Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Oxotremorine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1999

Synthesis and functional characterization of novel derivatives related to oxotremorine and oxotremorine-M.

Two subseries of nonquaternized (5a-10a) and quaternized derivatives (5b-10b) related to oxotremorine and oxotremorine-M were synthesized and tested. The agonist potency at the muscarinic receptor subtypes of the new compounds was estimated in three classical in vitro functional assays: M1 rabbit vas deferens, M2 guinea pig left atrium and M3 guinea pig ileum. In addition, the occurrence of central muscarinic effects was evaluated as tremorigenic activity after intraperitoneal administration in mice. In in vitro tests a nonselective muscarinic activity was exhibited by all the derivatives with potencies values that, in some instances, surpassed those of the reference compounds (i.e. 8b). Functional selectivity was evidenced only for the oxotremorine-like derivative 9a, which behaved as a mixed M3-agonist/M1-antagonist (pD2 = 5.85; pA2 = 4.76, respectively). In in vivo tests non-quaternary compounds were able to evoke central muscarinic effects, with a potency order parallel to that observed in vitro.

Animals↗
PubMed2000

New analogues of oxotremorine and oxotremorine-M: estimation of their in vitro affinity and efficacy at muscarinic receptor subtypes.

Two subsets of tertiary amines (1a-6a) and methiodides (1b-6b) with a structural resemblance to oxotremorine and oxotremorine-M were tested at rabbit vas deferens (M1), guinea pig left atrium (M2), guinea pig ileum and urinary bladder (M3) muscarinic receptor subtypes. The pharmacological profile of the derivatives under study has been discussed by evaluating their potency, affinity and efficacy as well as the regional differences in muscarinic receptor occupancy.

Animals↗
PubMed1977

The central and peripheral effectiveness of two oxotremorine-antagonists determined using oxotremorine-induced tremor and salivation.

Two oxotremorine antagonists have been examined using oxotremorine as the tremor salivation inducer and the ratios between the central and peripheral nervous systems determined. Under these conditions these compounds are still more effective antagonists centrally than peripherally. Differences in distribution to the various muscarinic receptors involved is believed to be the major factor in determining this separation of central and peripheral activities.

Alkynes↗
PubMed1994

Oxotremorine-M activates single nicotinic acetylcholine receptor channels in cultured Xenopus myocytes.

Oxotremorine methiodide (oxotremorine-M) is the quaternary amine derivative of oxotremorine and is known to be a potent and oft-reported pure, muscarinic receptor agonist. We report here, for the first time, that oxotremorine-M also has strong nicotinic actions at the single channel level. Although previous reports have suggested that oxotremorine-M has mixed cholinergic properties, its nicotinic actions have only been reported in systems which contain both muscarinic and nicotinic receptors, or in skeletal neuromuscular systems where the site of action of oxotremorine-M may have been ambiguous. We tested the possibility that oxotremorine-M is a nicotinic receptor agonist by examining the responses of single nicotinic acetylcholine receptors in primary cultures of myocytes from skeletal myotomes of Xenopus larvae. Myotomal myocytes are known to express the nicotinic acetylcholine receptor and no evidence exists that muscarinic receptors are expressed in these progenitors of the skeletal musculature. Furthermore, because we used aneural myocyte cultures, the effects of oxotremorine-M cannot be attributed to action on presynaptic receptors. Using cell-attached patches, we compared the responses of the nicotinic acetylcholine receptors to suberyldicholine and oxotremorine-M. Our results show that (1) both agonists activate the receptor channel in nanomolar concentrations; (2) the mean channel open-time is significantly smaller in oxotremorine-M; and (3) activation of the nicotinic acetylcholine receptor by oxotremorine-M is accompanied by a large percentage of short openings and a high frequency of event flickering. We conclude that oxotremorine-M is a mixed function agonist, showing partial blocking behavior, which effectively activates pure nicotinic acetylcholine receptors.

Animals↗
PubMed2001

Differential inhibition of [3H]-oxotremorine-M and [3H]-quinuclinidyl benzilate binding to muscarinic receptors in rat brain membranes with acetylcholinesterase inhibitors.

