Specific Plasticity Loci and Their Synergism Mediate Operant Conditioning
Yuto Momohara1, Curtis L Neveu1, Hsin-Mei Chen1,2
1Department of Neurobiology and Anatomy, W.M. Keck Center for the Neurobiology of Learning and Memory, McGovern Medical School at the, University of Texas Health Science Center, Houston, Texas 77030.
Summary
Operant conditioning (OC) in Aplysia involves decreasing neuron B4 excitability and its inhibitory connection to neuron B51. These changes, along with increased B51 excitability, synergistically enhance feeding behavior, revealing diverse plasticity mechanisms in OC.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Cellular Neuroscience
Background:
- Operant conditioning (OC) mechanisms are widely studied, yet the synergistic roles of diverse plasticity loci remain underexplored.
- The feeding neural circuit in Aplysia provides a model system to investigate OC plasticity.
- Appetitive OC in Aplysia typically enhances neuronal excitability and electrical coupling, promoting ingestive behavior.
Purpose of the Study:
- To investigate if OC reduces the excitability of neuron B4, which normally inhibits ingestive behavior.
- To examine the plasticity of the inhibitory connection from neuron B4 to neuron B51.
- To determine if OC-induced modifications in Aplysia's feeding circuit act synergistically.
Main Methods:
- Utilized an in vitro analog of appetitive operant conditioning in Aplysia.
- Measured changes in neuronal excitability of B4 and B8 neurons.
- Assessed the strength of inhibitory connections, specifically B4 to B51 and B4 to B8.
- Employed a conductance-based circuit model to simulate OC phenotypes.
- Investigated synergistic effects of combined plasticity modifications.
Main Results:
- Operant conditioning decreased the intrinsic excitability of neuron B4.
- OC reduced the strength of the inhibitory synapse from B4 to the decision-making neuron B51.
- These OC-induced changes were specific, not affecting neuron B8 or the B4-to-B8 connection.
- A computational model indicated that reduced B4-B51 synaptic strength or increased B51 excitability better explained the OC phenotype.
- Combined modifications, particularly those involving B51, synergistically enhanced feeding behavior.
Conclusions:
- Diverse plasticity loci, including intrinsic neuronal excitability and synaptic strength, mediate OC.
- These modifications exhibit synergistic interactions, crucial for behavioral changes in OC.
- The findings provide insights into dopamine-mediated reinforcement mechanisms in behavior.
- Specific neurons and synapses are well-suited for synergistic interactions in OC plasticity.
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