Individual variability in synaptic properties has functional consequences for susceptibility to and recovery from lesion of a central pattern generator.
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1
Georgia State University, Neuroscience Institute, United States
Neural circuits can contain considerable variability in synaptic and membrane properties across individuals and yet display a consistent output. The relevance of such variation in the network elements for behavior is not well understood. We found that in the central pattern generator (CPG) for swimming in the mollusc Tritonia diomedea, there is considerable animal-to-animal variability in synaptic properties and adaptive plasticity. The functional consequences of such individual differences are not apparent under normal conditions, but are unmasked when the CPG is impaired by injury.
The Tritonia swim CPG consists of three neuronal types: VSI, C2, and DSI, all of which make functional connections in each of the paired pedal ganglia by projecting axons through the pedal-pedal commissure. In the majority of individuals, C2 excites VSI in the pedal ganglion distal to the VSI soma, evoking antidromic spikes that travel back through the commissure. C2 produces a weaker excitation followed by a stronger inhibition in the proximal pedal ganglion. Cutting the commissure that contains the C2 and VSI axons disconnects the distal excitation of VSI by C2, and consequently impairs the swimming behavior and the fictive swim motor program of most, but not all individuals (Sakurai and Katz, 2009). The individual variability in the susceptibility to the lesion appears to be caused by differences in the synaptic actions of C2 onto VSI in the proximal pedal ganglion; there is an inverse correlation between the extent of impairment and the magnitude of C2-evoked depolarization of VSI at the time of lesion.
Most, but not all animals recover their ability to swim one day after lesion of the commissure (Sakurai and Katz, 2009). The variability in the extent of recovery appears to be caused by differences in the combined action of C2 and DSI. Since DSI is known to evoke serotonergic neuromodulatory actions within the CPG and is co-active with C2 during a swim motor pattern, these result suggests an involvement of serotonergic mechanisms in the network reorganization of the swim CPG after injury.
Our results suggest that individual variability in neural circuit properties might be “good enough” under normal conditions, but have functional consequences under demanding conditions, such as injury. Although the cellular mechanisms underlying this synaptic variability are not known, further study may provide insight into the inherited variability and adaptive plasticity of the neural functions that are applicable to other neural circuits.
References
Sakurai, A and Katz, PS (2009) Functional recovery after lesion of a central pattern generator. J Neurosci 29: 13115-13125.
Keywords:
individual variability,
injury,
mollusc,
Neuromodulation,
Serotonin,
SPIKE INITIATION ZONE,
synaptic plasticity,
Tritonia
Conference:
Tenth International Congress of Neuroethology, College Park. Maryland USA, United States, 5 Aug - 10 Aug, 2012.
Presentation Type:
Invited Symposium (only for people who have been invited to a particular symposium)
Topic:
Learning, Memory and Behavioral Plasticity
Citation:
Sakurai
A
(2012). Individual variability in synaptic properties has functional consequences for susceptibility to and recovery from lesion of a central pattern generator..
Conference Abstract:
Tenth International Congress of Neuroethology.
doi: 10.3389/conf.fnbeh.2012.27.00023
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Received:
25 Apr 2012;
Published Online:
07 Jul 2012.
*
Correspondence:
Dr. Akira Sakurai, Georgia State University, Neuroscience Institute, Atlanta, GA, 30302-5030, United States, akira@gsu.edu