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PubMed1983

Neuroeffector mechanisms of the defense reaction in the rat.

Electrical stimulation of the dorsal periaqueductal gray matter (DPAG) eliciting flight behavior in awake rats caused an increase in arterial blood pressure (BP), heart rate (HR) and respiration in rats anesthetized with urethane. The hypertension was markedly reduced by 5 mg/kg of intravenously injected hexamethonium or bretylium, virtually abolished by 5 mg/kg of phentolamine and partially antagonized by 0.1 mg/kg of the alpha 1-adrenoceptor blocker, prazosin. The tachycardia induced by DPAG stimulation was partially antagonized by hexamethonium or bretylium and abolished by propranolol (5 mg/kg, IV) or practolol (5 mg/kg, IV), but not affected by N-butylscopolamine (10 mg/kg, IV). Phentolamine increased basal HR and abolished the tachycardic response caused by either brain stimulation or intravenous noradrenaline. Prazosin moderately decreased the response to noradrenaline, but did not affect basal HR or the tachycardia induced by brain stimulation. The increase in respiratory amplitude occurring during brain stimulation was abolished by phentolamine as well as by prazosin, while the increase in respiratory rate was moderately reduced by phentolamine and propranolol. These results demonstrate that the cardiovascular component of the defense reaction of the rat is almost entirely due to a sharp increase in sympathetic tone. They also suggest that the hyperventilation induced by aversive brain stimulation is modulated by central and peripheral adrenergic mechanisms.

Animals↗
PubMed1992

Immunohistochemical, morphological and functional changes in the peripheral sudomotor neuro-effector system in elderly people.

Age-related changes in the human peripheral sudomotor neuro-effector system have been investigated in six 80-year-olds and six young adults. Histochemical and immunohistochemical studies on forearm skin biopsies showed diminished vasoactive intestinal polypeptide (VIP) and calcitonin gene related peptide (CGRP)-like immunoreactivity and a virtual absence of acetylcholinesterase in the elderly sudomotor nerve endings compared to the young. Reduced size of nerve bundles and decreased density of sympathetic nerve endings adjacent to the sweat glands of old people were shown by the neuronal marker, protein gene product (PGP 9.5), and by electron microscopy. Image analysis techniques were also used to demonstrate a marked regression in secretory coil size with age. Functional decrements accompanying the neurochemical and morphological changes in the neuro-effector system were measured in ten 80-year-olds by local quantitative nicotine axon reflex responses and compared with 12 young adults. These studies demonstrate marked regressive changes in both the nerve endings and target cells in old age and appear to express a significant loss of vigour in trophic interactions.

Acetylcholinesterase↗
PubMed1992

Sites at which neuropeptide Y modulates parasympathetic control of heart rate in guinea pigs and rats.

Immunohistological evidence indicates that neuropeptide Y (NPY) is present in the cardiac innervation of numerous species. The present experiments determined if NPY influences in vivo parasympathetic control of heart rate in guinea pigs and rats by either pre- or postganglionic mechanisms or by an interaction at muscarinic receptors at the sino-atrial node. Urethane-anesthetized animals were prepared with arterial and venous catheters, and ECG leads. The cervical vagi were sectioned and propranolol was administered to minimize reflex changes in heart rate. Methacholine injection, carbachol injection, or electrical stimulation of the peripheral end of the vagus nerve was performed to activate the neuroeffector site, intracardiac ganglion cells, or preganglionic neurons, respectively. All three trials were performed before, during, and after NPY infusion. No differences in methacholine- or carbachol-induced bradycardia were observed between control and NPY groups in either species. NPY infusion inhibited vagal-mediated bradycardia in guinea pigs and in rats. However, NPY inhibited vagal-mediated bradycardia at a lower dose in guinea pigs (1 microgram/kg/min) than in rats (4 micrograms/kg/min). These data indicate that NPY modulates cardiac vagal preganglionic, but not postganglionic nerve function or neuroeffector sites at the sino-atrial node, in guinea pigs and rats. Furthermore, due to the different effective dosages, NPY may play a greater modulatory role in guinea pigs than in rats.

Animals↗
PubMedDate not supplied

Effect of calcitonin gene-related peptide on the neuroeffector mechanism of sympathetic nerve terminals in rat vas deferens.

