Showing papers in "Neurochemistry International in 2008"

TL;DR: Astrocytes can release the excitatory transmitter glutamate which is capable of modulating activity in nearby neurons as mentioned in this paper, and this glutamate release can occur through six known mechanisms: reversal of uptake by glutamate transporters, anion channel opening induced by cell swelling, Ca2+-dependent exocytosis, glutamate exchange via the cystine-glutamate antiporter, release through ionotropic purinergic receptors and functional unpaired connexons, "hemichannels", on the cell surface.

TL;DR: A dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression and atherosclerosis.

TL;DR: Possible physiological functions of H2S include potentiating long-term potentials through activation of the NMDA receptors, regulating the redox status, maintaining the excitatory/inhibitory balance in neurotransmission, and inhibiting oxidative damage through scavenging free radicals and reactive species.

TL;DR: A review of recently published data underscores the growing importance of calcium ions in AD development and focuses on the relevant aspects of calcium homeostasis.

TL;DR: It is demonstrated for the first time that endotoxemia leads to inflammation in brain, with alteration in blood-brain barrier, up-regulation of AQP4 and associated edema, neutrophil infiltration, astrocytosis, as well as apoptotic cellular death, all of which appear to be mediated by TNF-alpha signaling through TNFR1.

TL;DR: Although it is difficult to extrapolate the findings to the human condition, the inhibition of mitochondrial respiratory chain by chronic stress may be one mechanism in the pathophysiology of depressive disorders.

TL;DR: Apigenin inhibited the production of nitric oxide and prostaglandin E(2) by suppressing the expression of inducible Nitric oxide synthase and cyclooxygenase-2 protein, respectively and was found to protect neuronal cells from injury in middle cerebral artery occlusion.

TL;DR: The article commences with an overview of how extrinsic factors modelling the brain at work: neurotransmitters, depolarising stimuli (potassium and voltage changes) and cyclic nucleotides as major signal transducing vehicles affect pH in the CNS.

TL;DR: Recent in vitro and in vivo experimental evidence relating to the amyloid cascade hypothesis and the cholinergic hypothesis of AD are surveyed, with particular attention to Bidirectional pathways linking them as regards theCholinergic neurotoxicity of Abeta and the regulatory mechanisms of Cholinergic receptor activation or enzyme inhibition in the processing of the ameloid precursor protein.

TL;DR: New studies indicate that endogenous extracellular adenosine is originated as a consequence of the release of gliotransmitters, namely ATP, which sets a global inhibitory tonus in brain circuits rather than in a single synapse.

TL;DR: It is proposed that aging causes brain mitochondrial complex I dysfunction which can be attributed to ROS-induced cardiolipin oxidation, and this finding may prove useful in elucidating the mechanism underlying mitochondrial dysfunction associated with brain aging.

TL;DR: Graft of adult mesemchymal stem cells reduces behavioral effects induced by 6-hydroxydopamine lesion and partially restores the dopaminergic markers and vesicular striatal pool of dopamine in Parkinson's disease.

TL;DR: Sal B is a better aggregation inhibitor than ferulic acid but less active than curcumin in the inhibition of Aβ1–40 aggregation, and has therapeutic potential in the treatment of AD, and warrants its study in animal models.

TL;DR: Recent progress in identifying the neurosteroid binding site on the GABA(A) receptor is reviewed, and how these discoveries will impact on understanding of the role of neurosteroids in health and disease is discussed.

TL;DR: It is hypothesized that alterations in the ratio of excitatory and inhibitory urothelial transmitters promote bladder hyperactivity in rat bladders following SCI that can be reversed, to a large extent, by treatment with BoNT-A.

TL;DR: This review of currently used experimental models of epilepsy in immature rats discusses more thoroughly seizure-induced acute and sub-acute cellular and molecular alterations, highlight the contribution of inflammatory-like reactions and intracellular cytoskeleton to the insult, and reveal changes in the structure and function of inhibitory GABA(A) and excitatory glutamate receptors.

TL;DR: It is demonstrated that the LC-MS/MS method allows the assessment of neuroactive steroids in the nervous system with high sensitivity and specificity and that diabetes strongly affects their levels, providing a further basis for new therapeutic tools based on neuro active steroids aimed at counteracting diabetic neuropathy.

TL;DR: It is suggested that acute treatment with caffeine improves recognition memory, and this effect may be related to an increase of the BDNF and TrkB immunocontent in the hippocampus.

TL;DR: Although available direct analytical methods have failed to detect levels of PREGS above 0.1-0.3 ng/g in brain tissue, it may be premature to completely exclude the local formation of biologically active PREGS within specific and limited compartments of the nervous system.

TL;DR: Impairment of the GPx (including glutathione)-mediated antioxidant system contributed to epileptogenesis in GEPR-9s, suggesting that mobilization of astroglial cells for synthesis of GPx protein is a response to KA insult, intended to decrease the neurotoxicity induced by peroxides.

TL;DR: The synthesis of astrocytic BDNF stimulated by noradrenergic neuronal activity is an adaptable process using multiple types (α 1 and β 1 /β 2 ) of adrenergic receptor activation.

TL;DR: Baicalin statistically blunted most of the effects induced by ischemia/reperfusion and was also found to be equally effective as EGCG to act as an antioxidant in the lipid peroxidation studies.

TL;DR: It was observed that lipid peroxidation started to increase and catalase, glutathione reductase, glucose-6-phosphate dehydrogenase enzyme activities and glutATHione levels started to decrease as amyotrophic lateral sclerosis progressed from 6 to 24 months, suggesting a correlation between these parameters and duration of amyotroph lateral sclerosis.

TL;DR: Findings show that endocannabinoid levels change in a disease phase- and region-specific way in the brain of R6/2 mice and indicate that an impaired endoc cannabinoidoid system is a hallmark of symptomatic HD, thus suggesting that drugs inhibiting endOCannabinoid degradation might be used to treat this disease.

TL;DR: This short commentary contrasts the principal molecular and functional components of the cholinergic signaling pathway with those of ATP and other nucleotides, highlighting pathways of their discovery and analyses tissue distribution, synthesis, uptake, vesicular storage, receptors, release, extracellular hydrolysis as well as pathophysiological significance.

TL;DR: There is substantial evidence confirming that expression of genes coding for key astrocytic and neuronal proteins are altered in HE, and findings consistent with the involvement of NS are summarized.

TL;DR: Analysis of major pre- and post-mortem variables showed that none were confounding for these between-group experimental comparisons, and known regulators of one of the key kynurenine-producing enzymes, tryptophan 2,3-dioxygenase (TDO2), were investigated.

TL;DR: It is demonstrated that neurochemical mechanisms underlying the pathophysiology of BPSD are both BPSd-specific and disease-specific which might have implications for future development of new and more selective pharmacological treatments of B PSD.

TL;DR: It is suggested that autonomic neural control of immune, epithelial and endothelial cells also involves non-synaptic transmission in autonomic neuroeffector junctions.

TL;DR: Observations demonstrate that LPA1 mediates LPA-induced stimulation of cell proliferation but not inhibition of glutamate uptake in astrocytes, demonstrating the role of LPA receptor subtypes in cortical astroCyte functions.