Biomedical subjects

M G Kolta

Publications and source records attributed to M G Kolta.

28 records · Page 2Linked to original sources

PubMed1985

Dietary choline affects response to acetylcholine by isolated urinary bladder.

Age-related increases occur in the response of isolated urinary bladders to the parasympathetic neurotransmitter acetylcholine (ACh). Experiments were carried out to determine whether long-term elevation or diminution in the amount of ingested choline can also affect the response of the urinary bladder to ACh. Female C57BL/6J mice were maintained on a choline-deficient chow and on drinking water supplemented with either 0, 1.5, or 4.0 mg/ml choline chloride from 8 to 20 months of age. Isolated bladders from choline deficient animals showed a 46% increase in the maximum response to ACh as compared to those from normal choline animals, while bladders from animals on choline enriched diets showed a 15% decrease in maximum contractile response. Radioligand binding experiments suggested that the functional changes result from alterations in the density of muscarinic receptors in the bladder. The results are consistent with the hypothesis that muscarinic receptors are down-regulated to compensate for increased parasympathetic activity associated with choline-enriched diets and up-regulated to compensate for decreased parasympathetic activity associated with choline-deficient diets.

Acetylcholine↗

PubMed1985

Time course of the development of the enhanced behavioral and biochemical responses to amphetamine after pretreatment with amphetamine.

These experiments were designed to examine the time course of development of the enhanced stereotyped behavioral response to amphetamine after withdrawal from chronic pretreatment with amphetamine and to determine whether this time course correlates with that of the enhancement in the amphetamine-induced stimulation of the release of dopamine (DA) from striatal slices. Rats were pretreated with amphetamine (5 mg/kg, i.p.) or saline, twice daily for 5 consecutive days. At 3, 15 and 30 days after withdrawal of the drug the stereotyped behavioral response and the release of endogenous DA from slices of striatum in response to a challenge dose of amphetamine were measured. At all 3 times tested, the stereotyped behavioral response to the challenge dose of amphetamine was enhanced in the rats pretreated with amphetamine, with the greatest degree of enhancement seen at 15 and 30 days after withdrawal of the drug. At these times, the responses were associated with a significant attenuation in the stimulation of locomotor activity produced by the challenge dose of amphetamine, which was probably related to the enhanced stereotyped behavioral response. Amphetamine stimulated the release of endogenous DA from slices of striatum in rats pretreated with saline and amphetamine. However, the release of endogenous DA from slices of rats pretreated with amphetamine was significantly greater than that of saline-pretreated rats at 15 and 30 days after withdrawal of the drug, but not at 3 days after withdrawal. Thus, pretreatment with amphetamine resulted in enhanced behavioral and biochemical responses to amphetamine which increased over time after withdrawal of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗

PubMed1985

Streptozocin-induced diabetes affects rat urinary bladder response to autonomic agents.

The response of the urinary bladder body and base to autonomic agents was studied in streptozocin (STZ)-diabetic rats. The bladder body region from 6-wk diabetic rats showed no changes in response to acetylcholine, phenylephrine, or isoproterenol. In contrast, the bladder base region showed a 39% increase in contractile response to acetylcholine and a 37% increased response to phenylephrine. In tissues from 47-wk diabetic animals, the bladder body showed a 51% increased contractile response to acetylcholine and a 37% increased relaxation response to isoproterenol. The bladder base showed a 66% increased contraction to acetylcholine. Thus, in the bladder base, enhanced responses to acetylcholine are detected soon after induction of diabetes and continue to increase as the diabetic state progresses. Moreover, in the same bladder region, an increase in responsiveness to alpha-adrenergic stimuli occurs. In the bladder body, enhanced responses to cholinergic and to beta-adrenergic stimuli occur, but are only observed in a more chronic diabetic state. The data suggest that an effect associated with autonomic diabetic neuropathy of the urinary bladder is an increased postsynaptic responsiveness to cholinergic stimuli in both regions.

Acetylcholine↗

PubMed1984

Age-related changes in sensitivity of rat urinary bladder to autonomic agents.

Experiments were done to determine if age-related changes occur in autonomic regulation of rat urinary bladder. The maximum contractile responses to acetylcholine were 63% and 15% greater in isolated bladders from 29-month and 17-month animals, respectively, as compared to 7-month animals. The amounts of [3H]quinuclidinyl benzilate bound to membrane preparations were 46% and 7% greater. In contrast, no age-related changes were observed in phenylephrine-induced contraction or in isoproterenol-induced relaxation of bladder. Thus, the urinary bladder of aged rats appears to develop increased sensitivity to cholinergic stimuli because of an increase in the number of muscarinic cholinergic receptors.

Acetylcholine↗

PubMed1984

Effect of hyperglycemia on biogenic amines, beta-endorphin and insulin of the rat brain.

