The proposed project is designed to examine the neural mechanisms underlying the ontogeny of cerebellar learning using short delay and trace eyeblink conditioning procedures. Previous findings from this projected showed that the ontogeny of delay eyeblink conditioning is highly correlated with developmental changes in the induction of neuronal plasticity within the cerebellum. A substantial body of evidence now indicates that the development of auditory input to the pontine nuclei plays a critical role in the ontogeny of cerebellar learning. The current proposal significantly extends these findings to elucidate the nature of developmental changes in auditory input to the pontine nuclei in Aim 1. It will also test the more general hypothesis that cerebellar learning depends on the development of sensory input to the pontine nuclei, not on the development of cerebellar plasticity mechanisms in Aim 2. That is, the cerebellum is capable of learning early in development but only with early developing sensory systems (olfactory, gustatory, and somatosensory), whereas cerebellar learning emerges later when late developing sensory systems (auditory and visual) are used. The scope of the project will be extended to examine the development of mechanisms underlying trace eyeblink conditioning, a cerebellar learning paradigm that requires the hippocampus and cortical projections to the pontine nuclei (Aim 3). New methods for recording neuronal activity in rat pups with moveable tetrodes will be used to examine the development of thalamic, pontine, and hippocampal activity during eyeblink conditioning. Nothing is known currently about the ontogeny of learning -related activity in the thalamus or hippocampus. Thus, the findings of these experiments will be novel and significant.

Public Health Relevance

The proposed experiments will provide novel data on fundamental developmental changes in cerebellar, thalamic, and hippocampal function. The findings of these experiments may then be used to guide studies of atypical neural development in models of developmental disorders such as autism, Down syndrome, fragile x syndrome, and fetal alcohol syndrome.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Research Project (R01)
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Study Section
Special Emphasis Panel (ZRG1-IFCN-L (03))
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Babcock, Debra J
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University of Iowa
Schools of Arts and Sciences
Iowa City
United States
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Freeman, John H (2015) Cerebellar learning mechanisms. Brain Res 1621:260-9
Goldsberry, Mary E; Elkin, Magdalyn E; Freeman, John H (2014) Sensory system development influences the ontogeny of eyeblink conditioning. Dev Psychobiol 56:1244-51
Campolattaro, Matthew M; Freeman, John H (2009) Cerebellar inactivation impairs cross modal savings of eyeblink conditioning. Behav Neurosci 123:292-302
Plakke, Bethany; Freeman, John H; Poremba, Amy (2009) Metabolic mapping of rat forebrain and midbrain during delay and trace eyeblink conditioning. Neurobiol Learn Mem 92:335-44
Freeman, John H; Campolattaro, Matthew M (2008) Ontogenetic change in the auditory conditioned stimulus pathway for eyeblink conditioning. Learn Mem 15:823-8
Campolattaro, Matthew M; Freeman, John H (2008) Eyeblink conditioning in 12-day-old rats using pontine stimulation as the conditioned stimulus. Proc Natl Acad Sci U S A 105:8120-3
Halverson, Hunter E; Poremba, Amy; Freeman, John H (2008) Medial auditory thalamus inactivation prevents acquisition and retention of eyeblink conditioning. Learn Mem 15:532-8
Freeman, John H; Duffel, Jessica W (2008) Eyeblink conditioning using cochlear nucleus stimulation as a conditioned stimulus in developing rats. Dev Psychobiol 50:640-6
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

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