SLC1 Glutamate Transporters and Diseases: Psychiatric Diseases and Pathological Pain.

SLC1 Glutamate Transporters and Diseases: Psychiatric Diseases and Pathological Pain.

Curr Mol Pharmacol. 2013 Jul 22;
Nakagawa T, Kaneko S

The solute carrier family 1 (SLC1) consists of two neutral amino acid transporters and five high-affinity excitatory amino acid transporters (EAAT1-5). EAATs are expressed in glial cells (EAAT1/GLAST and EAAT2/GLT-1), neurons (EAAT3/EAAC1 and EAAT4), and the retina (EAAT5), where they precisely regulate extracellular glutamate levels at both synaptic and extrasynaptic sites. EAATs play essential roles in the maintenance of normal excitatory synaptic transmission, protection of neurons from the excitotoxic action of excessive glutamate, and regulation of glutamate-mediated neuroplasticity. Therefore, dysfunction of EAATs can cause abnormal excitatory synaptic transmission, neuronal excitotoxicity, and the exaggeration of neuroplasticity-based events. EAAT dysfunction has been implicated in a variety of neurodegenerative and neurological diseases, including amyotrophic lateral sclerosis, Parkinson disease, Alzheimer disease, ischemia, and epilepsy. Recent evidence suggests that abnormalities of EAATs contribute to the pathogenesis of psychiatric diseases and pathological pain. The present review will briefly discuss novel findings on the roles of EAATs in the pathogenesis of psychiatric diseases such as schizophrenia, mood disorders, and drug dependence/addiction, and pathological pain, as well as the potential of EAATs as therapeutic targets. HubMed – addiction

Quality of Life Determinants in Patients of a Psychosocial Care Center for Alcohol and other Drug Users.

Issues Ment Health Nurs. 2013 Jul; 34(7): 524-30
Marini M, Schnornberger TM, Brandalise GB, Bergozza M, Heldt E

Quality of life assessments in patients receiving treatment for substance dependence can serve as one predictor of response to treatment. This study aimed to identify determinants of quality of life in patients of a Psychosocial Care Center for alcohol and other drug users (CAPSad). The sample consisted of 77 patients with a diagnosis of substance dependence being treated at CAPSad for more than six months. Severity of substance dependence was assessed using the Addiction Severity Index (ASI-6), quality of life was assessed using the World Health Organization Quality of Life assessment instrument-short version (WHOQOL-BREF), and depressive symptoms were assessed by the Beck Depression Inventory (BDI). Data on CAPSad activities, psychiatric diagnoses, and medications used were collected from the medical records. Quality of life was significantly impaired in more severe cases of substance dependence and in those with more severe depressive symptoms. As for other variables, poorer quality of life was significantly associated with a greater number of years of education, unemployment, use of medications, and greater use of individual sessions with the reference professional. Linear regression analysis revealed depressive symptom severity to be an independent determinant of quality of life impairment, accounting for over 50% of the variation in physical and psychological domains. These results demonstrate the need to consider other factors, such as depressive symptoms and quality of life, in the treatment of substance dependence. HubMed – addiction

Membrane potential and ph-dependent accumulation of decynium-22 (1,1′-diethyl-2,2′-cyanine lodide) flourencence through oct transporters in astrocytes.

Bol Asoc Med P R. 2010 Jul-Sep; 102(3): 5-12
Mikhail I, Yuri K, Lilia K, Priscilla S, Jiménez-Rivera C

1,1 ‘-Diethyl-2,2’-cyanine iodide (decynium22; D22) is a potent blocker of the organic cation family of transporters (EMT/OCT) known to move endogenous monoamines like dopamine and norepinephrine across cell membranes. Decynium22 is a cation with a relatively high affinity for all members of the OCT family in both human and rat cells. The mechanism through which decynium22 blocks OCT transporters are poorly understood. We tested the hypothesis that denynium22 may compete with monoamines utilizing OCT to permeate the cells. Using the ability of D22 to aggregate and produce fluorescence at 570 nm, we measured D22 uptake in cultured astrocytes. The rate of D22 uptake was strongly depressed by acid pH and by elevated external K+. The rate of uptake was similar to that displayed by 4-(4-(dimethylamino)-styryl)-N-methylpyridinium (ASP+), a well established substrate for OCT and high-affinity Na+-dependent monoamine transporters. These data were supported by measurement of electrogenic uptake using whole cell voltage clamp recording. Decynium22 depressed norepinephrine, but not glutamate uptake. These data are also consistent with the described OCT transporter characteristics. Taken together, our results suggest that decynium22 accumulation might be a useful instrument to study monoamine transport in the brain, and particularly in astrocytes, where they may play a prominent role in monoamine uptake during brain dysfunction related to monoamines (like Parkinson disease) and drug addiction. HubMed – addiction

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