A fundamental problem in neuroscience is to understand events occurring within Individual neurons and within neural networks that contribute to forms of plasticity underlying learning and memory. This proposal outlines both empirical and modeling studies that will examine the molecular, biochemical and biophysical properties of Identified neurons and the connectivity of neural circuits that have demonstrated capacities for nonassociative and associative plasticity. Specifically, the neural circuit that mediates the tail withdrawal reflex will be analyzed. Many of the sensory neurons, Interneurons, motor neurons and modulatory interneurons that control this behavior have been Identified and are accessible to study. Thus, molecular, biochemical and cellular neurophysiological techniques will be applied to analyze the particular processes that might explain associative and nonassociative learning. Formalisms of the cellular and network processes that underlie these forms of plasticity will be developed and incorporated into quantitative, real-time models of neuron-like elements and neural networks. The ability of these models to fit the experimental data and to predict simple and complex features of learning will be examined. The proposed research will provide for a fairly complete analysis of the mechanisms underlying the Induction, expression and maintenance of simple forms of nonassociative and associative learning as well as help address fundamental questions regarding the mechanistic relationship between short- and long-term memories.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Scientist Award (K05)
Project #
2K05MH000649-06A2
Application #
3075827
Study Section
Cognitive Functional Neuroscience Review Committee (CFN)
Project Start
1986-09-30
Project End
1998-06-30
Budget Start
1993-07-01
Budget End
1994-06-30
Support Year
6
Fiscal Year
1993
Total Cost
Indirect Cost
Name
University of Texas Health Science Center Houston
Department
Type
Schools of Medicine
DUNS #
City
Houston
State
TX
Country
United States
Zip Code
77225
Nargeot, R; Baxter, D A; Byrne, J H (1999) In vitro analog of operant conditioning in aplysia. I. Contingent reinforcement modifies the functional dynamics of an identified neuron. J Neurosci 19:2247-60
Nargeot, R; Baxter, D A; Patterson, G W et al. (1999) Dopaminergic synapses mediate neuronal changes in an analogue of operant conditioning. J Neurophysiol 81:1983-7
Nargeot, R; Baxter, D A; Byrne, J H (1999) In vitro analog of operant conditioning in aplysia. II. Modifications of the functional dynamics of an identified neuron contribute to motor pattern selection. J Neurosci 19:2261-72
Zwartjes, R E; West, H; Hattar, S et al. (1998) Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia. Learn Mem 4:478-95
Kabotyanski, E A; Baxter, D A; Byrne, J H (1998) Identification and characterization of catecholaminergic neuron B65, which initiates and modifies patterned activity in the buccal ganglia of Aplysia. J Neurophysiol 79:605-21
Smolen, P; Baxter, D A; Byrne, J H (1998) Frequency selectivity, multistability, and oscillations emerge from models of genetic regulatory systems. Am J Physiol 274:C531-42
Nakanishi, K; Zhang, F; Baxter, D A et al. (1997) Role of calcium-calmodulin-dependent protein kinase II in modulation of sensorimotor synapses in Aplysia. J Neurophysiol 78:409-16
Canavier, C C; Butera, R J; Dror, R O et al. (1997) Phase response characteristics of model neurons determine which patterns are expressed in a ring circuit model of gait generation. Biol Cybern 77:367-80
Liu, Q R; Hattar, S; Endo, S et al. (1997) A developmental gene (Tolloid/BMP-1) is regulated in Aplysia neurons by treatments that induce long-term sensitization. J Neurosci 17:755-64
Homayouni, R; Nunez-Regueiro, M; Byrne, J H et al. (1997) Identification of two phosphoproteins affected by serotonin in Aplysia sensory neurons. Brain Res 750:87-94

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