Glutamate-dependent long-term presynaptic changes in corticostriatal excitability.
We have previously shown that brief high frequency stimulation of the anteromedial prefrontal cortex induces a long-term decrease in excitability of the glutamatergic corticostriatal terminal field. In contrast, a long-term increase in presynaptic corticostriatal excitability may be induced by presenting two brief cortical tetanizing stimuli separated by 2-3 min such that the second tetanus coincides with a period of increased excitability elicited by the first. In the present study, we examined the glutamate receptor subtypes involved in these long-term changes in presynaptic excitability. A specific glutamate receptor antagonist was infused into the rat striatum 10-25 min prior to either a single or double cortical tetanic stimulation. To eliminate the participation of intrinsic striatal cells, a subset of animals received a striatal kainic acid lesion eight to 20 days before the recording experiment. Antagonists of the N-methyl-D-aspartate and metabotropic glutamate receptor subtypes were effective in blocking the decrease in excitability induced by single cortical tetanic stimulation whereas an antagonist of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainate receptor did not prevent the induction of a long-term reduction in excitability. In contrast, each of these antagonists prevented the induction of a long-term increase in excitability. These long-term modifications in excitability of the presynaptic glutamate axon terminals appear to be induced by similar mechanisms to those postulated to operate in long-term potentiation and depression. These enduring changes in presynaptic excitability are likely to represent important mechanisms for the selective modification of information processing in the striatum.
Garcia-Munoz
M
M
Department of Psychiatry, University of California San Diego, La Jolla 92093-0603, USA.
Patino
P
P
Masliah
E
E
Young
S J
SJ
Groves
P M
PM
D000200:Action Potentials / Q000502:physiology; D000613:Aminobutyrates / Q000633:toxicity; D000818:Animals; D002540:Cerebral Cortex / Q000201:enzymology / Q000502:physiology*; D004558:Electric Stimulation; D004789:Enzyme Activation / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005110:Extracellular Space / Q000502:physiology; D007608:Kainic Acid / Q000633:toxicity; D017774:Long-Term Potentiation / Q000502:physiology; D008297:Male; D018613:Microscopy, Confocal; D017072:Neostriatum / Q000201:enzymology / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017470:Receptors, Glutamate / Q000502:physiology*; D017661:Receptors, Presynaptic / Q000378:metabolism / Q000502:physiology*
D000613:Aminobutyrates; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D017470:Receptors, Glutamate; D017661:Receptors, Presynaptic; D011494:Protein Kinases; C012729:2-amino-4-phosphonobutyric acid; D007608:Kainic Acid