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At least 973 records · Page 54Linked to original sources
PubMed1983

Mediation of nicotine-induced convulsions by central nicotinic receptors of the 'C6' type.

The nature of the central receptors mediating the convulsant actions of nicotine has been investigated. Clonic tonic convulsions were seen in mice following intracerebroventricular (i.c.v.) injection of nicotinic agonists. (-)Nicotine was the most potent agonist tested, with a CD50 of 7.9 X 10(-9) mol. (+)Nicotine, cytisine, DMPP and lobeline were 10-100 times less potent than (-)nicotine. Nicotine induced convulsions were antagonized by ganglion blocking drugs administered intraventricularly. Pentolinium was the most potent antagonist, with an ED50 of 4 X 10(-11) mol. The ganglion-blockers also produced convulsions in their own right at doses 80-1000 times the anti-nicotine ED50 dose. 'C10' blockers, such as d-tubocurarine, did not antagonize nicotine-convulsions, but produced convulsions in their own right. alpha-Bungarotoxin had neither convulsant nor anticonvulsant activity at the doses tested. It is concluded that the central receptors mediating this nicotinic effect resemble ganglionic ('C6') receptors, rather than neuromuscular ('C10') receptors.

Animals↗
PubMed1985

Mechanism of the CNS-mediated pressor response to intracerebroventricular injection of noradrenaline in unanaesthetized rats.

Catecholamines administered intracerebroventricularly (i.c.v.) have cardiovascular effects mediated by the CNS. Although hypotension constitutes the more prominent response, an increase in blood pressure has also been reported after the intracerebroventricular injection of these amines. Anaesthesia interferes with pressor responses mediated by the CNS to a larger extent than with depressor mechanisms and constitutes one of the major factors influencing the pattern of response to the amines. The depressor response observed after the intracerebroventricular administration of noradrenaline is reversed into increases in blood pressure in awake animals. In the present experiment, the action of intracerebroventricularly injected noradrenaline was compared in anaesthetized and conscious rats. The results indicated that the pressor response in awake rats was not mediated by the sympathetic nervous system and involved the release of a pituitary humoral-factor, most probably vasopressin, whereas the depressor response observed in anaesthetized animals was not dependent on pituitary mediation. The involvement of histaminergic mechanisms in the CNS in the control of the pressor response to intracerebroventricularly administered noradrenaline in the rat is proposed.

Anesthesia↗
PubMed1992

Behavioural effects of anatoxin, a potent nicotinic agonist, in rats.

Preliminary behavioural studies with the nicotinic agonist (+)-anatoxin have been carried with procedures sensitive to (-)-nicotine. In experimentally naive rats, (+)-anatoxin decreased locomotor activity; this effect resembled that of (-)-nicotine, but it was not blocked by mecamylamine. In nicotine-tolerant rats, (+)-anatoxin differed from (-)-nicotine because it did not increase locomotion. However, in rats trained to discriminate nicotine from saline in an operant conditioning procedure, (+)-anatoxin produced a partial nicotine-like discriminative stimulus effect that was blocked by mecamylamine, and a decreased rate of responding that was insensitive to mecamylamine. The behavioural profile of (+)-anatoxin differs from that of (-)-nicotine and it can be used for further investigations of CNS nicotinic receptors.

Animals↗
PubMed1990

Microinjections of a nicotinic agonist into dopamine terminal fields: effects on locomotion.

Nicotine induces locomotion, a behavior associated with the mesocorticolimbic dopamine system. The present study determined the effects on locomotion of direct microinjections of the nicotinic agonist cytisine into four DA terminal fields were nicotinic receptors have been localized: nucleus accumbens (NAS, n = 20), caudate putamen (CPU, n = 9), olfactory tubercle (OT, n = 8), and medial prefrontal cortex (MPC, n = 12). Male Long-Evans rats were injected with cytisine (0.1, 1, 10 and 100 nanomoles per 0.5 microliters per side) or vehicle through indwelling cannulae, and locomotor activity was recorded during a 60-minute test session; each animal was tested with each dose in counterbalanced order. NAS injections of the three highest doses of cytisine increased locomotion relative to vehicle injections; injections in the CPU, dorsal to the NAS, were ineffective, as were MPC and OT injections. The data support the notion that systemic nicotine may interact with dopaminergic projections to the NAS to produce increases in locomotor activity.

Alkaloids↗
PubMed1991

Effect of captopril on plasma levels of neuropeptide Y (NPY)-like immunoreactivity in the pithed guinea pig.

The effect of exogenous angiotensin II (A II) and the angiotensin converting enzyme (ACE)-inhibitor captopril on plasma levels of neuropeptide Y-like immunoreactivity (NPY-LI) has been studied in the pithed guinea pig. Four periods of pre-ganglionic nerve stimulation (PNS, 8 Hz for 30s with 20 min intervals) were applied and the increases of mean arterial blood pressure (delta BP), heart rate (delta HR) and plasma NPY-LI (delta NPY-LI) in response to PNS were analysed in non-pre-treated and captopril pre-treated animals. Captopril (5 mg x kg-1 i.v.) reduced basal blood pressure and delta BP by 20% and 11%, respectively. Infusion of A II (0.5 microgram x kg-1 = min-1 i.v.) caused a significant increase in basal and PNS-induced maximal blood pressure response but reduced delta BP in captopril and non-pre-treated animals by 40% and 16%, respectively. A II elicited a long-lasting increase of basal heart rate by 12% but reduced delta HR by 36% in non-pre-treated animals. However, neither captopril alone nor A II infusion to captopril pre-treated animals significantly changed heart-rate values. The effects of exogenous A II on the cardiovascular responses were abolished by the A II-antagonist saralasin (a bolus injection, 40 micrograms x kg-1 i.v. followed by an infusion, 30 micrograms x kg-1 x min-1), which per se had no significant effect. Captopril pre-treatment reduced basal plasma NPY-LI levels by 38% and delta NPY-LI by 46% in response to PNS 1. However, neither in non-pre-treated nor in captopril pre-treated animals did infusion of A II significantly change the plasma NPY-LI level.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1981

Reflex cardiovascular responses induced by electrical stimulation of glossopharyngeal nerves in the rat.

