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Biomedical subjects

A Gulati

Publications and source records attributed to A Gulati.

At least 127 records · Page 7Linked to original sources
PubMed1988

Comparison of cortical adrenergic, cholinergic and benzodiazepine receptors between albino rat and desert rat (Mastomys natalensis) using radioreceptor binding.

Cortical alpha-adrenergic, beta-adrenergic, cholinergic (muscarinic) and benzodiazepine receptors have been studied in the albino rat and Mastomys natalensis (desert rat) using radioligand binding. Scatchard analysis was performed to determine affinity (Kd) and density (Bmax) of receptors. Compared to the albino rat, the desert rat was found to have higher affinity and density of alpha-adrenergic receptors. Beta-adrenergic receptors had similar Kd in both species but Bmax was significantly lower in the desert rat as compared to the albino rat. Cholinergic (muscarinic) receptors as well as the benzodiazepine receptors were in significantly higher density in the desert rat. The affinity was low for muscarinic receptors in the desert rat but equal for benzodiazepine receptors in both species. Since there are more alpha-adrenergic, muscarinic and benzodiazepine receptors in the desert rat, this species should be of value in screening compounds active at these sites.

Animals↗
PubMed1988

Binding of 3H-(3-MeHis2) thyrotropin-releasing hormone to spinal cord membranes of spontaneously hypertensive and Wistar-Kyoto normotensive rats.

Previous studies from this laboratory had indicated that in spontaneously hypertensive (SHR) rats the development of hypertension paralleled increases in brain receptors for thyrotropin-releasing hormone (TRH). The increase appeared to be confined to hypothalamus and striatum. The present studies were undertaken to determine the binding characteristics of TRH receptors in the peripheral tissues of SHR and normotensive Wistar-Kyoto (WKY) rats. TRH receptors were labeled with 3H-MeTRH. The binding of 3H-MeTRH to membranes prepared from spinal cord, heart, lung, kidney and adrenal gland of SHR and WKY rats was determined. In WKY rats, the binding of 3H-MeTRH to various tissue membranes was in the following order: spinal cord greater than kidney greater than lung greater than heart = adrenals. The binding of 3H-MeTRH to spinal cord membranes of SHR rats was significantly higher in comparison to WKY rat tissues, whereas the binding of 3H-MeTRH in kidney, heart, lung and adrenals of the two strains of rats did not differ. The increase in the binding of 3H-MeTRH to spinal cord of SHR rats was due to increases in the Bmax values and not in the Kd values. The results suggest that in addition to the brain, TRH receptors in the spinal cord of SHR rats are also up-regulated and may also play an important role in the regulation of blood pressure.

Animals↗
PubMed1988

Effect of methimazole-induced hypothyroidism on multiple opioid receptors in rat brain regions.

The effect of chronic administration of methimazole (0.05% w/v) in drinking water for 32 days to male Sprague-Dawley rats on the binding of opioid ligands, 3H-Tyr-D-Ala-Gly-MePhe-Gly-ol (DAGO, mu-receptors), 3H-Tyr-D-Ser-Gly-Phe-Leu-Thr (DSTLE, delta-receptors) and 3H-ethylketocyclazocine (EKC, kappa-receptors) to membranes of brain regions was determined. Chronic administration of methimazole to rats decreased their rate of body weight gain, colonic temperature, systolic blood pressure and heart rate in comparison to vehicle-treated rats. Administration of methimazole also decreased the serum concentration of triiodothyronine (total T3) and T4 when compared to vehicle-treated rats. The binding of 3H-DAGO to membranes of amygdala, pons and medulla, striatum, midbrain and cortex of methimazole-treated rats was greater than vehicle-treated rats, however, the binding to membranes of hypothalamus in the two treatment groups did not differ. The binding of 3H-DSTLE in amygdala and hypothalamus of methimazole-treated rats did not differ but it was significantly greater in pons and medulla, midbrain, cortex and striatum of methimazole-treated rats than vehicle-treated rats. The binding of 3H-EKC to membranes of pons and medulla was lower and of striatum and cortex of methimazole-treated rats was significantly greater than vehicle-treated rats, but the binding to membranes of amygdala, hypothalamus, and midbrain of the two treatment groups did not differ. The results indicate that brain, mu-, delta- and kappa-opioid receptors are differentially altered in hypothyroidism.

Animals↗
PubMed1988

Kappa opioid receptor activity in spontaneously hypertensive rats.

Earlier studies from this laboratory had indicated that there is a selective increase in the density of brain kappa opioid receptors labeled with [3H]ethylketocyclazocine in spontaneously hypertensive (SHR) rats in comparison to normotensive Wistar-Kyoto rats. The binding of a mu-ligand, [3H]naltrexone, and a delta-ligand, [3H]Tyr-D-Ser-Gly-Phe-Leu-Thr, to brain membranes of hypertensive and normotensive rats did not differ. The present studies were undertaken to determine further the role of kappa opioid receptors in hypertension. The binding of [3H]ethylketocyclazocine to brain membranes of hypertensive rats was much greater than those of normotensive rats. The density of kappa receptors was significantly higher in hypothalamic membranes of hypertensive rats as compared to normotensive rats. In order to determine the functional significance of the increased density of brain kappa opioid receptors in SHR rats, the effect of the kappa receptor agonists, tifluadom, U-50,488H and bremazocine, on two known actions associated with kappa receptors, namely analgesia and diuresis, were determined in SHR and normotensive rats. All three kappa agonists produced dose-dependent analgesia as measured by the tail-flick test. The intensity of the analgesic responses at each dose of the drugs in SHR rats was much greater than in normotensive Wistar-Kyoto rats. The kappa drugs also produced dose-dependent diuretic effects when the rats were loaded with 5% saline intragastrically. The increases in the volumes of urine produced by kappa drugs were much greater in SHR rats in comparison to normotensive rats. The basal tail-flick reaction time or urinary output in the two strains did not differ.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1987

On the mechanism of potentiation of apomorphine-induced stereotypy due to electroconvulsive shock.