The potential interaction of acetylcholinesterase inhibitors with cholinergic receptors may play a significant role in the therapeutic and/or side-effects associated with this class of compound. In the present study, the capacity of acetylcholinesterase inhibitors to interact with muscarinic receptors was assessed by their ability to displace both [3H]-oxotremorine-M and [3H]-quinuclinidyl benzilate binding in rat brain membranes. The [3H]-quinuclinidyl benzilate/[3H]-oxotremorine-M affinity ratios permitted predictions to be made of either the antagonist or agonist properties of the different compounds. A series of compounds, representative of the principal classes of acetylcholinesterase inhibitors, displaced [3H]-oxotremorine-M binding with high-to-moderate potency (ambenonium>neostigmine=pyridostigmine=tacrine>physostigmine> edrophonium=galanthamine>desoxypeganine) whereas only ambenonium and tacrine displaced [3H]-quinuclinidyl benzilate binding. Inhibitors such as desoxypeganine, parathion and gramine demonstrated negligible inhibition of the binding of both radioligands. Scatchard plots constructed from the inhibition of [3H]-oxotremorine-M binding in the absence and presence of different inhibitors showed an unaltered Bmax and a reduced affinity constant, indicative of potential competitive or allosteric mechanisms. The capacity of acetylcholinesterase inhibitors, with the exception of tacrine and ambenonium, to displace bound [3H]-oxotremorine-M in preference to [3H]quinuclinidyl benzilate predicts that the former compounds could act as potential agonists at muscarinic receptors. Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent. The capacity of these inhibitors to displace [3H]-oxotremorine-M binding preclude their utilisation for the prevention of acetylcholine catabolism in rat brain membranes, the latter being required to estimate the binding of acetylcholine to [3H]-oxotremorine-M-labelled muscarinic receptors. However, fasciculin-2, a potent peptide inhibitor of acetylcholinesterase (IC50 24 nM), did prevent catabolism of acetylcholine in rat brain membranes with an atypical inhibition isotherm of [3H]-oxotremorine-M binding, thus permitting an estimation of the "global affinity" of acetylcholine (Ki 85 nM) for [3H]-oxotremorine-M-labelled muscarinic receptors in rat brain.

Animals↗
PubMed1989

Central and peripheral muscarinic actions of physostigmine and oxotremorine on avoidance responding of squirrel monkeys.

The involvement of central and peripheral muscarinic cholinergic receptors in the behavioral effects of the cholinesterase inhibitor physostigmine was evaluated by comparing the ability of atropine and methylatropine to reverse the effects of physostigmine, the muscarinic agonist oxotremorine, or their quaternary analogs neostigmine and oxotremorine-M. Avoidance behavior was maintained under a schedule in which every lever press postponed delivery of electric shock for 20 s; shock occurred every 5 s in the absence of responding. Cumulative doses of physostigmine or oxotremorine produced dose-related decreases in response rates, and increases in response durations and rates of shock delivery. Similar effects occurred with neostigmine and oxotremorine-M. Methylatropine completely prevented the behavioral and parasympathetic effects of neostigmine and oxotremorine-M without having any behavioral effects of its own. However, methylatropine did not alter the behavioral effects of physostigmine or oxotremorine. Atropine prevented the peripheral manifestations as well as the behavioral effects of physostigmine and oxotremorine even though atropine decreased avoidance responding when given alone. These results suggest that in squirrel monkeys, central and peripheral muscarinic receptors may function in a redundant manner to control agonist-induced decrements in avoidance. When physostigmine or oxotremorine was given in conjunction with atropine, rates of avoidance responding were increased to 180% of control levels. Response rate increases after administration of oxotremorine or physostigmine in monkeys treated with atropine may reflect a non-muscarinic action of atropine, unmasked by the presence of cholinomimetics.

Animals↗
PubMed1983

Quantitation of tolerance development after chronic oxotremorine treatment.

