Paulose,C S; Amee,Krishnakumar; Anu, Joseph(Department of Biotechnology, October 25, 2006)
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Abstract:
The recent developments in neurobiology have rendered new prominence
and potential to study about the structure and function of brain and related disorders.
Human behaviour is the net result of neural control of the communication between
brain cells. Neurotransmitters are chemicals that are used to relay, amplify and
modulate electrical signals between neurons and/or another cell. It mediates rapid
intercellular communication through the nervous system by interacting with cell
surface receptors. These receptors often trigger second messenger signaling pathways
that regulate the activity of ion channels. The functional balance of different
neurotransmitters such as Acetylcholine (Ach), Dopamine (DA), Serotonin (5-HT),
Norepinephrine (NE), Epinephrine (EPI), Glutamate and Gamma amino butyric acid
(GABA) regulates the growth, division and other vital functions of a normal cell /
organism (Sudha, 1998). Any change in neurotransmitters' functional balance will
result in the failure of cell function and may lead to the occurrence of diseases.
Abnormalities in the production or functioning of neurotransmitters have been
implicated in a number of neurological disorders like Schizophrenia, Alzheimer's,
Epilepsy, Depression and Parkinson's disease. Changes in central and peripheral
neuronal signaling system is also noted in diabetes, cancer, cell proliferation,
alcoholism and aging. Elucidation of neurotransmitters receptor interaction pathways
and gene expression regulation by second messengers and transcriptional factors
in health and disease conditions can lead to new small molecules for development
of therapeutic agents to improve neurological disease conditions. Increased
awareness of the global effects of neurological disorders should help health care
planners and the neurological community set appropriate priorities in research,
prevention, and management of these diseases.
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.
Jackson,James; Pius S,Padayatti; Thomas,Paul; Paulose,C S(Department of Biotechnology, December 13, 1996)
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Abstract:
In the present study we assessed plasma and platelet
monoamine content using high performance liquid
chromatography (HPLC). The study included 22 subjects
consisting of 12 freshly-detected male diabetic
patients and 10 age and sex-matched healthy controls.
The same parameters were measured in streptozotocin
-induced diabetic rat models consisting of
controls , diabetic and insulin - treated diabetic rats.
The platelet counts were significantly reduced
(P < 0.05) in rat models as well as human diabetic
samples. The plasma norepinephrine (NE) and epinephrine
(EPI) concentrations were significantly increased
(P < 0.05). The platelet showed a significant
increase (P < 0.01) in NE, EPI and serotonin content.
Increase in the plasma and platelet content of neurotransmitters
may be due to increased sympathetic
function, which is an adaptation for the decreased
platelet count observed in our study . The results indicate
that changes in the neurotransmitter content
of the platelet may be a good index to assess the neurotransmitter
status in pathological condition such as
diabetes mellitus.
Sheelu,Varghese; Bake,Shameena; Lakshmy,P S; Biju,M P; Eswar Shankar,P N; Paulose,C S; Oommen,V Oommen(Department of Bio Technology, August 27, 2001)
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Abstract:
The effects of feeding of 6-propyllhiouracil (6-I'fU) and potyunsaturatcd fatty acids (I'UFA) independently and ill
combination and administration (ip) of a single close of Iriiodothyronine (I',) (2.51ig/IOOg body wl) along with feeding of 6-
PTU and PUFA were studied in cal brain. Dopamine (DA), 5-hydroxytryplophan (5-IIl'I'), serolouin (5-Ill), 5-hydioxy indole
acetic acid (5-111AA), norepinephrine (NF) :uul ceinephrinn (I?I'l) contenls were assayed in the hypothalannls and ccrc
bral cortex regions. It was found that 6-P"l'U Iccding resulted in decrease in dopamine, 5-III', 5 II I I' and 5 IIiAA in both
regions. In animals fed wills PUFA followed by adnliuislralion of T,. the I)A level was found normal.
Shreedevi,T T; Padayatti,P S; Kala,M S; Philip, J; Paulose,C S(Department of Biotechnology, May 25, 1994)
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Abstract:
Optical absorption characteristics of rat blood
affected by diabetes has been studied using photoacoustic
(PA) technique. PA spectrum of blood
depends on the molecular structure of haemoglobin.
The peak value ratio ylQ increases with increase in
the diabetic state. Externally added glucose to
normal blood does not show any increase in y//3 ratio
as seen in the diabetic condition . The increase in yl,8
ratio may be due to the decrease in DPG level and
the resultant shift from R -> T conformation of
majority of diabetic haemoglobin.
Paulose,C S; Athira, Babu; Anju, T R(Indian Journal of Biochemistry and Biophysics, April , 2009)
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Abstract:
Hypoxia is one of the major causes of damage to the fetal and neonatal brain and cardiac functions. in earlier studies we have reported the brain damage caused by hypoxia and resusciation with oxygen and epinephrine and have found that glucose treatment to hypoxic rats and hypoxic rats treated with oxygen shows a reversal of brain damage. during this study the findings may have clinical significance in the proper management of heart and brain functions.
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.
Paulose,C S; Thliveris,J A; Dakshinamurti,K; Viswanathan,M(Department of Biotechnology, 1989)
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Abstract:
We have studied testicular function in the biotin-
deficient rat biochemically and morphologically.
Serum testosterone and luteinizing hormone (LH) levels
were decreased significantly in the deficient rats. Administration
of biotin or gonadotropins to the deficient rats
reversed this decrease in serum testosterone. There was no
difference in the serum cholesterol level between the control
and biotin-deficient rats. A significant degree of sloughing
of seminiferous tubule germinal epithelium was noticed
in the biotin-deficient rat testes. Biotin treatment of biotindeficient
rats reversed this condition whereas testosterone
treatment was without any effect. The development and
maintenance of morphological and functional integrity of
the seminiferous tubules appears to require a biotin-mediated
step in addition to testosterone.
Dakshinamurti,K; Paulose,C S; Thliveris,J A; Vriend,J(Department of Biotechnology, August 15, 1984)
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Abstract:
In pyridopaminedoxine-deficient young rats hypothalamic serum TSH concentration was detected. Highly signifiserotonin
was decreased with no changes in the cant decreases in the content of pituitary TSH and in
and noradrenaline content. Serum the number of pituitary thyrotroph secretory granules
and tri-iodothyronine concentrations were were found. These results suo
mmuuchch lower in the deficient rats as compared to thyroidism of suggest that the hypocontrols.
No significant of hypothalamicp yorirdigoxinin.e -deficient young rats might bbee
difference between deficient and control groups in the