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Biomedical subjects

A G Chandorkar

Publications and source records attributed to A G Chandorkar.

At least 19 recordsLinked to original sources
PubMed2000

Effects of amantadine on modification of dopamine dependent behaviours by molindone.

Amantadine, a dopamine agonist is reported to act by releasing dopamine from the dopaminergic nerve terminals as an anti-Parkinsonian drug. In the present behavioural study in the rat, molindone-induced catalepsy and ptosis, which are dopamine dependent-behaviors are reversed by amantadine. Amantadine has also revered molindone-induced inhibition of traction response in mice. Our study indicates that amantadine, like other DA agonists, e.g. amphetamine and apomorphine can antagonize or even reverse the neuroleptic induced dopaminergic behaviors.

Amantadine↗
PubMed1990

Effects of yohimbine on dopamine dependent behaviours in rats and mice.

In the present study we have investigated the effect of yohimbine on dopamine-dependent behaviours in rats and mice. Yohimbine (1.25 to 10 mg/kg, ip) failed to block the conditioned avoidance response in rats, to inhibit the traction response in mice and to induce catalepsy in rats and mice. Pretreatment with yohimbine (1.25 to 10 mg/kg, ip) had no significant effect on apomorphine stereotypy in rats and apomorphine induced cage climbing behaviour in mice. However, pretreatment with yohimbine (1.25 to 10 mg/kg. ip) significantly increased the intensity of methamphetamine stereotypy and antagonised haloperidol catalepsy in rats. Our findings indicate that yohimbine does not possess postsynaptic striatal and mesolimbic D-2 dopamine receptor blocking activity.

Animals↗
PubMed1987

Effect of inhibition of lens membrane Na+-K+ ATPase by ouabain pre-treatment--an in vitro study.

The precise factors responsible for the cataract formation are not known. The role of Na+-K+-ATPase in maintaining ionic concentration of lens and lens membrane permeability and its involvement in the formation of cataracts has been of recent interest. Thus the present study was undertaken to study the effect of pre-treatment with Ouabain, a known Na-K-ATPase inhibitor, on the intra-lenticular ionic concentration and the rule of lens membrane permeability in cataractogenesis. Fresh goat lenses were used for the experimental work. Isolated lens culture technique was used. The electrolytes were estimated before and 24 hours after Ouabain pre-treatment. The electrolyte pattern showed significant changes after pre-treatment with Ouabain. Lens sodium ion concentration increased significantly with a concommitant decrease in potassium ion concentration. Intra-lenticular chloride concentration also showed a significant increase as compared to control. Calcium and magnesium ion concentrations also showed slight increase after the inhibition of Na+-K+-ATPase system by Ouabain.

Animals↗
PubMed1986

Head-twitch response induced by ergometrine in mice: behavioural evidence for direct stimulation of central 5-hydroxytryptamine receptors by ergometrine.

Ergometrine (2.5-80 mg/kg IP) induced head twitches in mice. Pretreatment with cyproheptadine (1.5 and 3 mg/kg), methysergide (5 and 10 mg/kg) and (-)-propranolol (2.5 and 5 mg/kg) significantly decreased the number of head twitches induced by ergometrine. Pretreatment with p-chlorophenylalanine (100 mg/kg/day X 4 days) and clomipramine (5 and 10 mg/kg) significantly decreased the number of head twitches induced by fenfluramine (10 mg/kg) and p-chloramphetamine (5 mg/kg) but had no significant effect on the number of head twitches induced by ergometrine. The results indicate that ergometrine induces head twitches in mice by directly stimulating central 5-hydroxytryptamine receptors.

Animals↗
PubMed1985

Effect of ergometrine on methamphetamine and apomorphine stereotypy in the guinea-pig.

Pretreatment with the DAi receptor antagonist ergometrine (10, 20 mg kg-1 i.p.) significantly potentiated methamphetamine stereotypy and facilitated the induction of biting, gnawing or licking behaviour by amantadine. However, ergometrine (5-20 mg kg-1) did not significantly influence the stereotyped behaviour induced by the DAe receptor agonist apomorphine. The results suggest that the DAi antagonist ergometrine is effective in modifying the behaviours induced by methamphetamine and amantadine, agents which through released DA simultaneously activate both DAe and DAi receptors, but fails to modify the stereotyped behaviour induced by apomorphine which specifically activates only DAe receptors. However, the possibility that ergometrine might have potentiated methamphetamine stereotypy and facilitated the induction of biting, gnawing or licking behaviour by amantadine through modulation of the activity of the central noradrenergic and 5-hydroxytryptaminergic systems, which are reported to influence DA-mediated behaviours, also needs to be considered.

Amantadine↗
PubMed1984

Effects of naloxone on methamphetamine and apomorphine stereotypy and on haloperidol catalepsy in rats.

Pretreatment with the opiate antagonist naloxone, at 1.25-5 mg/kg, increased the intensity of methamphetamine stereotypy, had no effect (over a range of 0.3125-5 mg/kg) on apomorphine stereotypy, and antagonized haloperidol catalepsy in rats at 1.25-5 mg/kg. It is suggested that naloxone, by blocking the opiate receptors located on the nigro-striatal and mesolimbic dopamine (DA) nerve terminals, releases the DA systems from endogenous inhibition, presumably caused by endogenous opiate systems, and thereby potentiates methamphetamine stereotypy and antagonizes haloperidol catalepsy. However, the possibility that naloxone might have affected methamphetamine stereotypy and haloperidol catalepsy by modulating the activity of the central noradrenergic and GABAergic systems, which are reported to influence dopaminergically mediated behaviours, also needs to be considered.

