The main goal of the proposed project is to provide more detailed information about the sensory input pathways that are necessary for cerebellar learning. We will initially focus on auditory and visual stimulus pathways in eyeblink conditioning. The PI's laboratory recently discovered that the medial auditory thalamic nuclei (medial division of the medial geniculate, posterior intralaminar nucleus, and suprageniculate nucleus) are necessary for auditory eyeblink conditioning in rats. The medial auditory thalamus is part of the auditory conditioned stimulus (CS) pathway in Pavlovian fear conditioning and tone-cued avoidance conditioning.
Specific Aim 1 is to further examine the role of the medial auditory thalamus in rodent eyeblink conditioning by identifying the afferent and efferent auditory projections of these nuclei that are necessary for eyeblink conditioning using lesions, neural tract tracing, microstimulation, unit recording, and pharmacological inactivation.
Specific Aim 2 is to examine the role of the inferior colliculus and its connections with the medial auditory thalamus in eyeblink conditioning.
Specific Aim 3 is to conduct an initial investigation of the visual CS pathways that are necessary for eyeblink conditioning. The findings of the proposed studies will provide more complete information regarding the auditory and visual CS pathways that are necessary for cerebellar learning. The findings will also have significant implications for developmental analyses of eyeblink conditioning, which have found evidence for developmental changes in auditory CS input to the cerebellum. Translational studies of cerebellar function in various developmental disorders and schizophrenia will also benefit from information derived from the proposed project. A better understanding of the sensory inputs to the cerebellum that are necessary for learning will help guide functional imaging studies to better assess abnormalities in sensory-motor interactions in patients with schizophrenia and various developmental disorders such as fetal alcohol syndrome, autism, and Down syndrome. A general goal of the translational research is to better understand the brain abnormalities underlying developmental disorders and schizophrenia in order to establish more effective treatments. ? ? ?

National Institute of Health (NIH)
National Institute of Mental Health (NIMH)
Research Project (R01)
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Special Emphasis Panel (ZRG1-IFCN-B (03))
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Osborn, Bettina D
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University of Iowa
Schools of Arts and Sciences
Iowa City
United States
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Steinmetz, Adam B; Freeman, John H (2018) Cannabinoid agonist administration within the cerebellar cortex impairs motor learning. Neurobiol Learn Mem :
Steinmetz, Adam B; Freeman, John H (2016) Cannabinoid modulation of memory consolidation within the cerebellum. Neurobiol Learn Mem 136:228-235
Kim, Jangjin; Wasserman, Edward A; Castro, Leyre et al. (2016) Anterior cingulate cortex inactivation impairs rodent visual selective attention and prospective memory. Behav Neurosci 130:75-90
Campolattaro, Matthew M; Buss, Eric W; Freeman, John H (2015) Cross-modal savings in the contralateral eyelid conditioned response. Behav Neurosci 129:683-91
Freeman, John H (2015) Cerebellar learning mechanisms. Brain Res 1621:260-9
Steinmetz, Adam B; Buss, Eric W; Freeman, John H (2013) Inactivation of the ventral lateral geniculate and nucleus of the optic tract impairs retention of visual eyeblink conditioning. Behav Neurosci 127:690-3
Steinmetz, Adam B; Harmon, Thomas C; Freeman, John H (2013) Visual cortical contributions to associative cerebellar learning. Neurobiol Learn Mem 104:103-9
Steinmetz, Adam B; Freeman, John H (2013) Differential effects of the cannabinoid agonist WIN55,212-2 on delay and trace eyeblink conditioning. Behav Neurosci 127:694-702
Steinmetz, Adam B; Freeman, John H (2011) Retention and extinction of delay eyeblink conditioning are modulated by central cannabinoids. Learn Mem 18:634-8
Campolattaro, Matthew M; Kashef, Alireza; Lee, Inah et al. (2011) Neuronal correlates of cross-modal transfer in the cerebellum and pontine nuclei. J Neurosci 31:4051-62

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