A transient, cocaine-mediated change in levels of Kal7 vs. ΔKal7 would be expected to have functional significance. While expression of exogenous Kal7 increases spine density in cortical and hippocampal pyramidal neurons and even in interneurons [13,21,24], expression of exogenous ΔKal7 does not. Expression of ΔKal7 does increase spine head size [24] and the cocaine-mediated increase in ΔKalrn promoter usage may contribute to the increase in spine width known to occur following cocaine administration [12,24]. Kal7 binding to its partners might be disrupted by ΔKal7, much as Homer-1a disrupts the clusters of proteins formed with the longer constitutive splice variants of the Homer family [60].
