Neurotransmitter receptors mediating excitatory input to cells in the cat lateral geniculate nucleus. II. Nonlagged cells.
1. We studied the type of receptor for excitatory amino acids (EAA) that mediates visual responses of nonlagged cells in the dorsal lateral geniculate nucleus (LGN) by recording the visual response of single cells to a stationary flashing spot before, during, and after iontophoretical application of antagonists and agonists to EAA receptors. 2. The visual response of the nonlagged cells was strongly suppressed, in a dose-dependent manner, by the specific quisqualate/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX). The average degree of suppression was 74%. Quisqualate enhanced the visual response. 3. Specific antagonists to the N-methyl-D-aspartate (NMDA) receptor had a weak suppressing effect on most nonlagged cells. The average degree of suppression was 22%. Measurement of such weak effects was complicated by the considerable spontaneous fluctuations of responsivity in the LGN cells. In the majority of cells where the visual response was suppressed by NMDA antagonists, the tonic response component was more strongly suppressed than the initial transient response component. The visual response was enhanced by NMDA, and this enhancement was antagonized by NMDA antagonists. 4. These findings suggest that the excitatory input from the retina to nonlagged LGN cells is mainly mediated by non-NMDA receptors. The non-NMDA receptors mediate fast EPSPs, and this can explain the fast onset and offset of the visual response of the nonlagged cells. 5. The generally small contribution from NMDA receptors to the visual response of the nonlagged cells might reflect a minor involvement of these receptors in the retinal input, or it could be related to the excitatory input to LGN from the visual cortex. 6. To study whether the expression of NMDA receptors was related to modulatory brain stem input to LGN, we examined the effects of the NMDA antagonists when the visual response was enhanced with gamma-aminobutyric acid (GABA) antagonists or acetylcholine (ACh). Neither of these pharmacologic manipulations consistently increased the relative contribution of NMDA receptors to the visual response. 7. No pharmacologic difference was found between nonlagged X- and Y-cells, or between ON- and OFF-center cells.(ABSTRACT TRUNCATED AT 400 WORDS)
Hartveit
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Institute of Neurophysiology, University of Oslo, Norway.
Heggelund
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D000344:Afferent Pathways / Q000502:physiology; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D002415:Cats; D005829:Geniculate Bodies / Q000166:cytology / Q000502:physiology*; D007608:Kainic Acid / Q000378:metabolism; D009474:Neurons / Q000502:physiology*; D010277:Parasympathomimetics / Q000494:pharmacology; D018091:Receptors, AMPA; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface / Q000502:physiology*; D018092:Kainic Acid Receptors; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D000596:Amino Acids; D007608:Kainic Acid; D010277:Parasympathomimetics; D018091:Receptors, AMPA; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface; D018092:Kainic Acid Receptors; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D005680:gamma-Aminobutyric Acid