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The opioid receptor mechanism involved in the morphine induced straub tail response was investigated in mice. Morphine (2.5, 5, 10 and 20 mg/kg s.c.) produced a dose dependent straub tail response and analgesia (hot plate test). Naloxone (5 mg/kg s.c.) and the mu-opioid receptor antagonist beta-funaltrexamine (10 micrograms i.c.v.) blocked both the straub tail response and analgesia while the mu 1-opioid receptor selective antagonist naloxonazine (35 mg/kg s.c.) blocked only analgesia and did not affect the straub tail response. Morphine (20 micrograms) administered by the i.c.v. route also produced the straub tail response as well as analgesia. Pretreatment with naloxonazine (35 mg/kg s.c.) antagonised i.c.v. administered morphine induced analgesia while the straub tail response was not affected. The results indicate that the morphine induced straub analgesia while the straub tail response was not affected. The results indicate that the morphine induced straub tail response is mediated by central mu 2-opioid receptors.

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Effect of oral feeding of Liv-52, on lipid peroxidation in normal liver and damaged liver induced by CCl4 of albino rats was studied. While Liv-52 did not show any effect on normal healthy liver cells, it had a significant protective effect against damage by CCl4 as shown by significant decrease in malonaldialdehyde content.

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In the present study, an attempt has been made to elucidate the role of alpha 2-adrenoceptors in reserpine-induced emesis in pigeons. Reserpine was found to induce dose-dependent emesis and a 500 micrograms kg-1 dose was found to be the 100% emetic dose. alpha 2-adrenoceptor agonists clonidine and alpha-methylnoradrenaline inhibited the reserpine induced emesis. Out of the two selective alpha 2-adrenoceptor antagonists idazoxan and yohimbine, only the latter induced a dose-dependent emesis. However, both the drugs potentiated reserpine-induced emesis and antagonised its inhibition by clonidine. Prior depletion of monoamines by reserpine also blocked the emetic response of reserpine. These observations indicate that release of monoamines is responsible for its emetic response in pigeons which is modulated by presynaptic alpha 2-adrenoceptors in a predictable manner.

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The possibility of a central component in the cardiovascular effects of peripherally administered calcium channel blockers has been explored through a comparison of the effects observed after intravenous (i.v.) and intracisternal (i.c.) administration of verapamil and diltiazem in chloralose-anesthetized and artificially ventilated cats. Both agents produced relatively greater effects after i.c. than after i.v. administration. The bradycardiac effect following i.c. as well as i.v. administration was totally abolished by bilateral cervical vagotomy, and the hypotensive effect was attenuated by this procedure. The results strongly suggest the existence of a central component in the cardiovascular effects of both agents.

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The effect of verapamil, a calcium channel blocker, was studied against stress (cold restraint), aspirin and pylorus ligation induced gastric ulcers in rats. Verapamil inhibited ulcerogenic response and ulcer index in all the three types of ulcers. Verapamil also decreased total and free gastric acidity without changing gastric secretory volume.

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The role of the central histaminergic system in depression was studied by using swimming despair test in mice - a behavioural model of depression. In this test, immobility of mice reflects a state of depression. Intracerebral (ic) injection of histamine (50-200 micrograms) increased significantly the immobility. The H1-receptor blocker mepyramine (2.5-20 mg/kg ip) had no effect while H2-receptor blocker cimetidine (100-200 micrograms ic) caused a significant decrease in immobility. The histamine induced facilitation was blocked completely by cimetidine and antidepressant drugs-imipramine and desipramine, but remained unaffected in mice pretreated with mepyramine or atropine. The H2 agonist impromidine (20-40 micrograms ic) also enhanced significantly, the immobility which was blocked by cimetidine and antidepressant drugs. It has been concluded that central H2-receptors facilitate depression and antidepressant drugs block central H2-receptors.