A new procedure was developed to quantitate the tolerance which develops as mice are chronically infused with the muscarinic agonist, oxotremorine. Cumulative dose-response curves were constructed for the effects of oxotremorine on body temperature and rotarod performance by administering sequential injections to individual animals. These dose-response curves compare favorably to those constructed by injecting individual animals with one of several doses. The sequential injection technique was used to assess the magnitude of tolerance development to oxotremorine. A linear relationship between oxotremorine infusion rate (dose) and magnitude of change of the ED50 value for impairment of rotarod performance was observed, with animals receiving an infusion rate of 1.0 mg/kg/hr showing a 24-fold increase in ED50. Dose-response curves for tolerant animals were parallel to those constructed for naive animals. The oxotremorine dose required to decrease body temperature to 35 degrees C (ED35 degrees) was 80-fold greater than control in the group treated with 1.0 mg/kg/hr. The dose-response curves for tolerant animals were not parallel to those seen in naive animals. Time courses of recovery from a challenge dose of oxotremorine suggest little change in metabolism occurred during chronic infusion. Chronic oxotremorine infusion resulted in a decrease in the total number of QNB binding sites. Both high- and low-affinity sites were reduced in number. Since no change in K1 for the muscarinic agonist, carbamylcholine, was observed, it seems unlikely that a change occurs in the affinity of the muscarinic receptor for agonists. Significant change in receptor number was detected only in animals that received higher doses of oxotremorine. Chronic oxotremorine treatment had no effect on choline uptake by synaptosomes prepared from any of five brain regions.

Animals↗
PubMed2001

Inhibition of oxotremorine-induced desensitization of guinea-pig ileal longitudinal muscle in Ca2+-free conditions.

The aim of this study was to investigate the differences between oxotremorine-induced and acetylcholine (ACh)-induced desensitization, particularly under Ca2+-free conditions, in guinea-pig ileal longitudinal muscle, and to elucidate the different mechanisms of desensitization that might exist between these two muscarinic agonists. Pretreatment of the tissue with 10(-7)-10(-5) M oxotremorine (desensitizing treatment) in normal Tyrode solution caused desensitization of the responses to ACh, as did the desensitizing treatment with ACh. However, Ca2+-free conditions significantly reduced oxotremorine-induced desensitization, contrary to the previous findings that Ca2+-free conditions enhanced ACh-induced desensitization. The desensitizing treatment with oxotremorine caused suppression of the responses to high K+ (tonic phase), as did the ACh treatment. Ca2+-free conditions removed this suppression, whereasthis condition enhanced ACh-induced suppression of the K+ response. A protein kinase C inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (10(-4) M) had no effect on oxotremorine-induced desensitization of the ACh response. The results suggest that a voltage-gated Ca2+ channel was involved in oxotremorine-induced desensitization, as in ACh-induced desensitization, but that the process of inactivation of Ca2+ channels was different between oxotremorine and ACh, and that oxotremorine-induced desensitization was due not only to Ca2+ channel, but also to other unknown factors. Protein kinase C did not participate in oxotremorine-induced desensitization.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1970

Effects of drugs on tremor and increase in brain acetylcholine produced by oxotremorine in the rat.

1. In rats the effect of drugs on oxotremorine tremor and oxotremorine-induced increase in brain acetylcholine has been investigated.2. Reserpine, (+/-)-alpha-methylmetatyrosine and diethyldithio-carbamic acid, drugs which have in common the ability to decrease tissue noradrenaline concentration, inhibited oxotremorine tremor without preventing the oxotremorine-induced increase in brain acetylcholine.3. (+/-)-p-chlorophenylalanine, a depletor of tissue 5-hydroxytryptamine, did not inhibit oxotremorine tremor.4. Phenoxybenzamine and propranolol inhibited oxotremorine tremor, and propranolol was without effect on oxotremorine-induced increase in brain acetylcholine.5. The toxicity of oxotremorine was increased by reserpine and phenoxybenzamine.6. The significance of these findings is discussed with regard to the mode of action of oxotremorine.

Acetylcholine↗
PubMed1975

Inhibition by oxotremorine of acetylcholine resting release from guinea pig-ileum longitudinal muscle strips.

