Search PubMed⌕ Search

Biomedical subjects

V Paul

Publications and source records attributed to V Paul.

85 records · Page 5Linked to original sources
PubMed1981

Changes in cognitive task performance across the menstrual cycle.

Menstrual-cycle-related changes in estrogen were expected to differentially affect various cognitive tests. Specifically, the estrogen peak occurring at midcycle in ovulatory women was expected to facilitate performance of highly practiced "automatized" tasks and to impair performance of "perceptual-restructuring" tasks, compared with performance of these tasks in the postovulatory phase of the cycle when progesterone is thought to counteract the action of estrogen. Perceptual-restructuring tasks are defined as tasks in which the initial percepts to obvious stimulus attributes are wrong and must be set aside in favor of percepts to less obvious stimulus attributes. Eight-seven regularly menstruating undergraduate women were studied. Odd-numbered subjects were tested first on or about Day 10 of their cycle and then again on Day 20; even-numbered subjects, in the reverse sequence. Daily basal body temperature records were obtained. These temperature records suggested that 21, or 24%, of the subjects did not ovulate in the cycle(s) studied. No main effect of Day 10 versus Day 20 occurred for any task in the 66 women who did appear to ovulate. However, the magnitude of predicted shifts in performance was significantly correlated with proximity of the "Day 10" testing day to the thermal nadir of the basal body temperature record, the presumed preovulatory estrogen peak; and to the "Day 20" proximity to the basal body temperature thermal peak, the presumed progesterone peak. Subjects tested 3 or fewer days before the thermal nadir and on or after the thermal peak had the predicted significant changes on three of the four administered tasks. No other temporally defined group produced significant changes. The results of the study support the experimental hypotheses and also indicate that precise timing is essential to demonstrate the phenomena.

Adult↗
PubMedDate not supplied

Effect of acute pretreatment of lead on picrotoxin-induced convulsions in rats.

The effect of acute exposure to lead acetate (LA)/lead nitrate (LN) on onset and severity of convulsions induced by a low dose of picrotoxin was examined in rats. Both LA and LN reduced the time of onset and exacerbated the severity of convulsions, with a resultant high lethality. On comparison, it was noted that in the LA-pretreated group, convulsion scores and incidence of tonus and mortality were much higher; the appearance of tonus was more delayed than in the LN-pretreated group. In lead-pretreated animals, the potentiation of picrotoxin-induced convulsions was accompanied by higher lead levels in blood (p < 0.001). However, the whole-brain lead levels were not significantly different in these animals compared to the controls. The difference in the degree of potentiation by the two forms of lead could possibly be attributed either to the role of a combination of anions and cations or to the variable cerebral uptake and regional distribution of lead or due partly to the extent of competitive interaction involving d-aminolaevulinic acid--whose level is known to be elevated consequent to lead-induced disruption of haem biosynthesis--at GABA receptors.

Animals↗
PubMedDate not supplied

The effect of beta-adrenoceptor antagonists alone and in combination with a GABA-elevating agent on isoniazid-induced convulsions in rats.

A delay in the onset of isoniazid-induced convulsions was found in rats pretreated with the beta 2-adrenoceptor blocker, butoxamine and the nonspecific beta-blocker, propranolol. In these animals the convulsive responses were inhibited in a dose dependent manner. These compounds were found to be effective even after the induction of convulsions. The beta 1-blocker, acebutolol was able to protect rats only when injected prior to the challenge. The anticonvulsant effect of acebutolol and propranolol but not that of butoxamine was found to be enhanced in animals pretreated with a gamma-aminobutyric acid (GABA) elevating agent, aminooxyacetic acid (AOAA). The findings indicate that the GABA-mediated anticonvulsant action of AOAA seems to be additive with that resulting from beta 1 but not beta 2-blockade.

Acebutolol↗
PubMedDate not supplied

The antimyoclonic action of clonazepam through a GABA--independent mechanism.

The present study investigates whether clonazepam exerts its antimyoclonic action through a GABA independent mechanism. We have studied the antimyoclonic effect of clonazepam and compared it with that of aminooxyacetic acid (AOAA), a GABA transaminase inhibitor, against myoclonus induced by picrotoxin, a GABA receptor antagonist and allylglycine, a drug which inhibits synthesis and release of GABA. We have also investigated the effect of clonazepam against picrotoxin-induced myoclonus in rats pretreated with either AOAA or submyoclonic dose of allylgylycine. Clonazepam pretreatment inhibited both picrotoxin and allylglycine-induced myoelonus whereas AOAA was effective in inhibiting only picrotoxin-induced myoclonus. The protective effect of clonazepam against picrotoxin-induced myoclonus was potentiated by AOAA pretreatment. Moreover, clonazepam afforded protection against picrotoxin-induced myoclonus in rats pretreated with a submyoclonic GABA reducing dose of allylglycine. These findings indicate that a GABA independent mechanism may also be involved in the antimyoclonic action of clonazepam.

4-Aminobutyrate Transaminase↗
PubMedDate not supplied

The role of adrenergic mechanism in tremorine-induced tremors in rats: antitremor effect of beta-adrenoceptor antagonists.

Tranylcypromine (TCP) pretreatment was found to accelerate the tremorogenic activity of tremorine in rats. Conversely, reserpinization delayed the onset of induction of tremors, and a significant diminution in their intensity was observed in these rats. A comparative study of the antitremor activity of beta-adrenoceptor antagonists against this tremor-model showed that butoxamine (beta 2-antagonist) and propranolol (nonselective antagonist) were able to afford a rapid and powerful protection, whereas a weaker and delayed effect was observed in rats treated with the beta 1-antagonist, acebutolol. Furthermore, the antitremor activity of butoxamine and propranolol but not that of acebutolol was found to be potentiated and diminished in rats pretreated with reserpine and TCP, respectively. It was inferred that beta 2-receptor modulated the tremorogenic activity of tremorine, and that inhibition by propranolol or butoxamine of this subtype beta-adrenoceptor resulted in rapid and powerful suppression of tremors, and that the antiadrenergic activity of acebutolol was unlikely to have a role in its antitremor effect.

Adrenergic beta-Antagonists↗