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PubMed1983

Enhancement of desynchronized sleep signs after pontine microinjection of the muscarinic agonist bethanechol.

The question of which brainstem neuronal receptors can mediate cholinergic REM sleep induction was investigated by injecting the pure muscarinic agonist bethanechol via glass micropipettes in the pontine tegmentum of cats. The REM sleep enhancement was observed to be equally potent, equally dose-dependent and its appearance equally site-dependent as that previously observed with carbachol, a mixed muscarinic/nicotinic agonist. The results suggest that the pharmacological activation of muscarinic receptors in pontine neurons is sufficient to trigger REM sleep.

Animals↗
PubMed1984

Accelerated regeneration of central catecholamine fibers in cat occipital cortex: effects of substance P.

Remarkably fast regeneration of central noradrenaline (NA) fibers was recently observed in the 6-hydroxydopamine (6-OHDA)-perfused occipital cortex. In the present study, we found that this reinnervation by NA fibers was further accelerated by substance P (SP) perfused into the fourth ventricle but not by SP directly perfused into the cortex. The site of SP's action is therefore most likely located in the soma-dendritic area of NA cells in the locus coeruleus (LC). The regeneration-stimulating effect of SP seems to be mediated by a process specific to SP, since the similar treatment with bethanechol in place of SP was ineffective.

Animals↗
PubMed1986

The role of striatal cholinergic mechanisms for the development of limb rigidity: an electromyographic study in rats.

The muscarinic cholinergic agonist bethanechol (0.25-1.0 micrograms) injected bilaterally into various parts of the rat neostriatum induced a tonic electromyogram (EMG) activity in the gastrocnemius muscle which is considered to be a measure of limb rigidity. This tonic EMG activity was found to be dose-dependent and muscarine-specific since it could be blocked by coadministration of the muscarinic antagonist N-methylscopolamine (1.0 micrograms). Tonic EMG activity of comparable amount was observed after injections of bethanechol (1.0 microgram) into all regions of the neostriatum but not into the globus pallidus, thalamus, zona incerta or cortex. The tonic EMG activity induced by intrastriatal injection of bethanechol (1.0 microgram) was abolished by a subsequent injection of the GABAmimetic drug muscimol (25 ng) into the posterior part of the substantia nigra pars reticulata suggesting that bethanechol-induced limb rigidity is mediated via impairment of GABAergic transmission within the substantia nigra pars reticulata.

Animals↗
PubMed1986

Desensitization of muscarinic acetylcholine receptors: possible relation to receptor heterogeneity and phosphoinositides.

The increases in firing rates of hippocampal cells were examined following microiontophoretic application of several muscarinic cholinergic receptor agonists. The agonists studied had been pharmacologically characterized previously and divided into two classes: class A agonists (e.g. acetylcholine, carbamylcholine, and oxotremorine-M) which maximally stimulate PI turnover and reveal mAChR heterogeneity, and class B agonists (e.g. bethanecol and oxotremorine-1) which poorly stimulate PI turnover and do not alter mAChR conformation/orientation in the hippocampus. While comparable stimulatory effects on hippocampal pyramidal cell firing rates were seen with both classes of agonists during short (20 s) ejection periods, longer applications (greater than 25 s) produced class-dependent differential firing patterns. Prolonged ejection of class A agonists selectively desensitized cells to further, continued application in the same ejection period, and the firing rates declined. Class B agonists produced stimulatory responses in hippocampal cells during the entire ejection period, and DE was not observed. This desensitization effect (DE) was observed only for bursts and not for simple spikes.

Acetylcholine↗
PubMed1988

Cholinergic brainstem sites for gain control of vestibulospinal reflexes in cats.

