Glucose-deprivation-induced [3H]D-aspartate release from isolated bovine and human retinae.
The glucose deprivation-induced release of [3H]D-aspartate was studied in bovine and human retinas in a superfusion apparatus. [3H]D-aspartate release was significantly increased upon omitting glucose in the superfusion buffer. This effect was dependent on external Ca2+ because L- and N-type Ca2+-channel blockers, such as diltiazem (1 microM), nitrendipine (1 microM), and omega-conotoxin (100 nM), significantly reduced the effect of glucose-deprivation induced release of [3H]D-aspartate. Furthermore, while glutamate receptor agonists (L-glutamate, N-methyl-D-aspartate, but not kainate) potentiated the effects of glucose deprivation, antagonists (MK-801, MCPG, ifenprodil, and L-AP3) at these receptors blocked the glucose deprivation-induced release process. Taken together, these studies have demonstrated that under conditions of glucose deprivation, as may happen during ischemic events in vivo, the retinal glutamatergic nerve endings and/or glial cells promote the efflux of [3H]D-aspartate into the extracellular environment. This process appears to be receptor-mediated and dependent on extracellular Ca2+ and is similar to previous reports pertaining to brain tissues.
Ohia
Sunny E
SE
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA. seohia@uh.edu
Awe
S Olubusayo
SO
Opere
Catherine A
CA
LeDay
Angela M
AM
Harris
Lydia C
LC
Kulkarni
Kaustubh
K
Sharif
Najam A
NA
D000409:Alanine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D001645:Biguanides / Q000008:administration & dosage; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002417:Cattle; D026603:D-Aspartic Acid / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000378:metabolism*; D004110:Diltiazem / Q000494:pharmacology; D016291:Dizocilpine Maleate / Q000494:pharmacology; D004357:Drug Synergism; D005947:Glucose / Q000037:antagonists & inhibitors / Q000172:deficiency* / Q000494:pharmacology*; D018698:Glutamic Acid / Q000494:pharmacology; D005998:Glycine / Q000008:administration & dosage / Q000031:analogs & derivatives*; D006801:Humans; D007608:Kainic Acid / Q000008:administration & dosage; D016202:N-Methylaspartate / Q000494:pharmacology; D009568:Nitrendipine / Q000494:pharmacology; D010477:Perfusion / Q000379:methods; D010880:Piperidines / Q000008:administration & dosage; D011073:Polyamines / Q000037:antagonists & inhibitors / Q000494:pharmacology; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism; D012160:Retina / Q000187:drug effects* / Q000378:metabolism*; D014316:Tritium / Q000737:chemistry / Q000378:metabolism; D014700:Verapamil / Q000494:pharmacology; D020960:omega-Conotoxins / Q000494:pharmacology
D001645:Biguanides; D002121:Calcium Channel Blockers; D010880:Piperidines; D011073:Polyamines; D017470:Receptors, Glutamate; C474696:methyl-(4-carboxyphenyl)glycine; D020960:omega-Conotoxins; C000211:2-amino-3-phosphonopropionic acid; D014316:Tritium; D018698:Glutamic Acid; D026603:D-Aspartic Acid; C006624:arcaine; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate; D009568:Nitrendipine; D014700:Verapamil; D004110:Diltiazem; D005947:Glucose; D000409:Alanine; C010739:ifenprodil; D007608:Kainic Acid; D005998:Glycine