In order to evaluate the mode of action of calcitonin gene-related peptide (CGRP) on the neuroeffector mechanism of peripheral sympathetic nerve fibers, the effects of CGRP were tested on the electrical stimulated and the non-stimulated preparations of the isolated rat vas deferens. The contractile responses, which were mediated predominantly by activation of postganglionic noradrenergic nerve fibers, were dose-dependently inhibited by CGRP in concentrations ranging from 0.1 to 10 nM. The inhibitory response produced by CGRP in high concentrations (greater than 2 nM) usually returned to the control level at 20-30 min and were rarely tachyphylactic. The inhibitory action of CGRP was not modified by pretreatment with 10(-7) M propranolol or 10(-7) M atropine. Contractions produced by exogenous norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in unstimulated preparations were not affected by pretreatment with CGRP in a low concentration (less than 2 nM). On the other hand, the contractions were slightly reduced 1 min after pretreatment with CGRP in high concentrations (greater than 5 nM), which recovered in 15 min after constant flow washout. High concentrations of CGRP also caused a concentration-dependent relaxation on the precontracted preparations produced by high potassium (60 mM K+) solution. These results suggest that CGRP in high concentrations (greater than 5 nM) may have a non-specific inhibitory action on the postsynaptic plasma membrane of the smooth muscle cell and a postulated CGRP receptor exists presynaptically in the rat vas deferens and that CGRP may inhibit the release of NE during adrenergic nerve stimulation.

Animals↗
PubMed1995

Excitatory action of [Leu13]motilin on the gastrointestinal smooth muscle isolated from the chicken.

The effects of a porcine motilin analogue, [Leu13]motilin (LMT) on the smooth muscle preparations isolated from the chicken gastrointestinal (GI) tract were investigated in vitro. In the proventriculus, LMT (100 nM to 30 microM) caused an atropine-sensitive contraction and enhanced the electrical field stimulation (EFS)- or 1,1-dimethyl-4-phenyl-piperazinium (DMPP)-induced contraction without affecting the response to acetylcholine (ACh). LMT also caused a concentration-dependent contraction of the intestinal tract (duodenum, jejunum, ileum, and colon). The responsiveness to LMT was strongest in the jejunum and weakest in the colon. The responses to LMT in the intestinal segments were not affected by tetrodotoxin, atropine, hexamethonium, pyrilamine, spantide, and 5-hydroxyltryptamine-induced desensitzation, but significantly decreased by verapamil or removal of external Ca2+. LMT did not enhance the EFS- or DMPP-induced contraction in the ileum. Canine motilin also contracted the intestinal segments in a similar concentration range to LMT with an equal potency, but erythromycin A (EMA) and N-ethyl-N-demethyl-8,9-anhydroerythromycin A, 6-9-hemiketal (EM523) showed only a weak contractile activity even at high concentration (up to 100 microM), indicating that motilin receptors in the chicken intestine were somewhat different from those of mammals. In conclusion, LMT produces an excitatory response in the chicken GI tract with a different sensitivity from region to region. The mechanisms of the action were different between the proventriculus and small intestine; that is, LMT contracts the small intestine through the direct action on the smooth muscle cells, but this peptide acts on the enteric cholinergic neurones and stimulates ACh release, and thus regulates autonomic neuroeffector transmission in the proventriculus.

Acetylcholine↗
PubMed1985

Functional and biochemical basis for multiple muscarinic acetylcholine receptors.

The novel antimuscarinic compound pirenzepine (PZ) has generated considerable interest in the basis and the implications of muscarinic acetylcholine receptor (mAChR) heterogeneity. [3H]PZ has been used extensively to identify and characterize the putative M1 (high affinity for PZ) mAChR subtype, which predominates in central nervous system (CNS) and ganglia. The heterogeneity sensed by PZ is not identical to the heterogeneity sensed by agonists. Differences in effector coupling do not necessarily provide a simple explanation for the molecular basis of these putative M1 and M2 subtypes. Therapeutic and untoward effects of muscarinic drugs may be mediated by independent mAChR subpopulations which may be pharmacologically exploited to produce more highly selective as well as efficacious new drugs.