Decerebrate cats were injected with carbachol into the locus coeruleus (LC) or with carbachol or bethanechol into the dorsal pontine reticular formation (pRF) of one side; recordings were made of the tonic contraction of forelimb extensor muscles of both sides and of their responses to sinusoidal roll tilt of the animal. Both drugs had similar effects when injected into the pRF: a decrease in the tonic contraction of limb extensors and a greatly enhanced amplitude and gain with slightly decreased phase lead in the responses to animal tilt of the forelimb extensor, triceps brachii, ipsilateral to the side of injection. Injected into the LC, carbachol produced a response opposite to the above: it increased the tonic contraction of limb extensors ipsilateral to the side of injection, but decreased the amplitude and gain of the EMG responses of limb extensor muscles to labyrinth stimulation induced by sinusoidal tilt. These findings did not depend on changes in posture since they were still observed when postural EMG activity was maintained constant by appropriate changes in static stretch of the muscle. Moreover, the magnitude of the effects increased in a dose-dependent manner. Results suggest that cholinergic activation of dorsal pRF neurons through muscarinic receptors increases the background discharge of medullary inhibitory reticulospinal (RS) system neurons, thus increasing their modulatory influence. Further, it is postulated that cholinergic activation of LC neurons would cause them to inhibit this tonic facilitatory drive by the pRF. Common to both sites of carbachol injection is the increase in phase lag of the EMG response of limb extensors to animal tilt.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Bethanechol-induced increase in hypothalamic estrogen receptor binding in female rats is related to capacity for estrogen-dependent reproductive behavior.

Neuroactive agents associated with different neurotransmitter systems can modulate the number of hypothalamic estrogen binding sites. It has been demonstrated previously that the muscarinic cholinergic agonist, bethanechol, administered 30 min prior to in vitro estrogen receptor assays increases the concentration of hypothalamic estrogen binding sites by 30-35% in female rats. Bethanechol was without effect on male hypothalamic preparations. In order to investigate further this sex difference and in an attempt to determine a relationship between the modulation of estrogen binding sites and a sexually differentiated function, bethanechol was given to female rats rendered either anovulatory and capable of displaying lordosis or anovulatory and behaviorally insensitive to estrogen. The results showed that bethanechol significantly increased the number of estrogen binding sites in females capable of displaying lordosis but not in females which did not show this estrogen-dependent behavior. It is possible that the capacity for drug-induced modulation of estrogen binding sites could be related functionally to the ability to display lordosis behavior.

Animals↗
PubMed1988

Age-related decrements in the muscarinic enhancement of K+-evoked release of endogenous striatal dopamine: an indicator of altered cholinergic-dopaminergic reciprocal inhibitory control in senescence.

Previous experiments have indicated that the release of striatal dopamine (DA) is controlled by inhibitory DA autoreceptors which are mediated by inhibitory cholinergic heteroreceptors (HTRs). Activation of the HTRs by muscarinic or nicotine agonists potentiates the K+-evoked release of DA from the striatum. Present experiments were carried out to determine if this relationship is altered as a function of aging. Cross-cut striatal tissue slices obtained from 3 age-groups (6, 12-18 and 24 months) Wistar rats were superfused with a modified Krebs-Ringer basal release medium containing 2.5 mM KCl. After a 30-min equilibration period, a 5-min baseline fraction was collected from each chamber. The medium was then switched to one containing 30 mM KCl, and depending upon the experiment, 1 of 4 concentrations of a particular muscarinic (oxotremorine, pilocarpine, carbachol or bethanecol) or nicotinic (nicotine) agonist. In some experiments DA autoreceptor function was assessed directly with haloperidol. Six 5-min fractions were taken during depolarization. DA release was assessed using high performance liquid chromatography coupled to electrochemical detection. Results indicated that the efficacy of the muscarinic agonists was reduced in an age-dependent manner with the oldest age groups showing the smallest enhancement. The age at which the decline was seen was dependent on the muscarinic agonist that was applied. Deficits were seen as early as 12 months when full agonists (e.g. carbachol) were applied, but did not appear until 18 months when partial agonists (e.g. oxotremorine) were applied. These age-related alterations were not seen when haloperidol or nicotine were used to enhance the K+-evoked release of DA.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Muscarinic cholinergic modulation of hypothalamic estrogen binding sites.