1. Longitudinal muscle strips of the guinea-pig ileum were incubated in Tyrode solution containing either DFP or physostigmine as cholinesterase inhibitor. After a 90 min preincubation period the acetylcholine resting release into the medium was determined. Acetylcholine was estimated by gas chromatography. 2. The resting release was 0.39 nmol/g times min irrespective of the cholinesterase inhibitor used. In the presence of hexamethonium, or after omission of external calcium, the resting release fell by 50 and 55 per cent, respectively. 3. Oxotremorine (10-5 and 10-4M) significantly inhibited the resting release of acetylcholine by 25 and 33 per cent, respectively. The inhibitory effect of oxotremorine was completely reversed by atropine (3 times 10-7 M). Oxotremorine did not reduce the spontaneous release of acetylcholine that occurred either in the presence of hexamethonium or in the absence of external calcium. 4. The acetylcholine content of the muscle strips was approximately doubled during the preincubation with a cholinesterase inhibitor. The subsequent incubation with oxotremorine did not lead to a further increase in the endogenous acetylcholine content. However, incubation of the muscle strips with oxotremorine in the absence of a cholinesterase inhibitor led to a rise in the endogenous acetycholine concentration. In in vivo experiments, oxotremorine also caused an increase in the acetylcholine content of the muscle strips. The possibility is discussed that the rise in the acetylcholine concentration following the administration of oxotremorine is a consequence of the decreased release. 5. It is concluded that oxotremorine inhibits the resting release of acetylcholine by activation of neuronal muscarinic receptors. The inhibitory effect of exotremorine is linked to that fraction of the acetylcholine resting release that is calcium-dependent and that arises from propagated activity in cholinergic neurones. The results are consistent with the hypothesis of a feed-back control of acetylcholine release mediated by inhibitory muscarinic receptors.

Acetylcholine↗
PubMed1990

Nicotinic actions of oxotremorine on murine skeletal muscle. Evidence against muscarinic modulation of acetylcholine release.

The effects of oxotremorine, arecoline and muscarine on neuromuscular transmission of mouse or rat phrenic nerve-diaphragm were investigated. For some studies of endplate potentials (e.p.p.s) the preparation was immobilized by cutting muscle fibers. Oxotremorine (0.3-10 microM) depolarized endplate membranes, reduced miniature e.p.p. amplitudes but increased frequency, induced spontaneous neural discharges and muscle fasciculations, and produced contracture of denervated mouse diaphragm. In mouse and young rat preparations pretreated with Mn2+, Co2+, Ni2+, Cd2+ or low Ca2+ Tyrode to depress evoked acetylcholine release, oxotremorine 0.3-1 microM increased indirect twitches as well as amplitudes and quantal contents of e.p.p.s. These increases were not observed when the synaptic transmission was not depressed, nor in adult rat preparations. The augmentation by oxotremorine of evoked acetylcholine release persisted in preparations pretreated with neostigmine (1 microM) and tetrodotoxin (20 nM), which inhibited acetylcholinesterase and oxotremorine-induced spontaneous neural discharges. These effects of oxotremorine were mimicked by arecoline but not by muscarine and were antagonized by tubocurarine (0.3 microM) but not by atropine (0.1-10 microM). Atropine alone did not affect indirect twitches, synaptic transmission, tetanic responses evoked by direct stimulation of diaphragms, nor the durations of muscle action potential. The direct twitch responses were only slightly increased by oxotremorine at 2-3 microM. Oxotremorine at high concentrations (greater than 2 microM), depressed indirect twitches and e.p.p. amplitude, and accelerated the run-down of trains of e.p.p.s. The IC50 on indirect twitches was reduced by pretreatment with diltiazem or proadifen, which are known to promote receptor desensitization.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1985

Tolerance, cross-tolerance, and receptors after chronic nicotine or oxotremorine.

Saline, 8.0 mg/kg/hr nicotine, or 1.0 mg/kg/hr oxotremorine was continuously infused into the jugular veins of DBA female mice. After 10 days of treatment, respiratory rate, Rotarod performance, Y-maze crossings, Y-maze rears, heart rate, and body temperature were measured after challenge with 2.0 mg/kg nicotine or saline or 0.2 mg/kg oxotremorine. Nicotine-infused mice were tolerant to the effects of nicotine for all six tests and oxtremorine-infused mice were tolerant to the effects of oxotremorine for all six tests and to the effects of nicotine on heart rate and body temperature. Oxotremorine infusion reduced the Bmax for [3H]-L-QNB binding, but had no effect on Bmax for either [3H]-DL-nicotine or [125I]-alpha-BTX binding. Conversely nicotine infusion did not alter the Bmax for [3H]-L-QNB binding, but increased the Bmax for both [3H]-DL-nicotine and [125I]-alpha-BTX binding. These results indicate that tolerance developed to the effects of two cholinergic agents, nicotine and oxotremorine, and that some cross-tolerance to the effects of nicotine occurred in oxotremorine-treated mice. Treatment with oxotremorine caused down-regulation of muscarinic receptors, while treatment with nicotine caused up-regulation of nicotinic receptors. Although some cross-tolerance to the effects of nicotine occurred in oxotremorine-treated mice, this did not appear to result from changes in nicotinic receptors.

