Paulose,C S; Dakshinamurti,K(Department of Biotechnology, April 24, 1984)
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Abstract:
The high-affinity of [3H]y-aminobutyric acid (GABA) to GABAA receptors and [3H]baclofen to
GABAB receptors were studied in the cerebellum of pyridoxine-deficient rats and compared to
pyridoxine-supplemented controls. There was a significant increase in the maximal binding ( Bmax) of both
GABAA and GABAB receptors with no significant difference in their binding affinities (Kd). The changes
observed suggest a supersensitivity of GABAA and GABAB receptors which seems to correlate negatively
with the concentration of GABA in the cerebellum of pyridoxine-deficient rats.
Biju,M P; Pyroja,Sulaiman; Rajeshkumar,Neelimmathara V; Paulose,C S(Department of Biotechnology, February 15, 2001)
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Abstract:
Gamma aminohutyric acid (GAB A.) receptor tunctionaI status was artaIV se(l in pa It ial hcpatcctoIn ised.II'II). lead
nitrate (LN) induced hyperplastic and N-nifrosodiethylantinc INDEAI treated nctplastic rat Iivers during peak DNA
synthesis. The high-affinity I'HJGALA binding significantly decreased in PII and NDEi\ rats and the receptor affinity
decreased in NDEA and increased in LN rats compared with control . in NDEA. displacement analysis of I'I IIGABA
with muscimol showed loss of low-allinity site and a shill of high-allinity cite towards low-allinity . ' 1 he affinity sites
shifted towards high-affinity in LN rats. 'file number of low-allinity 1'I Ilhicuc)lline receptors decreased cignilic:uttly
in NDEA and I'll whereas it increased in LN rats. (ir\Bi\t receptor :gunist. unrscinrul. disc dependcnllyinhihilcd
epidermal growth factor IEGI--) induced DNA synthesis :uul enhanced the tr:utsfnrnting grmvth )actor (Il I I'(il (tlI
mediated DNA synthesis suppression in prim:uy hepalucvte cultures . Our results suggest that GABA,t reccjhtor act
as an inhibitory signal fur hepatic cell prolifctatiun.
Biju,M P; Pyroja,Sulaiman; Rajeshkumar,Neelimmathara V; Paulose,C S(Department of Biotechnology, September 20, 2000)
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Abstract:
GABAergic alterations in hypothalamus during compensatory hyperplasia after partial hepatectomy (PH), lead nitrate (LN)
induced direct hyperplasia and N-nitrosodiethylamine (NDEA) induced neoplasia in liver were investigated. Serum GABA
levels were increased in all 3 experimental groups compared with the control. GABA content decreased in hypothalamus of
PH and NDEA treated rats, while it increased in LN treated rats. GABAA receptor number and affinity in hypothalamic membrane
preparations of rats showed a significant decrease in PH and NDEA treated rats, while in LN treated rats the affinity
increased without any change in the receptor number. The GABAB receptor number increased in PH and NDEA treated rats,
while it decreased in LN treated rats. The affinity of the receptor also increased in NDEA treated rats. Plasma NE levels
showed significant increase in PH and NDEA rats compared with the control while it decreased in LN treated rats. The results
of the present study suggests that liver cell proliferation is influencing the hypothalamic GABAergic neurotransmission
and these changes regulate the hepatic proliferation through the sympathetic stimulation.