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Biomedical subjects

S K Kulkarni

Publications and source records attributed to S K Kulkarni.

At least 235 records · Page 13Linked to original sources
PubMed1975

Influence of chemical stimulation of central dopaminergic system on the open field behaviour of rats.

Influence of some substances known to selectively modify the brain levels of dopamine, was studied on the Open Field behaviour in rats. Of the agents studied, I-dopa, benztropine and amantadine showed some similarity with amphetamine in exhibiting a high degree of complex stereotyped behaviour in rats. The complex stereotyped behaviour due to amphetamine and the similarity shown by these antiparkinsonian agents has been explained on the basis of brain dopamine levels. On the other hand apomorphine depressed the Open Field behaviour and produced a typical stereotyped biting in rats. Since 6-hydroxydopamine significantly prevented this biting behaviour, it has been suggested that the action of apomorphine is dependent on the presence of (i) functional state of catecholamine neurons and (ii) a separate receptor, responsible for the behavioural actions of apomorphine.

Amantadine↗
PubMedDate not supplied

Intrapelvic obturator neurectomy in cerebral palsy.

Results of 202 obturator neurectomies including 190 intrapelvic and 8 extrapelvic obturator neurectomies in 100 patients were evaluated. Obturator neurectomy, intrapelvic in particular, yielded gratifying results in properly selected patients. It controlled adductor spasticity, scissoring, improved perineal care and helped the patients in sitting and early ambulation. Pre- and post-operative intensive physiotherapy was necessary to get maximum benefit of the surgery. Poor motor status, low IQ, athetosis and inadequate post-operative care had adverse effect on final outcome.

Achilles Tendon↗
PubMedDate not supplied

Modification by GABA-ergic agents and clonidine of morphine-induced convulsions and toxicity in rats.

Intracerebroventricular (i.c.v.) administration of morphine produced dose-dependent behavioural changes in rats, the highest dose producing violent tonic convulsions. Naloxone (up to 10 mg/kg i.p., or 100 micrograms i.c.v.) failed to reverse morphine-induced toxicity. The conventional anticonvulsant drugs also failed to offer protection to morphine-induced seizures. GABA-ergic substances, GABA, piracetam and diazepam, on the other hand, protected the animals against morphine-induced convulsions and toxicity. Similarly, clonidine pretreatment also had a protective action against morphine-induced convulsions.

Animals↗
PubMedDate not supplied

Dopamine D4 receptors and development of newer antipsychotic drugs.

The last ten years have witnessed the generation of a large amount of information on the neurobiology of dopamine receptors. Molecular biology and pharmacology studies have revealed existence of at least five dopamine receptor subtypes, namely D1, D2, D3, D4 and D5. The discovery of D4 receptors and the putative affinity of clozapine for D4 receptors have kindled development of selective D4 receptor antagonists for the treatment of schizophrenia. Studies on expression of D4 receptor proteins have shown selective localisation of D4 receptors in mesolimbic/mesocortical areas which could probably explain the lack of motor side effects with atypical antipsychotics like clozapine and olanzapine. However, neuropathological and genetic studies on the role of D4 receptors in the pathophysiology of schizophrenia and preliminary clinical studies with selective D4 receptor antagonists have been disappointing. There have been, however, complimentary findings between selective D4 receptor antagonism and genetic approaches such as antisense treatment or gene targeting. The therapeutic potential of D4 receptors as a target for developing antipsychotics will be known only when selective D4 receptor-antagonists with varying D2/D4 and D4/5-HT2A ratios are developed and tested in psychiatric patients.

Animals↗
PubMedDate not supplied

Nitecapone and selegiline as effective adjuncts to L-DOPA in reserpine-induced catatonia in mice.

Reserpine-induced catatonia is a widely accepted animal model of Parkinson's disease. In the present study, reserpine (5 mg/kg i.p.) and alpha-methylpara-tyrosine (AMPT) (200 mg/kg i.p.) induced catatonia in mice 20 h and 1 h before the experiment, respectively, as assessed using the rota-rod and bar tests after reserpine treatment. There was a significant decrease in fall-off time in the rota-rod test and a significant increase in time spent on the bar in the bar test as compared to the untreated control mice. Combination therapy with L-DOPA (100 mg/kg i.p.) and carbidopa (10 mg/kg i.p.) was less effective in reversing catatonia as compared to higher doses of L-DOPA (200 mg/kg i.p.) and carbidopa (20 mg/kg i.p.), which showed intense hyperactivity in reserpinized mice. Pretreatment with nitecapone (30 mg/kg i.p.), a COMT inhibitor, or selegiline (10 mg/kg i.p.), a MAO-B inhibitor potentiated the motor stimulant actions of subthreshold doses of the L-DOPA (100 mg/kg i.p.) and carbidopa (10 mg/kg i.p.) combination. Amantadine (40 mg/kg i.p.), but not bromocriptine, potentiated the effects of L-DOPA treatment. The NMDA antagonistic action of amantadine may have beneficial effects. It is concluded that COMT and MAO-B enzymes play an important role in the metabolism of dopamine and administration of a COMT or MAO-B inhibitor may prove to be a better adjunct to L-DOPA therapy than a dopamine receptor agonist in Parkinson's disease.

