Masking effect of NMDA receptor antagonists on the formation of long-term potentiation (LTP) in superior colliculus slices from the guinea pig.
After electrical stimulation of the optic layer (OL) of superior colliculus (SC) slices, the postsynaptic potential (PSP) was recorded in the superficial gray layer (SGL) of the SC. The degeneration studies of retinotectal or corticotectal inputs to the SGL of the SC indicated that this PSP evoked in the SGL of the SC slices was retinotectal in origin. Neurotransmission in this pathway may be mediated by glutamate, because the PSP amplitude was reduced and blocked by application of kynurenate or quinoxaline dione (DNQX) to the medium. Furthermore, the concentration of glutamate in the right SGL was significantly reduced by 32% after left optic denervation and by 30% after ablation of the right visual cortex, compared with that in the left SGL. Long-term potentiation (LTP) in the SGL was induced by tetanic stimulation (50 Hz, 20 s) to the OL. The LTP formation was facilitated by the removal of Mg2+ from the medium. The effects of glutamate antagonists D-amino-5-phosphonovalerate (D-APV), gamma-D-glutamylglycine (gamma-DGG), and (+)-5-methyl-10,11-dihydro-5H-dibenzo, a,d-cycloheptene-5,10-imine maleate (MK-801) on the induction of LTP were investigated. D-APV (100 microM) or gamma-DGG (1 mM) masked the expression of LTP by tetanic stimulation, however LTP was induced after removal of the agents. LTP formation was observed without further tetanic stimulation following the removal of D-APV from the medium even 80 min after the tetanic stimulation. LTP once formed was not influenced by application of D-APV.(ABSTRACT TRUNCATED AT 250 WORDS)
Miyamoto
T
T
Department of Physiology, School of Medicine, Kobe University, Japan.
Sakurai
T
T
Okada
Y
Y
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D003714:Denervation; D003986:Dibenzocycloheptenes / Q000494:pharmacology; D004151:Dipeptides / Q000494:pharmacology; D016291:Dizocilpine Maleate; D005071:Evoked Potentials / Q000187:drug effects; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D066298:In Vitro Techniques; D007736:Kynurenic Acid / Q000494:pharmacology*; D008274:Magnesium / Q000494:pharmacology; D051379:Mice; D009410:Nerve Degeneration; D009900:Optic Nerve / Q000502:physiology; D011810:Quinoxalines / Q000494:pharmacology*; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects* / Q000502:physiology; D013477:Superior Colliculi / Q000187:drug effects / Q000502:physiology*; D014793:Visual Cortex / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D003986:Dibenzocycloheptenes; D004151:Dipeptides; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D011810:Quinoxalines; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; C028929:gamma-glutamylglycine; D001224:Aspartic Acid; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; C056723:FG 9041; D016291:Dizocilpine Maleate; D015763:2-Amino-5-phosphonovalerate; D007736:Kynurenic Acid; D008274:Magnesium