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.

Agency
National Institute of Health (NIH)
Type
Research Project (R01)
Project #
5R01NS038890-14
Application #
8652505
Study Section
Special Emphasis Panel (ZRG1)
Program Officer
Babcock, Debra J
Project Start
Project End
Budget Start
Budget End
Support Year
14
Fiscal Year
2014
Total Cost
Indirect Cost
Name
University of Iowa
Department
Psychology
Type
Schools of Arts and Sciences
DUNS #
City
Iowa City
State
IA
Country
United States
Zip Code
52242
Brown, Kevin L; Freeman, John H (2016) Retention of eyeblink conditioning in periweanling and adult rats. Dev Psychobiol 58:1055-1065
Freeman, John H (2015) Cerebellar learning mechanisms. Brain Res 1621:260-9
Goldsberry, Mary E; Kim, Jangjin; Freeman, John H (2015) Developmental changes in hippocampal associative coding. J Neurosci 35:4238-47
Harmon, Thomas C; Freeman, John H (2015) Ontogeny of septohippocampal modulation of delay eyeblink conditioning. Dev Psychobiol 57:168-76
Goldsberry, Mary E; Elkin, Magdalyn E; Freeman, John H (2014) Sensory system development influences the ontogeny of eyeblink conditioning. Dev Psychobiol 56:1244-51
Brown, Kevin L; Freeman, John H (2014) Extinction, reacquisition, and rapid forgetting of eyeblink conditioning in developing rats. Learn Mem 21:696-708
Ng, Ka H; Freeman, John H (2012) Developmental changes in medial auditory thalamic contributions to associative motor learning. J Neurosci 32:6841-50
Freeman, John H; Steinmetz, Adam B (2011) Neural circuitry and plasticity mechanisms underlying delay eyeblink conditioning. Learn Mem 18:666-77
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

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