Animals↗
PubMed1999

Oxotremorine-induced modifications of the behavioral and neuroendocrine responses to formalin pain in male rats.

In the present investigation, the antinociceptive effects of the muscarinic cholinergic agonist, oxotremorine, were evaluated in rats using the formalin test. In Expt. 1, two oxotremorine concentrations (0.1 and 0.2 mg/kg) and two administration times (15 and 1 min before formalin injection) were chosen. All spontaneous and formalin-evoked behavioral responses were considered. In Expt. 2, only the higher concentration of oxotremorine (0.2 mg/kg) was administered 15 or 1 min before the formalin test. The animals were killed 15, 30 or 60 min after formalin treatment. Blood was collected from the trunk to determine corticosterone plasma levels. Some brain areas (hypothalamus, septum and periaqueductal gray matter) were dissected for determination of the beta-endorphin content. Oxotremorine induced a dose- and time-dependent reduction of all formalin-evoked responses: licking was decreased during both the first and second phases of the formalin test, flexing was decreased during the second phase by the higher concentration only and paw-jerk was decreased during the first phase by both concentrations. Rearing and line-crossing were significantly decreased by oxotremorine while exploratory activity was only partially reduced; self-grooming was increased. These effects on exploratory activity and self-grooming were abolished by formalin treatment. beta-endorphin content in the septum was increased by oxotremorine administered 15 min, but not 1 min, before formalin-treatment. beta-endorphin in the hypothalamus increased in all formalin-treated groups independently of oxotremorine administration. These results confirm, and extend to tonic pain, the analgesic effect exerted by oxotremorine on phasic responses. Because of the different effects on each formalin-induced response, they also indicate both spinal and supraspinal CNS sites of action.

Analysis of Variance↗
PubMed1987

Nonmuscarinic neurotoxicity of oxotremorine.

The ability of various treatments to prevent peripheral parasympathetic actions, central effects and lethality of the muscarinic agonist oxotremorine was studied in rats. The percentage of animals exhibiting effects of oxotremorine was dose and time dependent. The ED50 for producing lacrimation, salivation, tremor, convulsions and death was 2.5, 1.3, 1.6, 3.2 and 8.3 mg/kg i.p., respectively. Pretreatment with 5 mg/kg of atropine completely prevented all observable effects of oxotremorine at doses of 5 mg/kg and below. Doses of oxotremorine in excess of 5 mg/kg produced tremor, generalized clonic convulsions and death that could not be prevented by atropine when given at up to 160 mg/kg; lacrimation and salivation were not present in atropine-treated rats. In the presence of 40 mg/kg of atropine, ED50 values for oxotremorine were shifted more than 12-fold for lacrimation, salivation and tremor, whereas convulsions and death were maximally altered by a factor of 2. Scopolamine, benactyzine and benztropine were also incapable of completely preventing tremor, convulsions and death induced by 10 or 15 mg/kg of oxotremorine. Atropine methyl nitrate had effects comparable to atropine sulfate on lacrimation, salivation and lethality induced by oxotremorine (10 or 15 mg/kg) but had no effect on tremor or convulsions. A similar profile of atropine-insensitive effects was produced by pilocarpine and arecoline. Doses of diazepam 4 times higher (4 mg/kg) than necessary to prevent tonic-clonic convulsions induced by pentylenetetrazol were ineffective against tremor, convulsions or death produced by oxotremorine (10 or 15 mg/kg) unless given in conjunction with atropine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Possible cholinergic-dopaminergic link in memory facilitation induced by oxotremorine in mice.