Studies from other laboratories have demonstrated that agents which interact with the dopaminergic and noradrenergic neurotransmitter systems alter the concentrations of cytosolic hypothalamic estrogen receptors. These results have led to the hypothesis that catecholamine systems are involved intimately with the regulation of brain estrogen receptors. The present study was undertaken to determine if agents from a different neurotransmitter system similarly affect [3H]estradiol binding. The data presented here show that the muscarinic cholinergic agonist, bethanechol, increases the number of cytosolic hypothalamic estradiol binding sites in ovariectomized female rats by as much as 38% above control values. Pretreatment with atropine sulfate, a highly specific muscarinic antagonist, blocked the bethanechol effect. Interestingly, bethanechol failed to alter the concentration of estradiol binding sites in castrated male rats. The results of the present experiments show not only that pharmacological modulation of cytosolic hypothalamic estradiol binding sites is not limited to drugs which interact with catecholaminergic systems, but that such effects may be sex-specific.

Animals↗
PubMed1992

Muscarinic nature of cholinergic receptors in the cerebellar flocculus involved in the enhancement of the rabbit's optokinetic response.

Intrafloccular micro-injection of the aselective cholinergic agonist carbachol enhances the optokinetic reflex (OKR)17. Histochemical and physiological studies have identified cholinergic receptors of the muscarinic as well as nicotinic type in the cerebellar cortex, and both have been implicated in cholinergic transmission. The present study was undertaken to elucidate the receptor type involved in the control of OKR. For that purpose, effects of injections of the nicotinic N1 agonist DMPP on the OKR and vestibulo-ocular reflex (VOR) were compared with injections of the muscarinic agonist betanechol and the aselective cholinergic agonist carbachol. Injection of betanechol mimicked the enhancement of the OKR by carbachol, while DMPP had no effect. We conclude that muscarinic receptors are involved in the positive modulatory action of the cholinergic system in the cerebellar flocculus.

Animals↗
PubMed1993

Activation of muscarinic receptors induces a long-lasting enhancement of Purkinje cell responses to glutamate.

The cerebellar cortex contains diffusely distributed cholinergic fibers and both muscarinic and nicotinic receptors. Behavioral studies suggest that an important function of this cholinergic innervation may be to modulate the effects of afferent input to the cerebellar cortex. The present study compared the effects of the muscarinic agonist bethanechol on basal firing rates and on glutamate-evoked firing of Purkinje cells in the vermis of the cerebellum of anesthetized rats. Microiontophoretic application of bethanechol produced a slowly developing, long-lasting enhancement of glutamate-evoked firing which was often disassociated from the bethanechol effect on the basal firing rate. Bethanechol increased the glutamate response of 22/33 Purkinje cells regardless of whether bethanechol increased, decreased or failed to alter the basal firing rate of the cell. The muscarinic antagonist scopolamine prevented the bethanechol-induced increase in the glutamate response. For 7/33 Purkinje cells, bethanechol decreased the glutamate-evoked response. However, this decrease did not appear to be mediated by muscarinic receptors because it was not blocked by scopolamine and it was mimicked by application of the vehicle alone. Acetylcholine application produced a long-lasting increase in the glutamate response of 4/5 Purkinje cells that was similar to the bethanechol effect. These data indicate that the cerebellar cholinergic system exerts a prominent modulatory influence on Purkinje cell excitability by acting through muscarinic receptors.

Acetylcholine↗
PubMed1993

Electrical communication between glomus cells of the rat carotid body.

Glomus cells of rat carotid bodies can be electrotonically coupled. This was determined by simultaneous intracellular recording and stimulation of two neighboring cells. Voltage applied into one cell (V1), was detected in the other cell as E2. The ratio E2/V1 or coupling coefficient (KC), varied from 0.003 to 1. R0 or input resistance (24.1-3,500 M omega), was calculated from the voltage elicited in the injected cell by current injection (V1/I1). The coupling resistance (RC) was estimated by using Bennett's model and was inversely related to KC. It ranged from 8.5 to 46,112 M omega. Values for KC are provisional since we may not have always recorded from immediately adjacent cells. Similarly, calculations of R0 and RC may not be accurate since, in all probability, there is a multicellular network. Stimulation by hypoxia (100% N2 or Na2S2O4), acidity (lactic acid or 100% CO2), dopamine, ACh, nicotine and bethanechol depolarized the majority of glomus cells, their input resistance decreased and cells became uncoupled. Fewer cells were either unaffected or coupling increased. There was a significant and negative correlation between changes in coupling coefficient and in coupling resistance.