Reflex cardiovascular responses to electrical stimulation of glossopharyngeal nerves (GPN) were studied in Dial-Urethane anesthetized rats. GPN stimulation at 3 V, 0.3 msec and 50 Hz produced maximal reflex depressor (34 +/- 2 mmHg) and bradycardia (21 +/- 2 beats/min) responses that were altered as follows: pentolinium (0.25 mg/kg, i.a.) blocked approximately 72% and 89% of control values of depressor and bradycardia responses, respectively; tripelennamine (5 mg/kg, i.a.) significantly reduced depressor responses (76%); whereas atropine (0.4 mg/kg i.a.) blocked only bradycardia (85%). Regional blood flow studies showed that GPN stimulation reduced systemic arterial pressure (approximately 25%), and increased iliac artery blood flow (5%), and decreased blood flow through the renal (14%) and superior mesenteric (13%) arteries. Hence, decreases in vascular resistance during GPN stimulation were greater in the hindlimb vascular bed (28%) than in the renal (14%) or the mesenteric vasculatures. In addition, the magnitude of decreases in hindlimb vascular resistance by GPN stimulation was reduced (80%) by pretreatment with tripelennamine, but not by atropine. The results suggest that reductions in arterial blood pressure and hindlimb vascular resistance of the rat in response to GPN stimulation may be mediated via a histaminergic vasodilator mechanism, and that there may be a differential pattern of reflex vascular adjustments of blood flow and vascular resistance among regional vasculatures of the rate.

Animals↗
PubMed1991

Development of a functional innervation of the iris dilator muscle by sympathetic nerve fibres in the rat.

These studies using both in situ and in vitro preparations were designed to determine the time of onset of a functional sympathetic innervation to the dilator muscle of the rat iris during postnatal development. The preganglionic nerve trunk to the superior cervical ganglion was stimulated and measurements made of pupil diameter. Alternatively, intracellular recordings were made from the dilator muscle cells and the response to stimulation of the intramural nerves was measured. During the second postnatal week, a decrease in the resting pupil diameter under low lighting conditions was observed, reflecting the normal developmental increase in size of the iris. On account of the small size of the iris in rats up to 10 days postnatal, the in vivo experiments were a reliable test of a functional innervation only in older animals. In all cases, stimulation of the preganglionic nerve trunk in situ caused dilatation of the pupil. Stimulation of the sympathetic nerves in vitro, in preparations of iris taken from rats of various ages, evoked a slow depolarisation mediated via alpha adrenoceptors. Such responses could be recorded in irides from rats as young as 3 days postnatal. Spontaneous activity was recorded in irides towards the end of the second postnatal week just prior to the time of normal eye opening, and may reflect the onset of photomechanical coupling. We conclude that the sympathetic nerves within the iris are capable of evoking membrane potential changes in the dilator muscle cells in the early postnatal period, well before the nerve plexus in the iris is fully differentiated.

Animals↗
PubMed1996

Activation of tyrosine hydroxylase by pituitary adenylate cyclase-activating polypeptide (PACAP-27) in bovine adrenal chromaffin cells.

The effect of pituitary adenylate cyclase-activating polypeptide (PACAP-27) on tyrosine hydroxylase activity has been studied in intact, cultured, bovine adrenal chromaffin cells. Tyrosine hydroxylase activity was determined in situ by measuring the production of 14CO2 following the hydroxylation and rapid decarboxylation of [14C]tyr offered to the cells. PACAP-27 increased tyrosine hydroxylase activity 3-fold over 10 min. With an EC50 of 10-20 nM. PACAP-38 was approximately 2-fold less potent. Removing extracellular Ca2+ reduced basal tyrosine hydroxylase activity and the activation produced by both PACAP-27 and forskolin by about 20%. In the absence of extracellular Ca2+, chelation of intracellular Ca2+ by treating cells with BAPTA-AM (50 microM) caused a consistent 40-50% reduction in basal tyrosine hydroxylase activity and in the responses to forskolin and PACAP-27. The tyrosine hydroxylase activation produced by PACAP-27 was unaffected by the protein kinase C inhibitor Ro 3l-8220 (3 microM), but was reduced by 85% by the protein kinase A inhibitor H89 (10 microM). PACAP-27 increased cellular cyclic AMP levels 3-fold at 100 nM. The results suggest that PACAP-27 activates tyrosine hydroxylase in bovine chromaffin cells through cyclic AMP formation and protein kinase A activation, and that both extracellular and intracellular Ca2+ modulate the effect of the adenylate cyclase/cyclic AMP/protein kinase A signalling pathway on tyrosine hydroxylase activity.

Animals↗