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.

Animals↗
PubMed1986

Antianxiety effect of cannabis: involvement of central benzodiazepine receptors.

The present work, involving clinical, behavioral, and biochemical studies, was undertaken to elucidate the probable mechanism of the observed antianxiety effects of cannabis. The population for the clinical study consisted of 50 male chronic cannabis users who were otherwise healthy and 50 matched controls. When evaluated on Taylor's Manifest Anxiety Scale (TMA), these subjects had low anxiety scores as compared with the controls. To explore the possible interaction of cannabis with the benzodiazepine receptors, behavioral and biochemical studies in mice were devised, involving acute and chronic cannabis administration. Behavioral study revealed that mice under chronic cannabis treatment scored significantly higher on foot shock-induced aggression, but this was significantly blocked by benzodiazepine receptor antagonist. Furthermore, chronic cannabis treatment significantly (p less than 0.001) increased the frequency of licking response periodically punished by shocks. This confirms the antianxiety effect of cannabis, which also appears to be mediated through a benzodiazepine receptor, as it was reduced significantly (p less than 0.001) by a benzodiazepine receptor blocker. Specific 3H-diazepam binding was carried out in frontal cortex to assess both the population and affinity of benzodiazepine receptors. Our results indicate that acute cannabis treatment has no significant effect, whereas chronic cannabis treatment significantly increased 3H-diazepam binding as compared with controls. Scatchard analysis further reveals that increased affinity is responsible for increased binding to these receptors. It is therefore our contention that the antianxiety effect of cannabis is mediated through central benzodiazepine receptors.

Adult↗
PubMed1986

Upregulation of brain benzodiazepine receptors by electroconvulsive shocks.

Locomotor activity and footshock-induced aggressive behaviour in rat was decreased in a dose-dependent manner by diazepam. These effects were significantly potentiated by chronic electroconvulsive shock (ECS). Specific 3H-diazepam binding showed an upregulation of benzodiazepine receptors in the rat frontal cortex by ECS. This upregulation can explain the decreased therapeutic benefit observed in patients receiving both benzodiazepines and electroconvulsive shocks.

Aggression↗
PubMed1985

The mechanism of opening of the blood-brain barrier by hypertonic saline.

The permeability of the blood-brain barrier was assessed in the cat, using Evan's blue as circulant. Regional blood flow and vascular resistance in various areas of brain were measured using radioactive microspheres. Cardiac output (CO), blood pressure (BP), heart rate (HR), pH, pO2 and pCO2 were also measured. Hypertonic saline (5 M, 0.5 ml/kg), administered intravenously, increased the staining of the brain substance. It also produced a marked increase in cerebral blood flow after 5 min and a marked decrease in blood flow to all the regions of the brain after 20 min. The flow returned to normal after 40 min. The vascular resistance decreased at 5 min, increased at 20 min and returned to normal at 40 min. Cardiac output increased significantly at 5 min and decreased at 20 min, while at 40 min it returned to normal. Blood pressure decreased at 5 min, increased at 20 min, while heart rate steadily decreased. A complete recovery of cardiac output, blood pressure and heart rate occurred in 1 hr. No change was observed in pH, pCO2 and pO2. It is concluded that intravenous administration of hypertonic saline causes marked haemodynamic changes and increases the permeability of the blood-brain barrier due to transient impairment of autoregulation.

Animals↗
PubMed1985

Evidence for the involvement of histamine in the regulation of blood-brain barrier permeability.

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.

Animals↗
PubMed1985

Effect of alcohols on the permeability of blood-brain barrier.

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.

1-Propanol↗
PubMed1984

Evidence for the lack of serotonergic mechanism in the regulation of blood-brain barrier.

Role of serotonergic mechanism in the regulation of blood-brain barrier in anaesthetised cats and dogs has been investigated. In cats, the circulant used was Evans blue. The drugs as well as the circulant were administered through the left carotid artery. The staining of the brain substance was scored at autopsy. 5-Hydroxy-tryptamine (5-HT), 5-hydroxytryptophan (5-HTP), 5-HT uptake-inhibitors, citalopram and fluvoxamine, as well as normal saline produced no staining whereas hypertonic sodium chloride solution produced significant staining of the brain substance. In experiments on dogs, sodium fluorescein was injected intravenously and the cerebrospinal fluid (CSF) was collected through a needle put in the cisterna magna for estimation of the dye. Normal saline, 5-HT, citalopram, fluvoxamine and methysergide failed to affect the entry of sodium fluorescein in the CSF while hypertonic sodium chloride solution increased it significantly. Furthermore, 5-HT did not affect the increased entry of sodium fluorescein induced by hypertonic sodium chloride. It is concluded that serotonergic mechanism does not play a significant role in the regulation of blood-brain barrier.

Animals↗