Alterations in dendritic spine morphology and postsynaptic structure are a hallmark of neurological
disorders. Particularly spine pruning of striatal medium spiny neurons and aberrant rewiring
of corticostriatal synapses have been associated with the pathology of Parkinson’s disease and LDOPA
induced dyskinesia, respectively. Owing to its low activation threshold the neuronal L-type
calcium channel CaV1.3 is particularly critical in the control of neuronal excitability and thus in the
calcium-dependent regulation of neuronal functions. CaV1.3 channels are located in dendritic spines
and contain a C-terminal class 1 PDZ domain-binding sequence. Until today the postsynaptic PDZ
domain proteins shank, densin-180, and erbin have been shown to interact with CaV1.3 channels and to modulate their
current properties. Interestingly experimental evidence suggests an involvement of all three PDZ proteins as well as
CaV1.3 itself in regulating dendritic and postsynaptic morphology. Here we briefly review the importance of CaV1.3 and
its proposed interactions with PDZ proteins for the stability of dendritic spines. With a special focus on the pathology associated
with Parkinson’s disease, we discuss the hypothesis that CaV1.3 L-type calcium channels may be critical modulators
of dendritic spine stability.
Keywords: CACNA1D, PDZ domain, voltage-gated calcium channels, synaptic transmission, δ-atenin, synapse stability,
Parkinson’s disease, autism spectrum disorders.
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