Three experiments were designed to study the changes in brain biogenic amines, beta-endorphin and insulin in response to hyperglycemia in adult male rats. In all three experiments, animals were decapitated 10 minutes post injection (IP) of either 2.5 ml of 40% glucose or 0.9% saline. In the first experiment brain DA, NE, 5-HT and 5-HIAA were measured using fluorometric method. Plasma glucose, insulin (RIA) and corticosterone (CPB) were also determined. In addition to these measurements, brain beta-endorphin was determined (RIA) in the second experiment and brain insulin (RIA) in the third experiment. In all three experiments the hyperglycemic groups showed a significant increase in plasma insulin, brain NE and 5-HT and a significant decrease in brain 5-HIAA and no significant change in plasma corticosterone, brain DA, beta-endorphin and insulin. The results obtained in these experiments suggest that high levels of glucose may have an inhibitory effect on the metabolism of NE and 5-HT resulting in increases in the level of both amines. They also suggest that brain insulin is independent of the pancreatic one since high blood glucose did not influence the central level.

Animals↗

PubMed1981

Effect of peripheral cholinergic activation on the adrenal cortex function.

The adrenocortical response to cholinergic agonist and antagonist agents were investigated in intact, hypophysectomized and medullectomized rats. The administration of peripherally active compound neostigmine, was found to cause a significant rise of corticosterone in the intact, and the hypophysectomized animals but not in the medullectomized animals. Meanwhile, the centrally and peripherally active cholinergic agent physostigmine caused a significant rise in the intact, hypophysectomized and medullectomized animals. The results also show that the administration of the ganglionic blocker (e.g. tetraethylammonium or hexamethonium), the muscarinic agonist (pilocarpin) or the muscarinic antagonist (atropin) did not result in any significant changes in corticosterone levels. The results of these experiments might indicate that peripheral cholinergic pathway is involved in the regulation of the adrenal cortex function.

Adrenal Cortex↗

PubMed1981

In vitro response of the regenerating adrenal gland to epinephrine.

In this experiment, the adrenal medulla was removed from male rats and after 11 days, animals were sacrificed and the adrenal glands were incubated. Addition of epinephrine to the regenerating gland resulted in significant increase in corticosterone content in the gland. However, no significant changes were observed in the intact glands after epinephrine administration. The results of this experiment suggest that epinephrine may be playing a role in the adrenal cortex function.

Adrenal Glands↗

PubMed1981

Tissue distribution of 3H-corticosterone in response to stress.

The level and distribution of 3H-corticosterone (3H-B) was investigated in adult male Sprague-Dawley rats in response to diethyl ether stress, epinephrine (EP) and/or dexamethasone (DXM) administration. Diethyl ether stress caused a significant increase in the 3H-B counts by some of the body tissues and brain regions studied. Plasma 3H-B counts in the stressed rats were found to be twice as much as in the control animals. When EP (1.0 mg/kg) was injected, the tissue-plasma ratios(TPR) of 3H-B were significantly lower (P less than 0.05) than those of the dexamethasone (1.0 mg/kg) treated animals or the control group. The high 3H-B count in the plasma in response to diethyl ether stress or EP may indicate a decline in rate of corticosterone metabolism.

Animals↗

PubMedDate not supplied

Hypothermic effect of ethanol in mice selected for differential sleep-time response to pentobarbital.

The hypothermic action of ethanol was investigated in genetically distinct lines of mice selected for sleep-time response to pentobarbital for six generations. Ethanol (3 g/kg, intraperitoneally) was administered to alcohol-naive males and females from each of the unselected control, long-, and short-sleep mouse lines. Rectal temperatures were measured immediately before, and at 15, 30, 60, 90, 120, and 240 min after ethanol injection. Eight female and eight male mice from each line were sacrificed at each time point, and trunk blood was collected for plasma ethanol analysis. The results show that short-sleep mice were less hypothermic (p < 0.05) compared to long-sleep mice at 15 and 30 min after ethanol administration. However, plasma ethanol concentrations were not significantly different between the mouse lines at any time point. Therefore, the line-dependent differential ethanol-induced hypothermia observed may be a result of differences in "brain sensitivity" rather than in the rates of ethanol metabolism among the mouse lines.

Animals↗

PubMedDate not supplied

The role of inducible nitric oxide synthase in cocaine-induced locomotor sensitization.

Experimentally naive male Sprague-Dawley rats (weighing 85-110 g) were used to examine the role of inducible nitric oxide synthase (iNOS) in cocaine-induced locomotor sensitization. Repeated administration of cocaine (15 mg/kg, ip) for 7 consecutive days produced locomotor sensitization. Pretreatment with iNOS inhibitors, L-N(6)-(1-iminoethyl) lysine (NIL) or (-)-epigallocatechin gallate (EGCG; 10 mg/kg, ip), 30 min before cocaine (15 mg/kg, ip) administration totally blocked the development of cocaine-induced locomotor sensitization. Dopamine (DA) receptor binding in the nucleus accumbens (NAC) showed a significant decrease in the density of D(2) receptor and the affinity of D(1) receptor after cocaine treatment. Pretreatment with EGCG or NIL abolished the cocaine-induced changes in these parameters. These results suggest that iNOS may participate in the process of development of locomotor sensitization through the modulation of DA receptors in the NAC.

Animals↗