Glutamatergic Nmda And Ampa Receptors Functional Regulation In Streptozotocin Induced Diabetic Rats: Effect Of Vitamin D3 And Curcumin Supplementation

The present study was designed to investigate the protective effect of curcumin and vitamin D3 in the functional regulation of glutamatergic NMDA and AMPA receptors in streptozotocin (STZ) induced diabetic rats. Alterations in glutamatergic neurotransmission in the brain were evaluated by analyzing the glutamate content, glutamate receptors - NMDA and AMPA receptors binding parameters and gene expression, GAD and GLAST gene expression. Immunohistochemistry studies using confocal microscope were carried out to confirm receptor density and gene expression results of NMDA and AMPA receptors. The role of glutamatergic receptors in pancreas was studied using the following parameters; glutamate content, GLAST expression, glutamate receptors - NMDA and AMPA receptor binding and gene expression. Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of diabetes. In the present study SOD assay and GPx gene expression were done to evaluate the activity of antioxidant enzymes in the brain regions and pancreas. NeuroD1 and Pdx1 gene expression were performed in pancreas of experimental rats to evaluate pancreatic islet survival. Gene expression profiles of caspase 8, Bax, and Akt in brain regions and pancreas were studied to understand the possible mechanism behind curcumin and vitamin D3 mediated neuroprotection and islet survival. Gene expression studies of vitamin D3 receptor localisation in the pancreas was done to understand the mechanism of vitamin D3 in insulin secretion. Curcumin and vitamin D3 mediated insulin secretion via Ca2+ release were studied using confocal microscope.

Adrenergic and serotonergic function in dna synthesis during rat liver regeneration and in hepatocyte cultures

The adult mammalian liver is predominantly in a quiescent state with respect to cell division. This quiescent state changes dramatically, however, if the liver is injured by toxic, infectious or mechanic agents (Ponder, 1996). Partial hepatectomy (PH) which consists of surgical removal of two-thirds of the liver, has been used to stimulate hepatocyte proliferation (Higgins & Anderson 1931). This experimental model of liver regeneration has been the target of many studies to probe the mechanisms responsible for liver cell growth control (Michalopoulos, 1990; Taub, 1996). After PH most of the remaining cells in the renmant liver respond with co-ordinated waves of DNA synthesis and divide in a process called compensatory hyperplasia. Hence, liver regeneration is a model of relatively synchronous cell cycle progression in vivo. In contrast to hepatomas, cell division is terminated under some intrinsic control when the original cellular mass has been regained. This has made liver regeneration a useful model to dissect the biochemical and molecular mechanisms of cell division regulation. The liver is thus, one of the few adult organs that demonstrates a physiological growth rewonse (Fausto & Mead, 1989; Fausto & Webber, 1994). The regulation of liver cell proliferation involves circulating or intrahepatic factors that are involved in either the priming of hepatocytes to enter the cell cycle (Go to G1) or progression through the cell cycle. In order to understand the basis of liver regeneration it is mandatory to define the mechanisms which (a) trigger division, (b) allow the liver to concurrently grow and maintain dilferentiated fimction and (c) terminate cell proliferation once the liver has reached the appropriate mass. Studies on these aspects of liver regeneration will provide basic insight of cell growth and dilferentiation, liver diseases like viral hepatitis, toxic damage and liver transplant where regeneration of the liver is essential. In the present study, Go/G1/S transition of hepatocytes re-entering the cell cycle after PH was studied with special emphasis on the involvement of neurotransmitters, their receptors and second messenger function in the control of cell division during liver regeneration

Dopamine receptor subtypes functional regulation in insulin induced hypoglycemic neonatal rats: Effect of Glucose, Bacopa monnieri and Bacoside A resuscitation

In the present work we studied the potential of Bacopa monnieri and Bacoside A treatment to enhance the antioxidant system and support the neuronal survival in the hypoglycemic neonatal brain. For achieving the aim, DAD1 and DAD2 receptors functional regulation, gene expression of growth factors, neuronal survival and apoptotic factors during insulin induced hypoglycemic neonatal brain in rats were studied.