Acetylcholine↗
PubMed1994

The muscarinic agonist, bethanechol, enhances GABA-induced inhibition of Purkinje cells in the cerebellar cortex.

An important function of cholinergic projections to the cerebellar cortex may be to modulate the effects of classical afferent inputs to the cerebellar cortex. This hypothesis is supported by the recent observation that cholinergic agonists act at muscarinic receptors in the cerebellar cortex to facilitate Purkinje cell responses to glutamate, the excitatory neurotransmitter of parallel fibers [Brain Res., 617 (1993) 28-36]. Since Purkinje cell excitability is influenced by inhibitory input from basket and stellate cells as well as by excitatory input from granule cells and climbing fibers, the present study investigated whether muscarinic agonists could also modify the Purkinje cell responses to GABA, the putative inhibitory transmitter of basket and stellate neurons. In anesthetized rats, microiontophoretic application of bethanechol produced a long-lasting enhancement of GABA-evoked inhibition of firing of Purkinje cells in the cerebellar vermis (22/25 cells) regardless of whether bethanechol increased, decreased or failed to alter the basal firing rate of the cell. The muscarinic antagonist scopolamine prevented the bethanechol-induced increase in the GABA response. It appears, therefore, that cholinergic activation of muscarinic receptors enhances not only the excitatory but also the inhibitory component of cerebellar cortex circuitry. Further experiments are required to investigate whether this combination of effects may potentiate the signal processing capabilities of the cerebellar cortex.

Action Potentials↗
PubMed1990

The salvage of rabbit ischaemic epigastric free flaps using the vasodilator calcitonin gene-related peptide.

The rabbit epigastric free flap, subjected to 21 hours of warm (25 degrees C) ischaemia, was used as an experimental model to test the ability of two endothelium-dependent vasodilators, calcitonin gene-related peptide (CGRP) and carbamyl beta-methylcholine chloride (MCh, bethanechol chloride, the stable acetylcholine analogue) to improve flap viability. After the period of ischaemia, flaps were infused intra-arterially with either Hanks balanced salt solution (controls), CGRP or MCh for 30 minutes, and received additional intravenous boluses of these drugs at 2 and 32 minutes after revascularisation. The area of flap surviving improved significantly (p less than 0.025) from 39.9% (n = 18) for controls to 70.2% (n = 14) for CGRP treatment at 2 micrograms/kg, but was unchanged at 47.1% (n = 14) for MCh treatment at 50 micrograms/kg. Both CGRP and MCh significantly increased blood flow (p less than 0.05) resulting in 34% lower peripheral resistances compared with controls. These results suggest that CGRP has considerable clinical potential for the salvage of ischaemic flaps. CGRP must have several, as yet undefined, beneficial effects on the ischaemic tissue, since MCh invoked a vasodilatory response but failed to salvage ischaemic flaps.

Abdominal Muscles↗
PubMed1975

Unusual cholinergic response of bullfrog sympathetic ganglion cells.

The membrane of bullfrog sympathetic ganglion cells was hyperpolarized by a direct action of ACh (more than 0.5 mM) in a solution containing both nicotine (0.24 mM) and atropine (0.14 mM). This ACh hyperpolarization could be imitated by neither carbachol nor bethanechol, suggesting that the ACh hyperpolarization was the response which was produced by a specific action of ACh, which appeared to be neither nicotinic nor muscarinic. The size of ACh hyperpolarization was increased during a conditioning hyperpolarization. The ACh hyperpolarization was completely blocked by ouabain (2 times 10(-3) mM) and eliminated in the Na-free lithium solution. These aspects of the ACh hyperpolarization suggested that generation of this hyperpolarization was associated with the sodium pump. The ACh hyperpolarization seemed to be partially responsible for the production of the slow IPSP, since a part of the slow IPSP remained occasionally in the presence of both nicotine and atropine.

Acetylcholine↗