Animals↗
PubMedDate not supplied

Involvement of normal physiological mechanisms in mediation of satiety by polyherbal antiobesity preparation, OB-200G, in female mice.

The first study investigated the effect of different doses (0.25, 0.5, 1 g/kg p.o.) of a polyherbal, antiobesity preparation, OB-200G, on the duration of a specific sequence of behaviors (activity, feeding, grooming and resting) associated with the onset of satiety. The recordings were taken at 0, 30 and 60 min, for 10-min periods, immediately after the presentation of sweetened chow to female mice that had been fasted for 16 h. At the end of a 70-min test session, the amount of sweetened chow consumed by each mouse was also recorded. The second study investigated the antagonism of hyperphagia mediated by 2-deoxy-D-glucose (2-DODG), by both OB-200G (0.5 g/kg) and fluoxetine (10 mg/kg). Ingestion of sweetened chow by control mice produced the typical sequence of behaviors associated with the onset of satiety, characterized by initial increase in duration of feeding and active behaviors. With time, these behaviors declined and there was an increase in grooming and resting behaviors. Prefeeding significantly (p < 0.01) decreased the percentage of time spent feeding but also significantly (p < 0.01) increased the duration of active behaviors at 0-10 and 30-40 min. Prefeeding for 20 min advanced the onset and increased the duration of grooming behavior. Treatment with fluoxetine (10 mg/kg) significantly decreased the duration of feeding behavior and increased the active behavior duration at 0-10 and 30-40 min as compared with the control group. There was also a significant (p < 0.01) increase in resting behavior duration with fluoxetine at 60-70 min. OB-200G (0.25-1 g/kg) administration significantly decreased the feeding behavior duration and increased the active-behavior duration at 30-40 min as compared with the control group during that period. However, OB-200G (0.25-I g/kg) did not elicit any significant change in grooming (except decrease at 60-70 min with a 0.5 g/kg dose) and resting behavior duration compared with the control or prefed groups. The amount of sweetened chow consumed significantly decreased (p < 0.01) in 10 and 20 min prefed, fluoxetine-treated and OB-200G-treated (0.5 and 1 g/kg) mice as compared with the control group. Furthermore, the hyperphagia mediated by 2-DODG was significantly antagonized by both OB-200G and fluoxetine. In conclusion, like fluoxetine, OB-200G mediates satiety through operation of normal physiological mechanisms. Antagonism of 2-DODG-hyperphagia by OB-200G and fluoxetine indicates the involvement of a common central pathway (or pathways) in their action.

Animals↗
PubMedDate not supplied

Antagonism of caffeine-induced convulsions by ethanol and dizocilpine (MK-801) in mice.

Ethanol (1 and 2 g/kg, i.p.) and MK-801 (1 mg/kg, i.p.), N-methyl-D-aspartate (NMDA) receptor antagonist, offered protection against caffeine-induced convulsions in mice. Subeffective doses of ethanol (0.5-g/kg, i.p.) and MK-801 (0.5 mg/kg, i.p.) when administered concurrently, did not provide a facilitatory anticonvulsant action against caffeine-induced convulsions. Ethanol (0.5 g/kg, i.p.) when administered concurrently with adenosine (100 mg/kg, i.p.) or dipyridamole (5 mg/kg, i.p.) elicited a facilitatory anticonvulsant action. However, concurrent administration of subeffective doses of MK-801 (0.5 mg/kg i.p.) with adenosine (100 mg/kg, i.p.) did not offer a facilitatory anticonvulsant action against caffeine-induced convulsions. The protective effect of ethanol (1 g/kg, i.p.) against caffeine-induced convulsions was reversed by an imidazobenzodiazepine, Ro 15-4513 (4 mg/kg, i.p.). Ro 15-4513 did not produce any proconvulsant effect with caffeine. It is suggested that ethanol and MK-801 elicit their anticonvulsant actions against caffeine-induced convulsions through different receptor mechanisms and that the anticonvulsant action of ethanol may be partly attributed to its ability to act via central adenosinergic mechanisms.

Animals↗
PubMedDate not supplied

Effect of baclofen, a GABAB-agonist, on forced swimming-induced immobility in mice.

The effect of baclofen, a GABAB-agonist, was studied on both forced swimming-induced immobility and isoprenaline-induced enhancement of forced swimming-induced immobility in mice. (+/-) Baclofen (0.5 and 1 mg/kg), and (-) baclofen (0.5, 1 and 2 mg/kg) attenuated forced swimming-induced immobility. The effect of baclofen was not reversed by bicuculline, a GABAA-antagonist. Baclofen also reduced isoprenaline-induced enhancement of forced swimming-induced immobility. On concomitant administration of a subeffective dose of baclofen with a subeffective dose of propranolol, desipramine and amitriptyline, a potentiating effect was observed. These results are corroborative of our previous finding that GABAergic agents, particularly GABAB-receptors, play a role in the modulation of despair behavior in mice and in the action of antidepressant drugs. Baclofen (5 mg/kg) did not produce any significant effect on forced swimming-induced immobility, but reduced significantly the locomotor activity of the animals. Lower doses (0.5 and 1 mg/kg) of baclofen, which reduced the forced swimming-induced immobility, did not affect the locomotor activity. At higher and lower tissue concentrations of the drug, involvement of different receptor populations is suggested.

Amitriptyline↗