Examination of the effects of cholecystokinin 26-33 and neuropeptide Y on responses of visual cortical neurons of the cat.
Extracellular recordings were made from 160 neurons in area 17 (n = 120) and area 18 (n = 40) of the visual cortex of anesthetized cats. Cells were classified according to their receptive field properties and their intracortical positions were evaluated histologically. Cholecystokinin 26-33, antagonists, (cholecystokinin 27-32, cholecystokinin 27-33 and proglumide), amino acids, neuropeptide Y and solvent vehicle (control), were administered to cells by microiontophoresis (cholecystokinin and neuropeptide Y) or by pressure (neuropeptide Y). The results of the tests with cholecystokinin 26-33 fell into four categories: enhancement (31%), suppression (24%), mixed, i.e. either biphasic responses or dose-related alterations in the direction of effect (20%), and no effect (25%). Enhancements of the visually elicited response were more prevalent in simple (43%) and unimodal/movement-sensitive (34%) cells than in complex (7%) cells. The converse was true for suppressions: 19% of simple cells, 24% of unimodal/movement-sensitive cells, and 31% of complex cells were suppressed. Thirty per cent of the unaffected cells were complex or unimodal/movement-sensitive; only 14% were simple. Cells in layers II-IV were more likely to have firing enhanced than suppressed by cholecystokinin 26-33. The converse was true for cells in layers V and VI, where 50% of responses were suppressed and only 22% were enhanced. Unaffected cells were found predominantly in layer III of areas 17, and the lower part of layer III and layer IV of area 18. Cholecystokinin 26-33 sometimes exerted delayed, response-suppressant effects; it also occasionally elevated responsiveness preferentially within the upper ranges (10-20 degrees/s) of velocity tuning curves. Cholecystokinin 26-33 altered the response-suppressant action of GABA in 11 of 19 visually sensitive cells. The peptide potentiated the visual responsiveness in half of the cells where cholecystokinin 26-33 diminished the GABA-induced suppressions (n = 8). The presumed antagonists either exerted no effect on firing or on cholecystokinin 26-33-induced effects, or had cholecystokinin 26-33-like actions themselves. There was a reversible partial antagonism of the effects of cholecystokinin 26-33 on only two of 11 cells tested. Neuropeptide Y injected by pressure or administered iontophoretically had variable and inconsistent effects on the visually evoked responses of 29 additional neurons from those described above. These effects were indistinguishable from those of the vehicle whether spontaneous activity, magnitude of the visually elicited response, spatial integrity of the RF substructure, orientation or velocity tuning was assessed.(ABSTRACT TRUNCATED AT 400 WORDS)
Hicks
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Department of Biology, College of Arts and Sciences, University of North Carolina, Greensboro 27412-5001.
Albus
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Kaneko
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Baumfalk
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D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D002415:Cats; D002766:Cholecystokinin / Q000494:pharmacology*; D005074:Evoked Potentials, Visual / Q000187:drug effects; D007478:Iontophoresis; D009431:Neural Conduction / Q000187:drug effects; D009474:Neurons / Q000187:drug effects*; D009478:Neuropeptide Y / Q000494:pharmacology*; D010775:Photic Stimulation; D011377:Proglumide / Q000494:pharmacology; D012844:Sincalide / Q000031:analogs & derivatives* / Q000494:pharmacology; D013618:Tachyphylaxis / Q000502:physiology; D014793:Visual Cortex / Q000166:cytology / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D009478:Neuropeptide Y; D005680:gamma-Aminobutyric Acid; C044201:cholecystokinin (26-33); D002766:Cholecystokinin; D011377:Proglumide; D001418:Baclofen; D012844:Sincalide