Mice with a loss-of-function mutation of calcium/calmodulin-activated adenylyl cyclase I (AC1) - barrelless mice - have strikingly abherrent cortical development: the thalamic afferents into the barrel cortex do not segregate into whisker-specific barrels. Our paper investigates the link between this mutation and the "barrelless" phenotype, and demonstrates that the loss-of-function mutation leads to deficits in presynaptic mechanisms at the thalamocortical synapse. How might presynaptic deficits disrupt whisker-specific segregation in the barrel cortex? We used a model to demonstrate one possibility: decrease in the release probability at the thalamocortical synapse (which is observed in the barrelless mutant) can influence the balance between LTP and LTD (in favor of LTD), which can disrupt whisker segregaton. Though how this occurs is easily explained with a conceptual model (described succinctly in the associated paper), we also produced a computational simulation of this phenomenon.
Model Type: Neuron or other electrically excitable cell
Simulation Environment: C or C++ program (web link to model)
Implementer(s): Butts, Dan [daniel_butts at hms.harvard.edu]
References:
Lu HC et al. (2006). Role of efficient neurotransmitter release in barrel map development. The Journal of neuroscience : the official journal of the Society for Neuroscience. 26 [PubMed]