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Biomedical subjects

D K Ganguly

Publications and source records attributed to D K Ganguly.

At least 55 records · Page 3Linked to original sources
PubMed1989

Tremorogenesis by LON-954 [N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride]: evidence for the involvement of 5-hydroxytryptamine.

LON-954 [N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride], a novel tremorogen known to affect the central dopaminergic system, has been investigated in rats for tremor and 5-hydroxytryptamine (5-HT) metabolism. Five, 10 and 20 mg/kg of LON-954 IP caused a reproducible and consistent tremor with a high frequency (16 Hz) within 2 minutes and lasting 30-45 minutes. 5-HT content of the tuberculum olfactorium and basal ganglia was found to be increased significantly at a time when 5-hydroxyindoleacetic acid (5-HIAA) content showed a decrease. 5-HT and 5-HIAA of medulla oblongata showed significant changes only after 15 minutes. The alterations in the levels of the indoleamine in tuberculum olfactorium and its relationship with dosage as well as duration and intensity of LON-954 tremor indicate the involvement of the mesolimbic system in its action. A direct role of 5-HT in LON-tremor was evidenced since the drug failed to produce tremor in rats pretreated with p-chlorophenylalanine (300 mg/kg IP) for 3 days.

Animals↗
PubMed1988

Alpha 2-antagonistic effect of N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride (LON-954).

The effect of N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride (LON-954) on alpha 2-adrenoceptors was studied in in vivo and in vitro preparations. Like yohimbine, LON-954 antagonised the clonidine-induced inhibition of twitch responses in the Auerbach's plexus of guinea pig ileum and rat vas deferens preparations. It also reversed the anti-convulsant effect of clonidine on pentylenetetrazol (PTZ)-induced convulsions in the rat, a property shared by yohimbine. However LON-954 failed to prevent the hypothermic response to clonidine in mice. The dissimilarity in action of LON-954 and yohimbine on clonidine-induced hypothermia could be due to the fact that the anticlonidine effect of yohimbine on hypothermia is mediated through its antiserotonin action. The results indicate that LON-954 acts as an alpha 2-antagonist both centrally and peripherally.

Adrenergic alpha-Antagonists↗
PubMed1987

Possible functional role of substance P on the mammalian motor nerve terminals.

The effect of substance P (sP) on mammalian skeletal myoneural transmission was studied employing innervated and denervated isolated rat diaphragm preparations. sP at a concentration of 3.7 nM facilitated the indirect twitch responses of the rat diaphragm and antagonised the paralytic effect of d-tubocurarine (d-Tc). sP failed to affect the direct twitch responses as well as the contractures induced by acetylcholine (ACh) and potassium chloride (KCl) in the denervated diaphragm. The amount of ACh released into the bathing medium in response to tetanic stimulation of the phrenic nerve was doubled in presence of sP. The study illustrates a presynaptic facilitatory involvement of sP on mammalian myoneural transmission.

Acetylcholine↗
PubMed1984

Effect of prostaglandin E2 on acetylcholine release from some peripheral cholinergic nerve terminals.

The effect of prostaglandin E2 (PGE2) on the acetylcholine (ACh) release evoked from rat phrenic nerve terminals and from Auerbach's plexus of the guinea-pig ileum was investigated. PGE2 enhanced the evoked release of ACh from phrenic nerve terminals and from Auerbach's plexus in a concentration-dependent manner. Preincubation with 7-oxa-13-prostynoic acid, the PGE receptor blocker, and indomethacin inhibited the PGE2-induced increase of evoked release of ACh while atropine failed to do so. Whereas a single administration of either 7-oxa-13-prostynoic acid or indomethacin significantly inhibited the control evoked release of ACh from the Auerbach's plexus, they failed to alter the control evoked release of ACh from the phrenic nerve terminals. The study indicates that the PGE2-induced increase in release of ACh from cholinergic nerve terminals is accomplished through activation of prostaglandin receptors and that PGE2 may play a physiological role in ACh liberation from the cholinergic autonomic nerve terminals but not from motor nerve terminals.

Acetylcholine↗
PubMed1982

Action of oxotremorine on the sub-cellular distribution of glycine in the rat spinal cord.

Intraperitoneal (i.p.) injection of 250 micrograms/kg of oxotremorine (OT) caused a 50% decrease in the glycine content of the synaptosomal-mitochondrial fraction of spinal cord homogenates prepared from rats killed 15 min after treatment. The glycine content of the supernatant fraction was correspondingly raised. In synaptosomes isolated from the spinal cord of OT-treated rats, the decrease in glycine content was 30%. Prior administration of atropine, but not of methylatropine, abolished this effect of OT on synaptosomal glycine content. Eserine exerted a potentiating effect on the action of OT in lowering the glycine content of spinal synaptosomes. Prior administration of L-DOPA, apomorphine, haloperidol, muscarine or mecamylamine had no significant effect on the action of OT on synaptosomal glycine content. OT alone or in combination with eserine, and acetylcholine (ACh) in combination with eserine, did not alter the rate of release of glycine from spinal synaptosomes of untreated rats incubated under appropriate conditions. OT was also without effect on the rate of release of glycine from normal spinal synaptosomes subjected to electrical stimulation, as well as on the eventual glycine content of the synaptosomes. On the basis of the present findings it has been suggested that (i) glycine may be released from Renshaw cells at their synapses with motoneurones in response to the muscarinic action of OT; (ii) dopaminergic modulation may not be involved in the OT-induced glycine release from Renshaw cells; and (iii) excessive release of glycine onto motoneurones may be the causative factor of the akinesia observed in OT-induced experimental Parkinsonism.