Alzheimer Disease↗
PubMed1983

Intraneural stimulation as a method to study sympathetic function in the human skin.

Intraneural electrical stimulation of sympathetic postganglionic axons was made in human skin nerves combined with recordings of skin resistance and a photoelectric pulse plethysmogram within the innervation zone. Tungsten microelectrodes were used first to record multiunit sympathetic activity in sural or median nerves. After blocking the nerve with local anaesthetics proximal to the recording site the electrodes were then used for intraneural stimulation. Stimulation led to reduction of skin resistance which was frequency dependent. A short train of stimuli reduced skin resistance transiently and the response was potentiated by a single stimulus delivered up to 2.5 min. prior to the train. Vasoconstrictor responses did not always occur and were relatively independent of stimulation frequency. The method may be useful for physiological and pathophysiological studies of sympathetic neuroeffector transmission in man.

Adult↗
PubMed1987

Immunoblockade of response to capsaicin in the rat vas deferens: evidence for the involvement of endogenous calcitonin gene-related peptide.

In the rat isolated vas deferens, capsaicin induced a transitory inhibition of the nerve-mediated contractions. This effect was not observed in preparations excised from capsaicin-pretreated rats nor following a first exposure to a high concentration of capsaicin in vitro. Exogenous calcitonin gene-related peptide (CGRP) induced a concentration-related inhibition of the nerve-mediated contractions. A highly avid and specific anti-CGRP serum raised in rabbits against conjugated synthetic rat CGRP inhibited selectively the capsaicin effect. These findings are consistent with the hypothesis that, in this preparation, the specific visceromotor response to capsaicin is brought about by the release of endogenous CGRP from sensory nerves.

Animals↗
PubMed1991

Modulation of neuroeffector transmission in the guinea pig pulmonary artery by endogenous nitric oxide.

The influence of endogenous nitric oxide (NO) on neuroeffector transmission in segments of guinea pig pulmonary artery was analyzed by application of NG-monomethyl-L-arginine (L-NMMA). L-NMMA enhanced contractile responses to nerve stimulation and this enhancement was counteracted by L-arginine. The enhancement remained after removal of the endothelium. L-NMMA enhanced contractions to exogenous noradrenaline. After blockade of adrenergic transmission by phentolamine, L-NMMA enhanced contractions induced by nonadrenergic-noncholinergic (NANC) neurotransmission. Stimulation-induced release of [3H]noradrenaline was unchanged by L-NMMA. The results suggest that endogenous NO exerts a postjunctional inhibition on adrenergic neurotransmission in the guinea pig pulmonary artery. A concomitant pre- and/or postjunctional inhibition of NANC transmission is implicated. The neuromodulation by NO does not require an intact endothelium.

Animals↗
PubMed1993

Neuropeptide Y modulation of A1 noradrenergic neuron input to supraoptic vasopressin cells.

A1 noradrenaline (NA) neurons provide a direct excitatory input to supraoptic nucleus (SON) vasopressin (VP) cells. Many A1 cells contain neuropeptide Y (NPY) and past studies have established that NPY exerts excitatory postsynaptic effects on VP cell activity. We have now investigated whether NPY might also modulate A1 input to VP cells via presynaptic mechanisms. Experiments done in pentobarbitone-anesthetized rats demonstrated that SON application of NPY (10 microM) excited VP cells but also depressed their response to activation of the A1 input. These two effects were not correlated, suggesting independent mechanisms. The putative Y1 agonist [Leu31,Pro34]NPY (10 microM) also excited VP cells but did not alter their response to activation of the A1 input. In contrast, the putative Y2 receptor agonist Ac-[Leu28,Leu31]NPY24-36 mimicked the synaptic depression produced by NPY but did not significantly alter spontaneous activity. These data are consistent with the proposal that NPY acts on Y1-like receptors to excite VP cells but can also act on a presynaptic Y2-like receptor to depress A1-VP cell synaptic transmission.

Animals↗
PubMed1992

Effects of S14001 on adrenergic neuroeffector interaction in isolated canine saphenous veins.

