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Biomedical subjects

R L Singhal

Publications and source records attributed to R L Singhal.

At least 55 records · Page 3Linked to original sources
PubMed1982

Effects of cholinergic and GABAergic drugs on apomorphine-induced gnawing behavior in rats.

The effects of cholinergic and GABAergic agonist and antagonist were studied on the apomorphine-induced gnawing behavior in rats. Physostigmine (0.5 mg/kg) decreased the biting scores, whereas atropine (5 mg/kg) had an opposite effect. Picrotoxin potentiated the physostigmine inhibitory action on gnawing responses. This inhibitory gnawing effect was antagonized by prior treatment with atropine. Pretreatment with amino-oxyacetic acid (25 mg/kg) also potentiated the inhibitory effect of physostigmine on gnawing behavior in animals. Such an additive inhibitory response could be antagonized by simultaneous pretreatment with cholinergic and GABAergic blockers such as atropine and picrotoxin, respectively. These findings indicate that the modulatory action of cholinergic neurons on DA system is probably influenced by changes in the GABAergic system.

Aminooxyacetic Acid↗
PubMed1981

Effects of apomorphine on behavioural activity and brain catecholamine synthesis in normal and L-triiodothyronine-treated rats.

The effect of chronic apomorphine treatment on behavioural activity as well as brain dopamine metabolism was studied in normal and neonatally L-triiodothyronine-treated rats. Neonatal hyperthyroidism was accompanied by an increase in spontaneous locomotor activity as well as by enhanced synthesis and release of dopamine as evidenced by increased catecholamine synthesis in crude synaptosomal preparation (P2 pellet), elevated tyrosine hydroxylase activity and higher concentrations of homovanillic acid and 3, 4-dihydroxyphenylacetic acid in striatum of rats. Repeated apomorphine treatment (1 mg/kg/day s.c) for 15 days, beginning from the 15th day of age, produced hypermobility and stereotyped behavior (consisting of sniffing, gnawing, rearing) which appeared to be more pronounced in neonatally hyperthyroid rats than in normal controls. In addition, apomorphine-treated hyperthyroid animals marched in a row with straub tail, and displayed increased aggressiveness and bizarre social behavior consisting of "mock fighting" when left in pairs. In contrast to normal rats, apomorphine-treated hyperthyroid animals displayed marked hyperactivity which was evident even at 24 hours after the last injection of apomorphine. Administration of apomorphine resulted in significant decreases in striatal tyrosine hydroxylase, catecholamine synthesis in crude synaptosomal preparation (P2 pellet) as well as dopamine metabolite levels in brains of both normal and hyperthyroid animals. Our present data showing that apomorphine potentiates behavioural activity in hyperthyroid rats suggest that L-triiodothyronine and apomorphine probably share certain features common to activating dopaminergic neurons in the brain.

Animals↗
PubMed1981

Effects of nortriptyline treatment on learned helplessness in the rat.

Using an escape delay procedure previously shown to elicit behavioral deficits in mice exposed to uncontrollable shock, rats treated with inescapable but not escapable shock or no shock displayed comparable interference effects when tested in a two-way shuttle box 24 hr later. Treatment with 12.5 mg/kg nortriptyline for 4 or 6 days counteracted the escape deficits produced by inescapable shock while the 0 or 2 day administration regimens were without any appreciable effect. The finding that interference effects produced by inescapable shock were sensitive to sub-acute but not acute drug administration supports the utility of the learned helplessness model in evaluating potential antidepressant agents in experimental animals.

Animals↗
PubMed1981

Thyrotropin releasing hormone potentiates the effects of imipramine on brain serotonergic system.

Daily administration of thyrotropin-releasing hormone (TRH) (20 mg/kg) for 10 days in 2 equally divided doses increased 5-hydroxytryptamine and/or 5-hydroxyindoleacetic acid levels in certain brain areas. Chronic imipramine treatment (10 mg/kg) for 10 days significantly decreased the levels of brain 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. When TRH was administered concurrently with imipramine (10 mg/kg), this neuropeptide significantly potentiated the effects of imipramine on lowering of endogenous levels of 5-hydroxytryptamine (striatum, hypothalamus) and 5-hydroxyindoleacetic acid (striatum, midbrain, pons-medulla). Our data provide a possible neurochemical basis for the reported potentiation of tricyclic antidepressant action by TRH.

Animals↗
PubMed1981

Testicular cyclic nucleotide and adrenal catecholamine metabolism following chronic exposure to cadmium.