Animals↗
PubMed1984

Psychopharmacological investigation of the monoamine oxidase inhibitory activity of molindone, a dihydroindolone neuroleptic.

24 h pretreatment with molindone enhanced the behavioural effects of L-dopa and 5-HTP, precursors of biogenic amines (catecholamines and 5-HT respectively) preferentially deaminated by MAO-A, confirming that a metabolite of molindone inhibits MAO-A. 24 h pretreatment with molindone enhanced the behavioural effects of tryptamine and antagonized reserpine-induced ptosis, and in molindone-pretreated rats L-tryptophan induced behavioural effects, probably because of the MAO-A inhibitory activity exerted by a metabolite of molindone. Since 24 h pretreatment with molindone, unlike 30 min pretreatment with clomipramine, failed to antagonize fenfluramine and p-chloramphetamine-induced behavioural syndromes, it suggests that molindone and/or its metabolites most probably do not exert 5-HT neuronal uptake blocking activity and the potentiation of 5-HTP-induced behavioural syndrome is due to a metabolite's MAO-A inhibitory activity. As 2 h pretreatment with molindone induced catalepsy and antagonized apomorphine-induced climbing behaviour in mice and stereotypy in rats, while 24 h pretreatment failed to induce catalepsy and to antagonize apomorphine-induced behaviour, it appears that, at 24 h, the tissue levels of molindone are inadequate to block postsynaptic striatal and mesolimbic DA receptors and that, though a metabolite of molindone is biologically active so far as inhibition of MAO-A is concerned, the metabolites are devoid of neuroleptic activity. Further, since 2 h pretreatment with molindone failed to enhance the behavioural effects of L-dopa, it suggests that at 2 h the degree of MAO-A inhibition induced by molindone and/or the metabolite is not sufficient to counteract the neuroleptic activity of the parent compound.

5-Hydroxytryptophan↗
PubMed1983

Effects of L-histidine and promethazine on apomorphine and amantadine stereotypy in rats.

Pretreatment with L-histidine, a precursor of brain histamine, and promethazine, a H1 receptor blocker, failed to modify apomorphine-induced stereotyped behaviour in rats. In contrast, pretreatment with L-histidine significantly decreased the intensity of amantadine stereotypy while pretreatment with promethazine significantly increased the intensity of amantadine stereotypy in rats. The results suggest that drugs which influence central histaminergic mechanisms are effective only in modifying the stereotyped behaviour induced by the indirectly-acting DA agonist amantadine, and fail to modify the stereotyped behaviour induced by apomorphine, a directly-acting DA agonist.

Amantadine↗
PubMed1983

Clofazimine in lepra (ENL) reaction, one year clinical trial.

Twenty patients of lepromatous leprosy with lepra reaction and suspected dapsone resistance were treated with tapering doses of clofazimine. Clinical assessment was carried out every week. Bacteriological examination was carried out every six month. Fifteen patients became reaction free at the end of three months and severity and frequency of reactions was reduced in other patients. Nerve tenderness, arthralgia, nodular eruptions and all other signs and symptoms except anaesthesia showed complete recovery in fifteen patients and severity of the reactions was reduced in others. Gynaecomastia regressed in two out of three patients within nine months. In a majority of patients, the BI and MI was reduced at the end of 3 months, and further reduced after 6 months, and in one case both BI and MI became negative. Clinical and bacteriological improvement is attributed to the antibacterial effect of clofazimine while reduction in incidence of (ENL) reactions was attributed to anti-inflammatory effect of clofazimine. Regression of gynaecomastia may be due to either improvement of involvement of testes or liver or both. Apart from dyschromia clofazimine did not produce any severe side effects or toxicity.

Adult↗
PubMed1983

The effect of clofazimine on liver function tests in lepra reaction (ENL).

Twenty patients with suspected DDS resistance and repeated attacks of lepra reactions were selected for the study. Clofazimine was administered in different doses over a period of 12 months. Elevated levels of transaminases and Alkaline phosphatase prior therapy attained values to near normalcy. Progressive fall in serum Bilirubin and Proteins with normal A/G ratio at the end of therapy was also observed. Clofazimine by its anti-inflammatory and antibacterial action could inhibit the process of liver damage and happened to have minimal deleterious effect on liver by studying the liver function tests.

Alanine Transaminase↗
PubMed1983

Effect of one year clofazimine therapy on autonomic functions in lepromatous leprosy with lepra (ENL) reaction.

Twenty patients of either sex of Lepromatous leprosy with frequent type II (ENL) reactions were selected for the study after exclusion of autonomic disorders. ANS functions were evaluated before and after Clofazimine therapy at an interval of two months for one year. Sweat function test, valsalva manoeuvre, Histamine triple response, cold pressor test and Homatropine instillation were carried out in twenty normal healthy volunteers (controls) and the (ENL) patients. Clofazimine was administered initially 100 mg three times daily for one month and then gradually reduced to a dose of 100 mg biweekly for the last three months. Before the clofazimine therapy, eighteen patients had abnormal sweat functions, five patients had abnormal valsalva score, five patients had abnormal cold pressor response and all the eighteen patients had abnormal histamine triple response test. Homatropine instillation test was normal in all the patients. ANS functions did not improve significantly with Clofazimine therapy, except in one patients with abnormal cold pressor response who showed slight improvement in pressor response which, however, did not reach the normal value. ANS function tests indicate complete involvement of local axon reflex and hyporeactivity of sympathetic system and cardiac regulatory mechanisms in these patients. Parasympathetic system seems to be normal as seen from Homatropine instillation test.

Autonomic Nervous System↗