In the retina, the glutamate transporter GLAST is expressed in Müller cells, whereas the glutamate transporter GLT-1 is found only in cones and various types of bipolar cells. To investigate the functional role of this differential distribution of glutamate transporters, we have analyzed GLAST and GLT-1 mutant mice. In GLAST-deficient mice, the electroretinogram b-wave and oscillatory potentials are reduced and retinal damage after ischemia is exacerbated, whereas GLT-1-deficient mice show almost normal electroretinograms and mild increased retinal damage after ischemia. These results demonstrate that GLAST is required for normal signal transmission between photoreceptors and bipolar cells and that both GLAST and GLT-1 play a neuroprotective role during ischemia in the retina.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC22547 | PMC |
| http://dx.doi.org/10.1073/pnas.95.8.4663 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dopamine loss alters glutamate synapses and transporters in the medial prefrontal cortex and anxiety-related behaviour in a male MPTP rodent model of Parkinson's disease.
Eur J Neurosci
November 2024
VA Medical Center/Portland, Portland, Oregon, USA.
Anxiety is a prominent non-motor symptom of Parkinson's disease (PD). Changes in the B-spectrum recordings in PD patients of the prefrontal cortex correlate with increased anxiety. Using a rodent model of PD, we reported alterations in glutamate synapses in the striatum and substantia nigra following dopamine (DA) loss.
View Article and Find Full Text PDFPositive allosteric modulation of glutamate transporter reduces cocaine-induced locomotion and expression of cocaine conditioned place preference in rats.
Eur J Pharmacol
December 2024
Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 191022, USA. Electronic address:
The glutamatergic system, located throughout the brain including the prefrontal cortex and nucleus accumbens, plays a critical role in reward and reinforcement processing, and mediates the psychotropic effects of addictive drugs such as cocaine. Glutamate transporters, including EAAT2/GLT-1, are responsible for removing glutamate from the synaptic cleft. Reduced expression of GLT-1 following chronic cocaine use and abstinence has been reported.
View Article and Find Full Text PDFGlutamate, the primary excitatory neurotransmitter in the CNS, is regulated by the excitatory amino acid transporters (EAATs) GLT-1 and GLAST. Following traumatic brain injury (TBI), extracellular glutamate levels increase, contributing to excitotoxicity, circuit dysfunction, and morbidity. Increased neuronal glutamate release and compromised astrocyte-mediated uptake contribute to elevated glutamate, but the mechanistic and spatiotemporal underpinnings of these changes are not well established.
View Article and Find Full Text PDFExogenous leptin alleviates glutamate-excitotoxic injury caused by cerebral ischemia-reperfusion in mice by affecting the expression of glutamate transporters.
Brain Res
December 2024
Department of Pathophysiology, Bengbu Medical University, Bengbu Anhui 233030, China; Basic and Clinical Key Laboratory of Cardiovascular and Cerebrovascular Diseases of Bengbu Medical University, Bengbu Anhui 233030, China. Electronic address:
Article Synopsis
- * This study investigates the effects of different doses of leptin on cerebral ischemia-reperfusion injury in mice, assessing its neuroprotective capabilities after a simulated stroke event.
- * Results indicated that leptin treatment improved neurological function, reduced brain damage, and altered the expression of certain proteins and glutamate levels, suggesting that leptin may protect the brain by mitigating excitotoxicity from excess glutamate.
NRICM101 prevents kainic acid-induced seizures in rats by modulating neuroinflammation and the glutamatergic system.
Int Immunopharmacol
October 2024
School of Medicine, Fu Jen Catholic University, New Taipei City 24205, Taiwan; Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan City 33303, Taiwan. Electronic address:
Article Synopsis
- The study investigates the effects of the Traditional Chinese medicine formula NRICM101 on epilepsy, specifically its ability to reduce seizures induced by kainic acid (KA) in rats.
- NRICM101 significantly decreases seizure behavior, neuronal loss, and glutamate levels while enhancing protective proteins in the brain, and its effects are comparable to the established antiseizure drug carbamazepine.
- The formula also shows promising neuroprotective effects by mitigating inflammation and cell death in the brain without causing harm to the liver or kidneys, suggesting its potential for managing epilepsy.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!