Target-specific regulation of synaptic efficacy in the feeding central pattern generator of Aplysia: potential substrates for behavioral plasticity?
The contributions to this symposium are unified by their focus on the role of synaptic plasticity in sensorimotor learning. Synaptic plasticities are also known to operate within the central pattern generator (CPG) circuits that produce repetitive motor programs, where their relation to adaptive behavior is less well understood. This study examined divergent synaptic plasticity in the signaling of an influential interneuron, B20, located within the CPG that controls consummatory feeding-related behaviors in Aplysia. Previously, B20 was shown to contain markers for catecholamines and GABA (Díaz-Ríos et al., 2002), and its rapid synaptic signaling to two follower motor neurons, B16 and B8, was found to be mediated by dopamine (Díaz-Ríos and Miller, 2005). In this investigation, two incremental forms of increased synaptic efficacy, facilitation and summation, were both greater in the signaling from B20 to B8 than in the signaling from B20 to B16. Manipulation of the membrane potentials of the two postsynaptic motor neurons did not affect facilitation of excitatory postsynaptic potentials (EPSPs) to either follower cell. Striking levels of summation in B8, however, were eliminated at hyperpolarized membrane potentials and could be attributed to distinctive membrane properties of this postsynaptic cell. GABA and the GABAB agonist baclofen increased facilitation and summation of EPSPs from B20 to B8, but not to B16. The enhanced facilitation was not affected when the membrane potential of B8 was pre-set to hyperpolarized levels, but GABAergic effects on summation were eliminated by this manipulation. These observations demonstrate a target-specific amplification of synaptic efficacy that can contribute to channeling the flow of divergent information from an intrinsic interneuron within the buccal CPG. They further suggest that GABA, acting as a cotransmitter in B20, could induce coordinated and target-specific pre- and postsynaptic modulation of these signals. Finally, we speculate that target-specific plasticity and its modulation could be efficient, specific, and flexible substrates for learning-related modifications of CPG function.
Díaz-Ríos
Manuel
M
Institute of Neurobiology and Department of Anatomy, University of Puerto Rico, 201 Blvd. del Valle, San Juan, Puerto Rico 00901.
Miller
Mark W
MW
D000818:Animals; D001048:Aplysia / Q000033:anatomy & histology / Q000502:physiology*; D004553:Electric Conductivity; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D005247:Feeding Behavior / Q000502:physiology*; D007395:Interneurons / Q000378:metabolism; D008564:Membrane Potentials; D008959:Models, Neurological; D009046:Motor Neurons / Q000378:metabolism; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology / Q000502:physiology*
D005680:gamma-Aminobutyric Acid