Polyunsaturated Fatty Acids (PUFA) Regulate Neurotransmitter Contents in Rat Brain

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.

ALPHA2 Adrenergic and High Affinity Serotonergic Receptor Changes in the Brain Stem of Streptozotocin induced Diabetic Rats

The brain stems (13S) of streptozotocin (STZ)-diabetic rats were studied lo see the changes in neurotransmitter content and their receptor regulation. The norepinephrine (NE) content determined in the diabetic brain stems did ^ control. an E showed la while PI turnover hri content increased significantly compared N^r eNveFa o the recep significant increase. The alpha2 adrenergic receptor IneP utisoulinntreat d ratsetheNE contentt dec^ sled was significantly reduced during diabetes. in versedcto reanorm sed ulcrea e tK reatment the state. while EPI content remained increased as in die diabetic B,, for a]pha2 adrenergic receptors slw^nificantly while Unlabelled clonidine inhibited [31-I]NE binding in BS of control, diabetic and insulin treated ulations bindi diabetic rats showed that alpha2 adrenergicre^ punks cojnidiabetic animal the ligand bound sites with Hill slopes significantly away from unity. weaker to the low affinity site than in controls. Insulin treatment reversed[ this allumbmn to control levels. The displacement analysis using (-)-epinephrine age in control and diabetic animals revealed two populations of receptor affinidtyo=tat ss. In control animals, when GTP analogue added with epinephrine, the curve nagnlde caofnfitnroit yS model; but in the diabetic BS this effect `not aobserved. In bintact oth the diabetic data thus showlthat the effects of monovalent cations on affinity alphaz adrenergic receptors have a reduced affinity v due in stem ialtered Itscppeomson(5- regulation. The serotonin (5-HT) coat hydroxy) tryptophan (5-HTP) showed an increase and its breakdown metabolite (5-hydroxy) indoleacetic acid (5-I{IAA) showed a significant decrease. This showed that in serotonergic which l nerves there is a disturbance in both synthetic and breankduomwnbers pretma'med ana increased 5-HT. The high affinity serotonin receptor um ese serotonerg decrease in the receptor affinity. The insulin ^treatmentsturtiy showsha decreased serotonergic receptor kinetic parameters to control level. receptor function. These changes in adrenergic and serotonergic receptor function were suggested to be important in insulin function during STZ diabetes.

Neurotransmitter Functional Role in Neurodegenerative Diseases: human Health

Neuroscience is the study of'tbe ne rvous system , including the i - ; . in, spinal cord and peripheral nerves . Neurons are the basic cells of the brain and nervous system which exerts its functional role through various neurotransmitters and receptor systems . The activity of a nen ren depends on the balance between the number of excitatory and inhibito r y processes affecting it, both processes occurring individually and sin ,tlte-' ,ieously. The functional bal,ince of different neurotransmitters such as Acct >>lcholine (Ach), Dopamine (DA), Serotonin (5-1-17), Nor epinepbri,te (N.1 j, Epinephrine (LPI), Glutamate and Gamma amino butyric acid (GA BA) regulates the growth , division and other vital functions ofa normal cell / organisin (Sudha, 1 998). The micro-environ ; nertt of the cell is controlled / the macro-environment that surrounds the individual. Any change in the cell environment causes imbalance in cell homeostasis and f,ntction. Pollution is a significant cause of imbalance caused iii the inacYcenvironment. Interaction with polluted environments can have an adverse impact on the health of humans. The alarming rise in enviromilmieil cont.iniin :rtion has been linked to rises in levels of pesticides, ndltstr al effluents, domestic Waste, car exhausts and other anthropogenic activities. Persistent exposures to contaminant cause a negative imp,-, on brain health and development . Pollution also causes a change in the neurotransmitters and their receptor function leading to earl.;' recurrence of neurodcge,terative disorders such as flypoxia , Alzbeimers's and Huntington 's disease early in life.