The release of endogenous amino acids from the rat visual cortex.
The release of endogenous taurine, GABA, glycine, aspartate, glutamate, glutamine and alanine from the rat visual cortex was measured using a cortical cup technique. The electrocorticogram (ECoG) was monitored throughout most experiments. 2. Spreading depression, evoked by the dropwise placement of 10% KCl solution on to the brain outside the cup was associated with a significant increase in the release of GABA and glutamine but a marked fall in that of glutamate. The evoked release of GABA and glutamate but not of glutamine was Ca2+ dependent. 3. A solution containing 50 mM-K+ placed within the cup elicited a significant increase in the release of taurine and GABA, whereas 100 mM-K+ additionally released aspartate and glutamate. The K+-evoked release of these amino acids with the exceptions of taurine and glutamine was Ca2+-dependent. 4. Three series of experiments were carried out in which the preparations were stimulated electrically. Bipolar stimulation (100 Hz, 1 msec pulse width, 2-5 mA for 5 min) with the electrode within the cup was followed by significant increases in taurine, GABA and glutamate release; using a 5 mA current, there was an additional release of aspartate and alanine. Only the evoked release of GABA and glutamate was Ca2+ dependent. 5. In the second and third series of experiments, the electrode was sited adjacent to the cup or on the contralateral cortex respectively. Following stimulation (100 Hz, 1 msec pulse width, 2-5 mA for 5 min) there was a significant increase in taurine and GABA release and a significant fall in the release of aspartate and glutamate. With the exception of taurine, these changes in release were Ca2+ dependent. Reducing the stimulus current to 1-5 mA or the period of stimulation to 2-5 min initiated similar but statistically insignificant changes in release. A range (10-100 Hz) of stimulation frequencies was examined: the evoked release of GABA was linearly related to frequency whereas that of taurine was frequency-independent. The fall in aspartate and glutamate release was maximal at a frequency of about 50 Hz. 6. The results are discussed in relation to (a) the possible sites of release of the amino acids and (b) the proposed neurotransmitter roles of the physiologically active amino acids.
D000409:Alanine / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D013181:Cortical Spreading Depression; D004558:Electric Stimulation; D005971:Glutamates / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D008297:Male; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D013268:Stimulation, Chemical; D009435:Synaptic Transmission; D013654:Taurine / Q000378:metabolism; D014793:Visual Cortex / Q000187:drug effects / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000596:Amino Acids; D005971:Glutamates; D005973:Glutamine; D013654:Taurine; D001224:Aspartic Acid; D005680:gamma-Aminobutyric Acid; D000409:Alanine; D011188:Potassium; D005998:Glycine