Jackson,James; Paulose,C S(Department of Biotechnology, May 1, 2000)
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Abstract:
5-HT2A receptor binding parameters were studied in the cerebral cortex and brain stem of
control, diabetic, insulin, insulin + tryptophan and tr3yptophan treated streptozotocin diabetic
rats. Scatchard analysis using selective antagonist, [-H](±)2,3-dimethoxyphenyl-l-[2-(4-piperidine)-
methanol] ([3H]MDL100907) in cerebral cortex of diabetic rats showed a significant
decrease in dissociation constant (Kd) without any change in maximal binding (Bm). Competition
binding studies in cerebral cortex using ketanserin against [3H]MDL100907 showed
the appearance of an additional site in the low affinity region during diabetes. In the brain
stem, Scatchard analysis showed a significant increase in Bmax and Kd. Displacement studies
showed a shift in the receptor affinity towards a low affinity state. All these altered parameters
in diabetes were reversed to control level by insulin, insulin + tryptophan and tryptophan
treatments. Tryptophan treatment is suggested to reverse the altered 5-HT2Abinding and
blood glucose level to control status by increasing the brain 5-HT content.
Paulose,C S; Dakshinamurti,K; Subah,Packer; Newman,L Stephens(Department of Biotechnology, 1986)
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Abstract:
Pyridoxal phosphate (PLP) is the coenzyme of various decarboxylases involved in the
formation of monoamine urotransmitters such as y-aminobulyric acid (GAE3A),
serotonin (5-HT) and dopamine. 1-lowever; in the pyridoxine-deficient rats GABA and
5-HT are decreased in various brain areas including the hypothalamus, with no change
in the catecholamine levels. Serotonin and GABA are known to be involved in blood
pressure control mechanisms. In this study adult Sprague-Dawley rats placed on a
pyridoxine-deficient diet for 8 weeks showed significant hypertension compared with
pyridoxine-supplemented controls. This was associated with a general sympathetic
stimulation. Treatment of deficient rats with a single dose of pyridoxine (10 mg/kg body
weight) reversed the blood pressure to normal levels within 24 h, with concomitant
restoration of hypothalamic 5-HT and GABA, as well as the return of plasma
norepinephrine to nornr;l levels. The results indicate that there is a cause-and-effect
relationship between pyridoxine deficiency and hypertension.
Dakshinamurti,K; Paulose,C S; Viswanathan,M; Siow,Y L(Department of Biotechnology, 1988)
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Abstract:
Veuruenducrim lri v j p .rim,
deficienc:v. NEUROSCI BIOBEHAV REV 12(3/4) 189-193. 1988.- Dihydroxyphenylalanine decarboxvlase and
5-hydroxytryptophan decarboxvlase respectively have high and low affinities for pyridoxal phosphate. In the pyridoxinedeficient
animal. hypothalamic serotonin content is significantly reduced without any change in catecholamine levels.
Hypothalamic neurotransmitters affect the hvpothalamo-pituitary-end organ axes. Specifically, the decrease in hypothalamic
serotonin in the pyridoxine-deficient rat results in tertiary hypothyroidism. In addition. pineal function is affected in
deficient animals due to decreased synthesis of melatonin.
Viswanathan,M; Siow,Y L; Paulose,C S; Dakshinamurti,K(Department of Biotechnology, May 24, 1988)
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Abstract:
Pvridoxine deficiency causes physiologically significant decrease in brain serotonin (5-HT) due to decreased decarboxylation of 5-
hvdroxvtrvptophan (5-HTP). We have examined the effect of pyridoxine deficiency on indoleamine metabolism in the pineal gland, a
tissue with high indoleamine turnover. Adult male Sprague-Dawley rats were fed either a pyridoxine-supplemented or pyridoxinedeficient
diet for 8 weeks. Pyridoxine deficiency did not alter the pattern of circadian rhythm of pineal 5-HT. 5-hvdroxvindoleacetic
acid (5-HIAA), V-acetvlserotonin (NAS). and melatonin. However the levels of these compounds were significantly lower in the
pineal glands of pyridoxine-deficient animals. Pineal 5-HTP levels were consistently higher in the pyridoxine-deficient animals and a
conspicuous increase was noticed at 22.00 h. Increase in pineal NAS and melatonin levels caused by isoproterenol (5 mg kg at 17.00 h)
were significantly lower (P < 0.05) in the pyridoxine-deficient animals. Treatment of pyridoxine-deficient rats with pvridoxine restored
the levels of pineal 5-HT, 5-HIAA. NAS. and melatonin to values seen in pyridoxine-supplemented control animals. These results
suggest that 5-HT availability could be an important factor in the regulation of the synthesis of pineal NAS and melatonin.
Paulose,C S; Dakshinamurti,K; Subah,Packer; Newman,L Stephens(Department of Biotechnology, December 8, 1987)
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Abstract:
Pyridoxal phosphate is the coenzyme of various decarboxylases involved in the formation
of monoamine neurotransmitters such as y-aminobutyric acid , serotonin , dopamine, and norepinephrine
. Adult male Sprague-Dawley rats placed on a pyridoxine -deficient diet for 8 weeks showed
significant hypertension compared with pyridoxine -supplemented controls . Hypothalamic contents of
pyridoxal phosphate , y-aminobutyric acid, and serotonin in the pyridoxine - deficient rats were significantly
lower than those in pyridoxine -supplemented controls . Hypertension was associated with
sympathetic stimulation . Treatment of pyridoxine-deficient rats with a single dose of pyridoxine (10
mg/kg body weight) reversed the blood pressure to normal levels within 24 hours, with concomitant
restorations of hypothalamic serotonin and y-aminobutyric acid as well as the return of plasma
norepinephrine and epinephrine to normal levels . Also, pyridoxine treatment reversed the hypothalamic
hypothyroidism observed in pyridoxine -deficient rats . These results indicate an association
between pyridoxine deficiency and sympathetic stimulation leading to hypertension.