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Electroconvulsive shock-induced changes in the intensity of stereotype induced by apomorphine, the binding of [3H]spiroperidol in the corpus striatum, the accumulation of [3H]dopamine in brain and the permeability of the blood-brain barrier, were monitored in rats 30 min after single, or 24 hr after chronic (once daily for 7 days) electroconvulsive shock. There was significant potentiation in stereotypy induced by apomorphine after chronic electroconvulsive shock. The binding of [3H]spiroperidol did not show any change in the affinity (Kd) or density (Bmax) of receptors in the striatum after acute or chronic electroconvulsive shock. The accumulation of dopamine increased significantly in the hypothalamus after acute electroconvulsive shock and in the corpus striatum and hypothalamus after chronic electroconvulsive shock. A significant increase in the entry of sodium fluorescein into the hypothalamus occurred after acute electroconvulsive shock; it increased in all the regions of the brain after chronic electroconvulsive shock. Alteration in the blood-brain barrier (BBB) by electroconvulsive shock leading to increased accumulation of dopamine in the corpus striatum may be responsible for the potentiation of stereotypy.

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Role of histaminergic mechanisms in the regulation of blood-brain barrier (BBB) was assessed in dog. Histamine increased the entry of sodium fluorescein from the blood to the cerebrospinal fluid (CSF) in a dose-dependent manner. Histamine receptor antagonists, mepyramine (H1) and metiamide (H2) per se did not affect the entry of dye in the CSF. Mepyramine failed to affect the change induced by histamine whereas metiamide completely blocked the histamine-induced entry of sodium fluorescein in CSF. 2-Methyl histamine, a specific H1-agonist, did not affect the barrier permeability. However, 4-methyl histamine, a specific H2 receptor agonist significantly increased the permeability of BBB. This increase was blocked by metiamide. Forskolin, a stimulant of adenylate cyclase, also increased the entry of dye in the CSF which could be significantly blocked by metiamide. It is concluded that histamine increases the permeability of BBB by affecting H2-receptors linked to adenylate cyclase.

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Effect of alcohols on the permeability of blood-brain barrier was studied in anaesthetised dogs using sodium fluorescein as circulant. Entry of sodium fluorescein in the cerebrospinal fluid (CSF) was measured spectrophotofluorometrically. Methyl, ethyl, propyl and butyl alcohols were used in the study. Methyl alcohol did not increase the entry of sodium fluorescein in CSF compared to control. However, ethyl, propyl and butyl alcohols significantly increased the entry of sodium fluorescein. The increase was dependent upon the length of alkyl chain of alcohols. Longer was the aliphatic chain more marked was the effect. The increase in permeability was also dependent upon the concentration of the alcohol. Thus 90% ethyl alcohol was more effective than 30% and this effect was concentration-dependent. The increase in permeability of blood-brain barrier could be correlated to the lipid solubility of alcohols.

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Sensitivity of central cholinergic (muscarinic) receptors was studied in rats after application of single and repeated (once daily for 7 days) electroconvulsive shocks (ECS). Oxotremorine-induced tremor was significantly enhanced after single as well as chronic exposure to ECS; [3H]QNB binding in frontal cortex was also significantly increased by chronic ECS. The results indicate that ECS develops supersensitivity in central muscarinic receptors.

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The role of central histaminergic system in foot shock induced aggression was studied in mice. Histamine administered by intracerebral (IC) injection (25-200 micrograms) produced a significant increase in fighting episodes in a dose dependent manner. It was observed that mepyramine (H1 blocker) given intraperitoneally (IP) significantly increased and metiamide (H2 blocker) given IC decreased significantly the fighting response. To determine the nature of receptors involved in histamine induced facilitation of aggressive behaviour, histamine was administered IC in mice pretreated with mepyramine or metiamide. Mepyramine pretreatment further increased the facilitatory effect of histamine while metiamide blocked the enhancement of aggressiveness by histamine. Combined pretreatment with metiamide and mepyramine decreased significantly the fighting counts which remained unaffected after histamine. Haloperidol did not block the enhancement of aggression by histamine or mepyramine. However, atropine pretreatment partially inhibited the histamine induced increase in the fighting counts. Results of pretreatment with metiamide and atropine were similar to those obtained with pretreatment of metiamide and mepyramine. Metiamide alone or in combination with atropine failed to affect the facilitatory effect of amphetamine on the foot-shock aggression. It is concluded that central histamine H2 receptors have a facilitatory role and H1 receptors an inhibitory role on aggressive behaviour in mice induced by foot-shock. Since histamine per se had a facilitatory effect on foot-shock induced aggression, the central H2 receptors seem to dominate over the H1 receptors.

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