Serotonergic modulation of Aplysia sensory neurons (Baxter et al 1999)

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Accession:33986
The present study investigated how the modulation of these currents altered the spike duration and excitability of sensory neurons and examined the relative contributions of PKA- and PKC-mediated effects to the actions of 5-HT. A Hodgkin-Huxley type model was developed that described the ionic conductances in the somata of sensory neurons. The descriptions of these currents and their modulation were based largely on voltageclamp data from sensory neurons. Simulations were preformed with the program SNNAP (Simulator for Neural Networks and Action Potentials). The model was sufficient to replicate empirical data that describes the membrane currents, action potential waveform and excitability as well as their modulation by application of 5-HT, increased levels of adenosine cyclic monophosphate or application of active phorbol esters. The results provide several predictions that warrant additional experimental investigation and illustrate the importance of considering indirect as well as direct effects of modulatory agents on the modulation of membrane currents. See paper for more details.
Reference:
1 . Baxter DA, Canavier CC, Clark JW, Byrne JH (1999) Computational model of the serotonergic modulation of sensory neurons in Aplysia. J Neurophysiol 82:2914-35 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Aplysia sensory neuron;
Channel(s): I Na,t; I A; I K; I K,Ca; I CAN; I Potassium;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s): Serotonin;
Simulation Environment: SNNAP;
Model Concept(s): Action Potentials; Invertebrate;
Implementer(s): Baxter, Douglas;
Search NeuronDB for information about:  I Na,t; I A; I K; I K,Ca; I CAN; I Potassium; Serotonin;
 
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