Cadmium (Cd) produces injurious effects on reproductive function and has been implicated in the pathogeneses of hypertension. The present article summarizes available data on alterations in the cyclic AMP system of testicular and prostatic tissue as well as in catecholamine metabolism in adrenal glands following exposure to Cd and subsequent withdrawal. Daily Cd (1 mg/kg IP) for 45 days decreased prostatic and testicular weights of mature male rats. In prostate, chronic treatment with Cd reduced cyclic AMP levels to 57% of normal values which appeared to be due to the decrease in adenylate cyclase activity since cyclic AMP metabolism by phosphodiesterase was not significantly altered. Cyclic AMP binding to prostatic protein kinase was increased following Cd administration as was the activity of the cyclic AMP-dependent form of protein kinase. In contrast to the prostate, testicular adenylate cyclase was stimulated by Cd treatment. However, the endogenous cyclic AMP levels remained unaffected since the increase in testicular adenylate cyclase was offset by a concomitant increase in the activity of phosphodiesterase. Although the activities of the cyclic AMP-dependent and the independent forms of testicular protein kinase were significantly depressed, the binding of cyclic AMP to protein kinase from testes of Cd-treated rats was not affected. Discontinuation of treatment for 28 days in rats that had previously been given the heavy metal for 45 days resulted in at least a partial reversal of several of the cadmium-induced changes in cyclic AMP metabolism of the rat prostate and testes. However, the weight of the prostate glands remained essentially in the same range as that seen in the "treated group."Data suggest that cyclic AMP metabolism in both the primary and the secondary reproductive organs is altered following chronic Cd treatment and that some changes persist even 28 days following the termination of daily exposure to the heavy metal.Cd treatment also increased adrenal weights and augmented the levels of adrenal norepinephrine and epinephrine as well as the activity of tyrosine hydroxylase. Discontinuation of the heavy metal treatment for 28 days, in rats previously injected with Cd for 45 days, restored the activity of tyrosine hydroxylase as well as the amount of norepinephrine and epinephrine. In contrast, adrenal weights were restored only partially following withdrawal of Cd treatment. Evidence indicates that the changes in adrenal catecholamine metabolism may be the result of stress induced by chronic exposure to this heavy metal. In addition, some of the untoward effects such as hyperglycemia and arterial hypertension seen during Cd toxicity might be related to increased synthesis of epinephrine in adrenal glands.

Adrenal Glands↗
PubMed1981

MK-771 enhances the turnover of norepinephrine in brain.

Single injection of MK-771, an analog of thyrotropin-releasing hormone (10 mg/kg) increased the soluble tyrosine hydroxylase activity in striatum and olfactory tubercles by 22% and 31%. The endogenous levels of norepinephrine in olfactory tubercles, striatum, hypothalamus, mid-brain, pons medulla and cerebral cortex remained unchanged; in hippocampus, it was lowered to 71% of controls. Furthermore, the concentration of 3-methoxy-4-hydroxy-phenylethylene glycol was enhanced by 33%. Data suggest that MK-771 increases the synthesis and release of norepinephrine and that MK-771 elicits its CNS stimulant action partly by augmenting the turnover of this biogenic amine.

Animals↗
PubMed1980

Diabetogenic effects of chronic oral cadmium adminstration to neonatal rats.

1 Chronic exposure of neonatal rats to oral cadmium (Cd) (0.1 and 1.0 micrograms/g daily for 45 days) disturbed glucose homeostasis, as reflected by hyperglycaemia, reduced liver glycogen and enhanced gluconeogenic potential of hepatic tissue. 2 This Cd-exposure regimen also increased hepatic cyclic adenosine 3',5'-monophosphate (cyclic AMP) which was accompanied by enhancement of basal, adrenaline and glucagon-stimulated form(s) of adenylate cyclase. 3 In order to assess the responsiveness of pancreatic beta cells to glucose, islets isolated from control as well as Cd-exposed animals were incubated in vitro and their rate of insulin secretion determined. In the presence of glucose 0.5 mg/ml, there was no significant difference in the rate of insulin release. However, at higher glucose concentrations (1.5 and 3.0 mg/ml), the islets from Cd-exposed rats released significantly less insulin than those of control animals. 4 The results are discussed in relation to the possible mechanism of the diabetogenic effect of Cd.

Adenylyl Cyclases↗
PubMed1980

Effect of low-dose lithium administration and subsequent withdrawal on biogenic amines in rat brain.

1 The effects of low-dose lithium administration (2 mEq/kg, daily) and its subsequent withdrawal have been examined with reference to changes in biogenic amine systems in several discrete regions of rat brain. 2 Increased levels of striatal tyrosine and midbrain tryptophan were found following lithium administration together with slight decreases in striatal tyrosine hydroxylase and midbrain tryptophan hydroxylase activities. Withdrawal resulted in a decrease in tyrosine content with increased tyrosine hydroxylase activity, whilst tryptophan levels and tryptophan hydroxylase activity were increased. 3 Lithium treatment and withdrawal resulted in altered levels of noradrenaline and dopamine, these changes being regionally variable. 3-Methoxy-4-hydroxyphenylglycol content was depressed in both treated and withdrawal rats as were 3,4-dihydroxyphenylacetic acid levels. Homovanillic acid decreased as a result of lithium treatment, but was greatly elevated in the withdrawal group. 4 5-Hydroxytryptamine content decreased in some brain regions following lithium treatment with return towards control values in withdrawal rats. 5-Hydroxyindoleacetic acid levels also displayed a regional variation as a result of lithium treatment and withdrawal. 5 The implications of these observations in elucidating the pharmacological effect of lithium treatment and its subsequent withdrawal are discussed.

Animals↗