Enhanced NMDAR1, NMDA2B and mGlu5 receptors gene expression in the cerebellum of insulin induced hypoglycaemic and streptozotocin induced diabetic rats

Joseph, Abin John; Kumar, T. Peeyush; Nandhu, Mohan S.; Paulose, C S

doi:10.1016/j.ejphar.2009.12.024

Cited by 27 publications

(11 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the diabetic brain the content of glutamate transporters and the α 1A subunit of P/Q type Ca 2+ channels are changed. In the cerebellum of STZ rats the expression of the glutamate transporter GLAST gene was decreased, which indicates a decrease of glutamate reuptake (Anu et al, 2010). In the hippocampus a decrease of the level of glutamate transporters was transient, being evident mainly at the early stages of DM.…”

Section: Fig 3 Signaling Pathways Responsible For Glutamate Toxicitymentioning

confidence: 88%

“…Excessive glutamate over-activates the cognate receptors, specifically NMDA receptors, which gives the influx of high level of Ca 2+ in the post-synaptic cell. In the diabetic brain the glutamate level and the number of GluRs are significantly increased, which is the main cause of neurodegenerative changes in DM (N. Li et al, 1999;Tomiyama et al, 2005;Joseph et al, 2008;Anu et al, 2010) (Fig. 3).…”

Section: Glutamate Signalingmentioning

confidence: 99%

“…The activity of mGlu 5 R was increased, which led to stimulation of the activity of PLC coupled with mGlu 5 R via G q protein and to an increase of the content of intracellular inositol 1,4,5-triphosphate receptors interacting with the second messenger phosphatidyl inositol 1,4,5-triphosphate generated by PLC. The increase of activity of NMDA receptors and the mGlu 5 R-associated stimulation of PLC activity mediated Ca 2+ overload in cells causing neuronal cell damage and neurodegeneration in the diabetic brain, affecting as it did the motor learning and memory ability (Anu et al, 2010). In the dorsal horn of the lumbar spinal cord of STZ rats the levels of mRNAs coding several AMPA receptor subunits (GluR1, GluR2, and GluR3), NMDA receptor subunits (NR2A and NR2B), as well as mGlu 1 R and mGlu 5 R were also up regulated (Tomiyama et al, 2005).…”

Section: Fig 3 Signaling Pathways Responsible For Glutamate Toxicitymentioning

confidence: 99%

“…The various neurotransmitter systems, including dopaminergic, serotonergic, cholinergic, glutamatergic, and GABAergic, undergo a significant change in DM (Jackson & Paulose, 1999;Gireesh et al, 2008;Antony et al, 2010a;Anu et al, 2010; T.P. Kumar et al, 2010) (Fig.…”

Section: Neurotransmitter Signaling Systems In the Diabetic Brainmentioning

confidence: 99%

See 3 more Smart Citations

Hormonal Signaling Systems of the Brain in Diabetes Mellitus

Шпаков¹,

Chistyakova²,

Derkach³

et al. 2011

Neurodegenerative Diseases - Processes, Prevention, Protection and Monitoring

View full text Add to dashboard Cite

Section: Fig 3 Signaling Pathways Responsible For Glutamate Toxicitymentioning

confidence: 88%

Section: Glutamate Signalingmentioning

confidence: 99%

Section: Fig 3 Signaling Pathways Responsible For Glutamate Toxicitymentioning

confidence: 99%

Section: Neurotransmitter Signaling Systems In the Diabetic Brainmentioning

confidence: 99%

See 2 more Smart Citations

Hormonal Signaling Systems of the Brain in Diabetes Mellitus

Шпаков¹,

Chistyakova²,

Derkach³

et al. 2011

Neurodegenerative Diseases - Processes, Prevention, Protection and Monitoring

View full text Add to dashboard Cite

“…29 In insulin-induced hypoglycemiant and diabetic rats, an upregulation of mGlu5 receptors leads to increased inositol triphosphate (IP3) content which mediates Ca 2+ overload that causes cell damage and neurodegeneration. 30 However, endogenous activation of mGlu5 receptors is required for optimal insulin response to glucose in mice and is also involved in the correct glucagon response to insulin challenge. 31 Specific agonists for Group I and II mGlu receptors increased the release of insulin in the presence of glucose, whereas Group III agonists inhibited insulin release at high glucose concentrations.…”

Section: Modulation Of Growth Hormone and Prolactin Release By Mglu Rmentioning

confidence: 99%

mGlu receptors in endocrine organs

Durand

Carniglia

Lasaga

2011

WIREs Membr Transp Signal

View full text Add to dashboard Cite

Metabotropic glutamate (mGlu) receptors in the central nervous system are known to be essential for neuroplasticity associated with normal brain functions and are also critically involved in various neurological and psychiatric disorders. A recent surge of publications supports the presence, importance, and functionality of mGlu receptors outside the central nervous system with a unique distribution within various tissues. Group I, II, and III mGlu receptors are found in a wide range of peripheral organs including parts of the peripheral nervous system and nonneural organs such as hypophysis, pancreas, adrenal medulla, and the reproductive system. The distinct distribution of mGlu receptors in peripheral tissues is discussed in terms of possible functional endocrine implications. 

show abstract

Increased neuronal survival in the brainstem during liver injury: Role of γ-aminobutyric acid and serotonin chitosan nanoparticles

Joy

Anitha

Paulose

2013

Journal of Neuroscience Research

View full text Add to dashboard Cite

γ-Aminobutyric acid (GABA)- and serotonin (5-HT)-mediated cell signaling, neuronal survival enhancement, and reduced neuronal death in brainstem during liver injury followed by active liver regeneration have a critical role in maintaining routine bodily functions. In the present study, GABAB and 5-HT2A receptor functional regulation, interrelated actions of neuronal survival factors, and expression of apoptotic factors in the brainstem during GABA and 5-HT chitosan nanoparticles-induced active liver regeneration in partially hepatectomized rats were evaluated. Partially hepatectomized rats were treated with the nanoparticles, and receptor assays and confocal microscopic studies of GABAB and 5-HT2A receptors, gene expression studies of GABAB and 5-HT2A receptors, nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), Akt-1, phospholipase C, Bax, and caspase-8 were performed with the brainstems of experimental animals. A significant decrease in GABAB and 5-HT2A receptor numbers and gene expressions denoted a homeostatic adjustment by the brain to trigger the sympathetic innervations during elevated DNA synthesis in the liver. The neuronal apoptosis resulting from the loss of liver function after partial hepatectomy was minimized by nanoparticle treatment in rats compared with rats with no treatment during regeneration. This was confirmed from the gene expression patterns of NF-κB, TNF-α, Akt-1, phospholipase C, Bax, and caspase-8. The present study revealed the potential of GABA and 5-HT chitosan nanoparticles for increasing neuronal survival in the brainstem during liver injury following regeneration, which avoids many neuropsychiatric problems.

show abstract

Enhanced NMDAR1, NMDA2B and mGlu5 receptors gene expression in the cerebellum of insulin induced hypoglycaemic and streptozotocin induced diabetic rats

Cited by 27 publications

References 63 publications

Hormonal Signaling Systems of the Brain in Diabetes Mellitus

Hormonal Signaling Systems of the Brain in Diabetes Mellitus

mGlu receptors in endocrine organs

Increased neuronal survival in the brainstem during liver injury: Role of γ-aminobutyric acid and serotonin chitosan nanoparticles

Contact Info

Product

Resources

About