The immediate post-trial injection of the centrally active muscarinic agonist oxotremorine (0.025, 0.050 and 0.100 mg/kg, IP) can facilitate the retention of a passive-avoidance response in mice, as indicated by performance on a retention test 24 h later. Injections given 10 min after training also significantly facilitated retention, but given 120 min after training did not affect retention. These findings suggest an action of oxotremorine on memory mechanisms. The enhanced retention was neither the result of a punishing effect of oxotremorine nor of a nonspecific proactive pharmacological action of the drug. The memory facilitation produced by oxotremorine (0.050 mg/kg, IP) was not antagonized by pretreatment with phentolamine (10 mg/kg, 30 min, IP), phenoxybenzamine (10 mg/kg, 120 min, IP) or piperoxane (20 mg/kg, 30 min, IP). The alpha-noradrenergic blocking agents had no effect by themselves. On the other hand, the immediate post-trial injection of oxotremorine (0.050 mg/kg, IP) did not enhance retention when mice were pretreated with haloperidol (0.5 mg/kg, 120 min, IP). Haloperidol injected either before training or before the retention test did not alter performance during the retention test. This suggests that haloperidol impairs neither acquisition of the avoidance response nor its retrieval. Thus, it is probable that haloperidol pretreatment impaired oxotremorine-induced memory facilitation. We suggest a possible participation of brain catecholamines in memory facilitation induced by oxotremorine in mice.

Adrenergic alpha-Antagonists↗
PubMed1981

The effect of 6-hydroxydopamine on the antinociceptive action of oxotremorine.

Mice received intraventricular 6-hydroxydopamine (6-OHDA) to deplete brain noradrenaline (NA) and dopamine (DA). 6-OHDA reduced the reaction time of mice to nociceptive stimulus (hot plate) and attenuated the antinociceptive action of oxotremorine. The administration of 6-OHDA to desipramine treated mice prevented both the loss of cerebral NA and the antagonism of oxotremorine's antinociceptive action. The administration of 6-OHDA to pargyline-treated mice increased the depletion of cerebral DA, but the antagonism of oxotremorine's antinociceptive action persisted. Catecholamines were measured in mouse brain at intervals from 1 h to 3 days after administration of 6-OHDA. DA levels failed to correlate with either the reduction in the hot plate reaction time or the antagonism of oxotremorine analgesia, whereas these effects were usually accompanied by a loss of brain NA. Centrally acting DA agonists failed to restore oxotremorine's antinociceptive action in 6-OHDA-treated mice. Intraventricular administration of the acetylcholine synthesis inhibitor triethylcholine to mice did not effect the antinociceptive action of oxotremorine. It is concluded that the antinociceptive action of oxotremorine in mice is initiated by stimulation of muscarinic receptors and involves noradrenergic neurones.

Analgesics↗
PubMed1994

The muscarinic receptor agonist oxotremorine methiodide evokes a nicotinic response in mammalian sympathetic neurons.

Oxotremorine methiodide, a congener of oxotremorine, is used as a muscarinic receptor agonist. Responses to oxotremorine methiodide and nicotinic receptor agonists were examined in cultured guinea-pig celiac ganglion neurons using whole-cell voltage clamp techniques. At holding potentials between -30 and -60 mV, a brief application of oxotremorine methiodide produced fast and slow inward current transients, depending upon the concentration applied. Slowly developing inward current transients, characteristic of muscarinic responses, were produced by lower concentrations (EC50: 0.3 microM) and were blocked by atropine. Rapid inward current transients, characteristic of nicotinic responses, were produced by higher concentrations of oxotremorine methiodide (EC50: 168 microM) and were blocked by d-tubocurarine. Thus oxotremorine methiodide, at concentrations of 10 microM and greater, produced an initial nicotinic fast inward current transient followed by a slow muscarinic inward transient. The fast inward transients were similar to responses evoked by the nicotinic receptor agonists acetylcholine, nicotine and 1,1-dimethyl-4-phenyl-piperazinium iodide and were not antagonized by atropine. We conclude that oxotremorine methiodide acts as a nicotinic and muscarinic receptor agonist in celiac sympathetic ganglion neurons.

Animals↗