Inhibitory conditioning is a central component of theoretical models of associative learning but its neural basis has not been fully elucidated. Conditioned inhibition is generally thought to be due to the development of an association between a conditioned stimulus (CS) and the omission of an unconditioned stimulus (US). The proposed project will initiate a research program to examine the neural mechanisms of inhibitory classical conditioning. The eyeblink conditioning preparation will be used in these experiments in order to compare the neural mechanisms of inhibitory conditioning with the previously identified neural mechanisms of excitatory conditioning. The experiments of Specific Aim 1 will investigate the role of the cerebellar cortex in conditioned inhibition using excitotoxic lesions, unit recording, and reversible inactivation. In the experiments of Specific Aim 2, pharmacological inactivation will be used to assess the roles of several possible sites within the neural circuitry underlying the acquisition and expression of excitatory eyeblink conditioning in the acquisition of conditioned inhibition. The experiments of Specific Aim 3 will determine whether conditioned inhibition involves neural systems that are distinct from the neural systems that mediate excitatory conditioning. The fundamental importance of inhibitory learning underscores the need to study its neural mechanisms. The proposed research project will provide important initial steps toward determining the neural mechanisms of inhibitory classical conditioning. A successful analysis of the neural mechanisms of inhibitory classical conditioning may lead to the application of this experimental approach to the study of excitatory and inhibitory processes that occur in other learning situations. The results of these studies may also lead to a better understanding of the functional pathology associated with various psychiatric disorders that involve deficits in behavioral inhibition.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Project (R01)
Project #
5R01MH065483-03
Application #
6817534
Study Section
Special Emphasis Panel (ZRG1-BBBP-1 (01))
Program Officer
Anderson, Kathleen C
Project Start
2002-12-01
Project End
2007-11-30
Budget Start
2004-12-01
Budget End
2005-11-30
Support Year
3
Fiscal Year
2005
Total Cost
$147,500
Indirect Cost
Name
University of Iowa
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
062761671
City
Iowa City
State
IA
Country
United States
Zip Code
52242
Campolattaro, Matthew M; Schnitker, Kathleen M; Freeman, John H (2008) Changes in inhibition during differential eyeblink conditioning with increased training. Learn Behav 36:159-65
Plakke, Bethany; Freeman, John H; Poremba, Amy (2007) Metabolic mapping of the rat cerebellum during delay and trace eyeblink conditioning. Neurobiol Learn Mem 88:11-8
Freeman, John H; Halverson, Hunter E; Hubbard, Erin M (2007) Inferior colliculus lesions impair eyeblink conditioning in rats. Learn Mem 14:842-6
Campolattaro, Matthew M; Halverson, Hunter E; Freeman, John H (2007) Medial auditory thalamic stimulation as a conditioned stimulus for eyeblink conditioning in rats. Learn Mem 14:152-9
Campolattaro, Matthew M; Freeman, John H (2006) Perirhinal cortex lesions impair simultaneous but not serial feature-positive discrimination learning. Behav Neurosci 120:970-5
Campolattaro, Matthew M; Freeman, John H (2006) Perirhinal cortex lesions impair feature-negative discrimination. Neurobiol Learn Mem 86:205-13
Halverson, Hunter E; Freeman, John H (2006) Medial auditory thalamic nuclei are necessary for eyeblink conditioning. Behav Neurosci 120:880-7
Nolan, Brian C; Freeman, John H (2006) Purkinje cell loss by OX7-saporin impairs acquisition and extinction of eyeblink conditioning. Learn Mem 13:359-65
Freeman Jr, John H; Halverson, Hunter E; Poremba, Amy (2005) Differential effects of cerebellar inactivation on eyeblink conditioned excitation and inhibition. J Neurosci 25:889-95
Nolan, Brian C; Freeman Jr, John H (2005) Purkinje cell loss by OX7-saporin impairs excitatory and inhibitory eyeblink conditioning. Behav Neurosci 119:190-201

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