Animals↗
PubMed1980

Release of prostaglandin E from the isolated urinary bladder of the guinea-pig.

1 Release of prostaglandin E (PGE) from guinea-pig urinary bladder in vitro has been demonstrated both in the resting state and during electrical stimulation. 2 The electrically evoked release of PGE was significantly higher than the resting release and was frequency-dependent. 3 The released substance was characterized as PGE pharmacologically by (a) blockade of its response by SC-19220 on guinea-pig ileum, (b) reduction of the amount of the released substance by indomethacin and (c) the inhibitory effect of the released substance on adrenergic neurotransmission in guinea-pig vas deferens. 4 The prostaglandin seemed to originate from the muscle since tetrodotoxin treatment did not abolish the release during direct muscle stimulation; however, concomitant release from neuronal tissue could not be excluded in the present experiments. 5 Indomethacin failed to inhibit the mechanical responses of the bladder to transmural stimulation. 6 The present experiments suggest that PGE is not involved in mediating the non-cholinergic non-adrenergic neurotransmission in the guinea-pig urinary bladder.

Animals↗
PubMed1980

Anti-tremor action of C10Dichol, a peripheral acetylcholine synthesis inhibitor.

1 Anti-tremor action of decamethylene bis-(hydroxyethyl)-dimethylammonium bromide (C10Dichol), a peripheral acetylcholine synthesis inhibitor, was investigated. 2 C10Dichol inhibited tremor induced by oxotremorine, nicotine and physostigmine and afforded partial protection from physostigmine-induced mortality in mice. 3 In non-paralysing doses, C10Dichol antagonized the neuromuscular effects of oxotremorine, nicotine and physostigmine. 4 Prior administration of C10Dichol failed to prevent tremor and neuromuscular paralysis induced by harmine and arecoline. 5 In the absence of any antimuscarinic property of C10Dichol, its neuromuscular effects appeared to be casually related to its anti-tremor action. 6 This study reveals a possibility for the development of peripherally acting anti-Parkinson drugs.

Acetylcholine↗
PubMed1978

Enhancement by oxotremorine of acetylcholine release from the rat phrenic nerve.

Oxotremorine (10.5 micron) produced a paralytic effect on twitch responses of rat diaphragm in vitro to direct and indirect stimulation. 2 The paralytic effect of oxotremorine was absent when the diaphragm was stimulated directly in the presence of hemicholinium-3 (0.42 mM), at a time when twitch responses to indirect stimulation ceased completely. 3 Oxotremorine, at two different pharmacologically active doses, strikingly increased the resting as well as electrically evoked release of acetylcholine into the bathing fluid from the phrenic nerve-diaphragm preparation. 4 This presynaptic effect of oxotremorine may explain its pharmacological effects at the cholinergic synapses studied so far.

Acetylcholine↗
PubMed1978

Rat isolated phrenic nerve-diaphragm preparation for pharmacological study of muscle spindle afferent activity: effect of oxotremorine.

1. Muscle spindle afferent discharges exhibiting an approximately linear length-frequency relation could be recorded from the phrenic nerve in the isolated phrenic nerve-diaphragm preparation of the rat. 2. Muscle spindle afferent discharges could be identified by their characteristic "spindle pause" during muscle contraction and by their response to succinylcholine. 3. Cholinergic influence on spontaneous and stretch-induced afferent discharges was indicated by the augmentation produced by physostigmine and acetylcholine. (+)-Tubocurarine, but not atropine, prevented this augmentation indicating the presence of curariform cholinoceptors in muscle spindles. 4. Acetylcholine did not appear to be involved in the genesis of spindle afferent discharges as incubation with hemicholinium-3 and (+)-tubocurarine failed to affect the rate of spontaneous and stretch-induced spindle discharges. 5. Oxotremorine markedly increased the rate of spontaneous and stretch-induced spindle afferent discharges and this effect was prevented in the presence of hemicholinium-3 and (+)-tubocurarine. 6. These results with oxotremorine are of interest in connection with the observation that muscle spindle afferents and hyperactive in Parkinsonian patients.

Animals↗
PubMed1978

Influence of triethylcholine on autonomic transmission in vitro.

The influence of triethylcholine (TEC) on isolated autonomic transmission has been investigated in some isolated preparations. The guinea-pig hypogastric nerve-vas deferens-urinary bladder preparation for studying both cholinergic and adrenergic transmission simultaneously is described. Incubation with TEC caused impairment of cholinergic transmission but failed to inhibit adrenergic transmission. Employing TEC as a pharmacological tool, no evidence for a cholinergic link could be obtained in adrenergic transmission in the isolated vas deferens and rabbit ileum preparations.

Animals↗