1. The effects of (S) fluoro-6 (morpholinyl-2 methoxy)-8-tetrahydro-1,2,3,4 quinoleine (S14001) on adrenergic neurotransmission in isolated canine saphenous veins were investigated in experiments which measured the accumulation, overflow and metabolism of 3H-norepinephrine. 2. S14001 inhibited the accumulation of total tritium (3H-norepinephrine and 3H-metabolites of norepinephrine) in a concentration-dependent manner. 3. Under basal conditions, S14001 increased tension and basal effiux of total tritium; the latter consisted predominantly of 3H-DOPEG. The increases in these parameters were not inhibited by desmethylimipramine (DMI). 4. During electrical stimulation, S14001 increased the contraction and overflow of total tritium; the latter consisted predominantly of 3H-DOPEG. The increases in these parameters were inhibited by DMI. 5. These experiments suggest that S14001 has dual effects on adrenergic neurotransmission in the canine saphenous vein: (a) an inhibitory action on the neuronal accumulation; and (b) a pharmacological displacement of the transmitter from adrenergic nerve terminals.

Animals↗
PubMed1994

Pre- and postjunctional muscarinic receptor subtypes in the vas deferens of rat.

1. A pharmacological study of the pre- and postjunctional muscarinic receptors of the isolated rat vas deferens was carried out using more selective agonists and antagonists. 2. The prejunctional receptor was characterized on electrically stimulated preparations, while the postjunctional receptor was studied on vasa deferentia without stimulation. 3. The results indicate that atropine exhibited a similar affinity for the two populations of muscarinic receptor subtypes of this tissue. 4. 4-DAMP was able to differentiate with high affinity a subtype located at postjunctional level which had pharmacological similarities with the M3-ACh subtype and with low affinity a subtype located at prejunctional level. 5. The selective M1-ACh agonist McN-A-343 was not able to activate the postjunctional receptor, but showed a similar affinity to ACh for the prejunctional one. 6. At present, the prejunctional receptor can be considered as an atypical M1-ACh subtype based on the results obtained with the selective drugs available.

Animals↗
PubMed1996

Does motilin stimulate the gastrointestinal motility of the pig? In vitro study using smooth muscle strips and dispersed muscle cells.

To clarify the physiological role of motilin in the pig gastrointestinal (GI) tract, effect of Leu13-porcine motilin (LMT) on the contractility of GI smooth muscle was investigated in studies using isolated muscle strips and dispersed muscle cells. LMT produced no contraction in either longitudinal muscle (LM) or circular muscle (CM) of the stomach (fundus, corpus, antrum), duodenum, ileum and colon even at 1 microM. Pretreatment with LMT (1 nM-1 microM) did not potentiate the contractile response to acetylcholine (ACh) in each muscle strip. Dispersed cells from the duodenum responded to ACh in a concentration-dependent manner (EC50 = 10 pM), but not to LMT even at a high concentration (10 microM). Electrical field stimulation (EFS) caused a frequency-dependent (0.2-10 Hz) contraction of the duodenal LM that was almost completely inhibited by atropine or tetrodotoxin. EFS caused the relaxation of duodenal CM in a frequency-dependent manner (0.1-10 Hz). This relaxation was not inhibited by atropine, propranolol, phentolamine or guanethidine, indicating the involvement of noncholinergic, nonadrenergic (NCNA) nerves. NG-nitro L-arginine methylester (L-NAME, 100 microM) attenuated the EFS-induced relaxation and the inhibition at low frequency was larger than that at high frequency. L-Arginine prevented the inhibition by L-NAME but D-arginine did not. LMT (1 nM-1 microM) had no influence on EFS-induced cholinergic contraction of LM and EFS-induced NCNA relaxation of CM layer. The present in vitro studies indicate that motilin is ineffective in producing contraction and in modulating the autonomic neuroeffector transmission of the pig GI smooth muscle, and suggest that pig GI smooth muscle lacks functional motilin receptors.

Acetylcholine↗
PubMed1980

Candidate mechanisms for inhibition of neurotransmitter release by narcotic analgesics and endorphins.

