caa a22 4500 465738230 CHVBK 20180323111801.0 cr unu---uuuuu 170327e19900801xx s 000 0 eng 10.1007/BF02244222 doi (NATIONALLICENCE)springer-10.1007/BF02244222 A possible role of AA2 excitatory amino acid receptors in the expression of stimulant drug effects [Elektronische Daten] [William Freed, H. Cannon-Spoor] GDEE, an antagonist of the AA2 or quisqualic acid category of excitatory amino acid receptor, decreases behavioral activity and locomotor stimulation induced by cocaine and amphetamine when locally injected into the nucleus accumbens. The present experiment was intended to examine the effects of systemic GDEE and other excitatory amino acid antagonists on stimulant-induced locomotor activity. GDEE markedly attenuated the stimulant effect of amphetamine, and partially blocked the effects of phencyclidine (PCP). Apomorphine-induced cage climbing behavior was partially decreased by lower dosages of GDEE, but was almost completely blocked by the highest dosage tested. Amphetamine-induced stimulation of locomotor activity was not decreased by any of the other excitatory amino acid antagonists that were tested, including MK-801, 2-amino-7-phosphonophetanoic acid (APH), or CNQX. APH decreased stereotypy only at a high dosage (250 mg/kg), which also produces ataxia. Several other compounds, includingl-glutamic acid gamma ethyl ester (GMEE),l-glutamic acid, glycine, andl-glutamine did not block amphetamine-induced stimulation in molar dosages equivalent to the highest dosage of GDEE (8 mmol/kg). It is concluded that the AA2 excitatory amino acid receptor is important in the expression of activating effects of stimulant drugs. Springer-Verlag, 1990 Glutamic acid diethyl ester nationallicence Excitatory amino acids nationallicence Stimulants nationallicence Amphetamine nationallicence Phencyclidine nationallicence Freed William Preclinical Neurosciences Section, Neuropsychiatry Branch, NIMH Neuroscience Center at Saint Elizabeths, 2700 Martin Luther King Jr. Avenue, 20032, Washington DC, USA aut Cannon-Spoor H. Preclinical Neurosciences Section, Neuropsychiatry Branch, NIMH Neuroscience Center at Saint Elizabeths, 2700 Martin Luther King Jr. Avenue, 20032, Washington DC, USA aut Psychopharmacology Springer-Verlag 101/4(1990-08-01), 456-464 0033-3158 101:4<456 1990 101 213 https://doi.org/10.1007/BF02244222 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02244222 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Freed William Preclinical Neurosciences Section, Neuropsychiatry Branch, NIMH Neuroscience Center at Saint Elizabeths, 2700 Martin Luther King Jr. Avenue, 20032, Washington DC, USA aut NATIONALLICENCE 700 1- Cannon-Spoor H. Preclinical Neurosciences Section, Neuropsychiatry Branch, NIMH Neuroscience Center at Saint Elizabeths, 2700 Martin Luther King Jr. Avenue, 20032, Washington DC, USA aut NATIONALLICENCE 773 0- Psychopharmacology Springer-Verlag 101/4(1990-08-01), 456-464 0033-3158 101:4<456 1990 101 213 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer