulation was 1.2 +/- 0.5 (SE) s and its duration was 15.9 +/- 1.9 s. The PPT-elicited suppression of the slow cellular oscillation was accompanied by an activation of the electroencephalogram (EEG) having a similar time course. Fast Fourier transform analyses of EEG activities before and after PPT stimulation showed that the PPT-evoked changes consisted of decreased power of slow rhythms (0-8 Hz) and increased power of fast rhythms (24-33 Hz); these changes were statistically significant. 3. The blockage of the slow cellular oscillation was mainly achieved through the diminution or suppression of the long-lasting hyperpolarizations separating the rhythmic depolarizing envelopes. This effect was observed even when PPT pulse trains disrupted the oscillation without inducing overt depolarization and increased firing rate. The durations of the prolonged hyperpolarizations were measured during a 40-s window (20 s before and 20 s after the PPT pulse train) and were found to decrease from 1.5 +/- 0.2 to 0.7 +/- 0.1 s. The values of the product resulting from the duration (in seconds), the amplitude (in millivolts), and number of such hyperpolarizing events within 20-s periods were 51.5 +/- 5 and 5.1 +/- 1.9 before and after PPT stimulation, respectively. 4. The PPT effect was suppressed by systemic administration of a muscarinic antagonist, scopolamine, but not by mecamylamine, a nicotinic antagonist. 5. The PPT effect on cellular and EEG cortical slow oscillation survived, although its duration was reduced, in animals with kainate-induced lesions of thalamic nuclei projecting to areas 5 and 7 (n = 3) as well as in animals with similar excitotoxic lesions leading to extensive neuronal loss in nucleus basalis (n = 2). These data indicate that the PPT effect is transmitted to neocortex through either thalamic or basal forebrain relays.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2003

Different synaptic mechanisms of long-term potentiation induced by nicotine and tetanic stimulation in hippocampal CA1 region of rats.

AIM: To investigate whether long-term potentiation (LTP) induced by nicotine and tetanic stimulation in the hippocampal CA1 region shares different mechanisms. METHODS: Extracellular population spikes of the pyramidal cell layer in the hippocampal CA1 region were recorded in vitro. RESULTS: LTP induced by the tetanic stimulation could be facilitated by nicotine 10 micromol/L, meanwhile, the tetanic stimulation did the same effect on LTP induced by nicotine 10 micromol/L. MK-801 10 micromol/L or NG-nitro-L-arginine methyl ester (L-NAME) 20 micromol/L blocked LTP induced by tetanic stimulation, but did not inhibit LTP induced by nicotine. CONCLUSION: LTP induced by nicotine shares different synaptic mechanisms with LTP induced by tetanic stimulation.

Animals↗
PubMed1991

[3H]tetraphenylphosphonium accumulation in cerebral cortical synaptosomes as a measure of nicotine-induced changes in membrane potential.

The effect of nicotine on synaptosomal membrane potential in P2 preparations of rat cerebral cortex was investigated using a membrane permeant, lipophilic cation, [3H]tetraphenylphosphonium ([3H]TPP+). [3H]TPP+ accumulated in synaptosomes in a time-dependent manner and its accumulation was decreased when the extracellular potassium concentration was increased and in the presence of the sodium channel toxin, veratridine. Nicotine (1-1000 microM) decreased the accumulation of [3H]TPP+ in both P2 synaptosomal preparations and in synaptosomes purified using Percoll gradients. This effect of nicotine was mimicked by other nicotinic agonists (1,1-dimethyl-4-phenylpiperazinium iodide, cytisine, suberyldicholine and acetylcholine) and was partially blocked by 10 microM mecamylamine and 30 microM hexamethonium. Atropine (1 microM) and the removal of calcium from the incubation mixture both enhanced the effect of nicotine while the addition of physostigmine (10 microM) reduced the nicotine-induced decrease in [3H]TPP+ accumulation, evidence that acetylcholine released from the synaptosomes by nicotine may produce hyperpolarization of synaptosomes via stimulation of presynaptic muscarinic receptors. It is concluded that the effect of nicotine on [3H]TPP+ accumulation is mediated by nicotine stimulation of a ganglionic-type nicotinic cholinergic receptor and that this method of determining synaptosomal membrane potential will provide a functional measure of presynaptic nicotinic receptor activation.

Animals↗