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V Radhakrishnan

Publications and source records attributed to V Radhakrishnan.

29 records · Page 2Linked to original sources
PubMed1991

NMDA receptor antagonist blocks the facilitation of the tail flick reflex in the rat induced by intrathecal administration of substance P and by noxious cutaneous stimulation.

This study examined effects of the N-methyl-D-aspartate (NMDA) receptor antagonist, 2-amino-5-phosphonovaleric acid (APV), on facilitation of the tail flick reflex (1) by intrathecal administration of 6.5 nmol of substance P at the lumbar spinal level in awake rats and (2) by noxious cutaneous stimulation in anesthetized rats (by immersing the tip of the tail in hot water at 55 +/- 1 degrees C for 1.5 min). Reaction time was decreased by about 70% by intrathecal administration of substance P and by about 40% by tail immersion. Intrathecal administration of APV (2 nmol) or cerebrospinal fluid (CSF) failed to alter the baseline responses. However, APV but not CSF blocked the facilitation induced by intrathecal administration of substance P and by tail immersion. These results indicate that while NMDA receptors do not appear to be involved in mediating the tail flick reflex, they may be involved in expression of the facilitation of this reflex by substance P and/or by a related peptide.

2-Amino-5-phosphonovalerate↗
PubMed1990

Selective blockade of NMDA-activated channel currents may be implicated in learning deficits caused by lead.

The effect of Pb2+ on glutamate receptor activity in rat hippocampal neurons was investigated with a view of explaining the cognitive and learning deficits produced by this heavy metal. Pb2+ (2.5-50 microM) selectively inhibited N-methyl-D-aspartate (NMDA)-induced whole-cell and single-channel currents in a concentration-dependent but voltage-independent manner, without significantly altering currents induced by either quisqualate or kainate. The frequency of NMDA-induced channel activation was decreased by Pb2+. Neither glycine (10-100 microM), nor Ca2+ (10 mM) reversed the effect of Pb2+. Pb2+ also inhibited the [3H]MK-801 binding to rat hippocampal membranes in vitro. The elucidation of the actions of Pb2+ on the NMDA receptor ion channel complex provides important insights into the clinical and toxic effects of this cation.

Animals↗
PubMed1987

Mitotic chromosome organization of neuroblastomas induced by the recessive oncogene Lethal(2)giant larvae4 of Drosophila melanogaster.

Mitotic chromosomes in neuroblastomas of Drosophila melanogaster homozygous for the recessive oncogene Lethal(2)giant larvae4 were studied at different larval ages. There was a progressive increase in mitotically active cells with increasing period of tumorous growth. The karyotype of the neuroblastomas generally remained stable. The metaphase chromosomes of the neuroblastomas, however, showed widely varying levels of condensation ranging from highly condensed to highly extended. Staining with the AT-specific fluorescent dye Hoechst 33258 showed extensive resolution of AT-rich heterochromatic blocks in the third and Y chromosomes suggesting their lack of coalescence in the extended metaphases of neuroblastomas. Our results suggest aberrant condensation as a major chromosomal lesion in Drosophila neuroblastomas.

Animals↗
PubMed1986

Effect of selective gastric vagotomy on gustatory behavior in rats.

Gustatory responses were investigated in sham vagotomized (SVgX) and selective gastric vagotomized (VgX) male rats by 1-h single-bottle tests using 3% sucrose, 13% glucose, 0.2% saccharin, 0.9% sodium chloride, 0.16% citric acid, 0.001% quinine sulphate and tap water as test solutions. The intakes of sucrose, glucose, saccharin and sodium chloride were significantly less in VgX rats, compared to SVgX ones. When all these rats were exposed to graded concentrations of sucrose (0.1%, 0.5%, 1% and 5%), a maximum preference was shown to 5% and the least to 0.1% sucrose by both SVgX and VgX rats, even though the VgX rats consumed less than SVgX ones. Vagotomy produced a maximum suppression of 5% sucrose intake, a moderate suppression of 1% and 0.5% sucrose intake and no significant change in the intake of 0.1% sucrose. The results also indicated a probable reduction in the ability of VgX rats to discriminate taste intensities within a close range. Pharmacological blocking of vagal efferents with atropine methyl nitrate (5 mg/kg) did not produce any significant change in the intakes. The possibility of an excitatory input through the gastric vagal afferents selectively influencing the intake of sapid substances is suggested.

Animals↗
PubMed1985

Cardiorespiratory changes following chemical applications to gut serosa.

Application of 0.2-0.3 ml of 1 M ammonium chloride, 100 mM citric acid, 100 mM hydrochloric acid, 1% potassium chloride, 1% ammonium oxalate, 1% oxalic acid, 0.5% sodium hydroxide, 200 micrograms% bradykinin or 20 mg% capsaicin to gastrointestinal serosa produced a fall in blood pressure and inhibition of respiration in hypertensive as well as normotensive rats. In 6 (8%) of the animals studied, a fall in heart rate was also seen which was blocked by atropine. The blood pressure changes were independent of changes in heart rate. After acute abdominal vagotomy, while the respiratory inhibition following chemical application on gut serosa was enhanced, the cardiovascular responses were the same as before. In animals subjected to sympathetic denervation by spinal section at T5, celiac ganglionectomy or splanchnicotomy, a similar application produced an augmented respiratory response while the cardiovascular parameters were unaffected. These results show that the above inhibitions were mediated through the sympathetic afferents and a minor stimulation of respiration, via vagal afferents. The efferent pathway for the cardiac changes seems to be via vagus and the vascular changes via the sympathetics. In chronic vagotomized animals, the same stimulation produced a response similar to that seen in animals with intact vagus. An adaptive response may be operating in chronic animals reverting the status back to normal.

Ammonium Chloride↗