Some neurones are endowed with receptors for endorphins and narcotic analgesics. Activation of these receptors results in a depression of the release of transmitter per impulse. It is currently believed that narcotic analgesics and endorphins depress the stimulus-induced influx of calcium (Ca2+) into the terminal and thereby modify the amount of the ion which triggers the release of the transmitter from intracellular stores. The influx of Ca2+ is largely governed by the Ca2+ "channel", which opens during depolarization of the neuronal membrane either after an action potential (electrical stimulus) or in the presence of high extracellular potassium (K+) or nicotinic stimulants (chemical stimulus). The evoked influx of Ca2+ can be affected by a direct action on the Ca2+ "channel" or by primary actions on other membrane properties that subsequently regulate the Ca2+ "channel". In many tissues narcotic analgesics and endorphins fail to inhibit transmitter release. This may be accounted for by the possibility that either such neurones lack presynaptic opiate receptors or that the function of existing receptors remains latent under the experimental conditions employed. Currently, there is insufficient evidence for endorphins physiologically modulating transmitter release.

Analgesics, Opioid↗
PubMed1988

Modulation of peripheral sympathetic nerve transmission.

The past 15 years have been witness to a remarkable growth in knowledge regarding the modulation of "sympathetic traffic" to neuroeffector organs, including vascular tissue. The release of norepinephrine from peripheral sympathetic neurons is now known to be under both negative and positive feedback control. Norepinephrine, when released from peripheral neurons, acts on presynaptic alpha 2-receptors to inhibit further neurotransmission. Vascular postsynaptic alpha 2-receptors, sensitive to circulating catecholamines, subserve vasoconstriction. The antihypertensive agents clonidine, guanabenz and guanfacin likely reduce blood pressure by acting centrally on alpha 2 postsynaptic neurons to limit sympathetic transmission to blood vessels. Clonidine can produce venoconstriction and thereby improve orthostatic hypotension by activating venous alpha 2-receptors. Additional presynaptic dopaminergic receptors (DA2), muscarinic receptors (acetylcholine), opioid receptors, prostaglandin receptors, adenosine receptors (A1) and histamine (H2) receptors are present on sympathetic nerve membranes and, when engaged with the appropriate ligand, can limit the exocytotic process. Gamma-aminobutyric acid and serotonin demonstrate similar roles in reducing sympathetic nerve activity. In contrast to these inhibitory presynaptic mechanisms, facilitation of norepinephrine release appears to occur by way of neuronal angiotensin II receptor activation and perhaps through stimulation of sympathetic nerve membrane beta 2-receptors. An appreciation of these inhibitory and facilitator mechanisms is useful in the treatment of a variety of clinical conditions, including hypertension, heart failure, orthostatic hypotension, septic shock and a number of common withdrawal syndromes.

Animals↗
PubMed2003

Fe2+ decreases the taurine-induced Cl- current in acutely dissociated rat hippocampal neurons.

The effects of ferrous ions (Fe(2+)) on taurine-induced Cl(-) current (I(tau)) recorded from single neurons, which was freshly isolated from the rat hippocampal CA1 area, were studied with conventional whole-cell recording under voltage-clamp conditions. Using standard pharmacological approaches, we found that the currents gated by concentrations of taurine (<or=10 mM), which existed in about 90% of the hippocampal neurons tested, were predominantly mediated by strychnine-sensitive glycine receptors. When co-applied with taurine, Fe(2+) effectively depressed I(tau) in a concentration-dependent manner, with an IC(50) of 3.76 mM and Hill coefficient of 1.01, while preincubation with 1 mM Fe(2+) alone did not affect the following membrane currents elicited by taurine. The result suggests that resting taurine-gated channels are insensitive to Fe(2+). Since internal cell dialysis with 3 mM Fe(2+) failed to modify I(tau), it was deduced that the site of action of Fe(2+) is extracellular. Furthermore, the Lineweaver-Burke double reciprocal plot of normalized response to taurine against the concentration of taurine illustrated that the depression of I(tau) was noncompetitive, therefore Fe(2+) may act on the glycine receptor-chloride ionophore complex at a site distinct from where taurine binds. Various concentrations of Fe(2+) ranging from 0.1 to 20 mM depressed I(tau) and this extracellular depression was independent of membrane voltage. These results indicate that Fe(2+) decreases I(tau) in acutely dissociated rat hippocampal neurons and the inhibition of glycine receptors by Fe(2+) might be one possible approach through which Fe(2+) induces seizures.

Animals↗