Following acquisition of conditioned inhibition (CI) of the nictitating membrane, response, rabbits received radio-frequency lesions of the mesencephalon. The reinforced conditioned stimulus (CS) was light onset and the nonreinforced CS was the same light compounded with a tone. The unconditioned stimulus was electric shock to the paraorbital region of the eye. In accord by an earlier study by Mis , lesions disrupted conditioned inhibition by reducing the capacity to suppress conditioned responses on nonreinforced trials; conditioned responding on reinforced trials was unaffected. Lesions of the pretectum in the region of the posterior commissure and of the periaqueductal grey produced the greatest disruption CI, and fiber degeneration from these regions, as assessed by the Fink-Heimer method, projecting in a ventro-anterior direction to the posterior hypothalamus was implicated in CI disruption. This observation, together with indirect evidence that the dorsal noradrenergic bundle is involved in CI, suggested that conditioned inhibitors may act via a brainstem-hypothalamus reward system to antagonize the motivational support of the conditioned response. © 1980, All rights reserved.
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