Terminal excitability of the corticostriatal pathway. II. Regulation by glutamate receptor stimulation.
The influence of impulse activity and glutamate receptor stimulation on the electrical excitability of the corticostriatal terminal field was explored. Antidromic responses were recorded from prefrontal cortical neurons the electrical stimulation of their terminal field in the contralateral striatum. Terminal excitability was assessed by determining the percentage of subthreshold current stimulus presentations eliciting an antidromic response. Terminal excitability was found to be positively correlated with variations in spontaneous firing rate: increases and decreases in firing rate were accompanied by corresponding changes in the percentage of antidromic responses elicited by a subthreshold stimulus. Drugs were applied to the striatal stimulation site in a volume of 312 nl delivered over 5 min. Striatal administration of either the competitive NMDA antagonist D-alpha-aminoadipate (DAA) or D-2-amino-7-phosphonoheptanoate (AP-7) or the competitive non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3 dione (CNQX) blocked the correlation between excitability and firing rate. Further examination revealed that the terminal field was rendered more excitable for a period of 20-80 ms following the arrival of an action potential. This post-impulse facilitation of terminal excitability was attenuated after local application of AP-7 (10 microM) or CNQX (20 microM). At half these doses, AP-7 or CNQX produced a non-significant effect, however when administered simultaneously a significant attenuation was observed. The participation of interneurons in these excitability effects was ruled out since they were still seen following kainic acid lesions. We propose that this impulse-dependent enhancement in terminal excitability results from the release of glutamate induced by the action potential in the terminal field and the subsequent stimulation of glutamate autoreceptors on the terminals.
Garcia-Munoz
M
M
University of California, School of Medicine, Department of Psychiatry, San Diego, La Jolla 92093.
Young
S J
SJ
Groves
P M
PM
D015763:2-Amino-5-phosphonovalerate / Q000031:analogs & derivatives*; D015074:2-Aminoadipic Acid / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology / Q000502:physiology*; D003342:Corpus Striatum / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004594:Electrophysiology; D005971:Glutamates / Q000378:metabolism; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D009411:Nerve Endings / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D017981:Receptors, Neurotransmitter / Q000502:physiology*
D000596:Amino Acids; D005971:Glutamates; D011810:Quinoxalines; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D015074:2-Aminoadipic Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D015763:2-Amino-5-phosphonovalerate; C031231:2-amino-7-phosphonoheptanoic acid; D007608:Kainic Acid