. Alterations in the ankyrin domain of TRPV4 cause congenital distal SMA, scapuloperoneal SMA and HMSN2C. Nat Genet. 2010 Feb;42(2):160-4. PubMed.


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  1. It's interesting that Ilya Bezprozvanny mentions the known interaction of TRP channels with PIP2. Di Pialo and colleagues report that Aβ disrupts PIP2 metabolism, which can be prevented in mice haploinsufficient for synaptonanin1 (1). This follows a study in which reduced PIP2 levels are reported in presenilin mutants (2). Several genes in the Down syndrome critical region have been reported to be involved in the expression synaptojanin 1, and reduced PIP2 expression is reported in the mouse model (4). TRPV1-expressing neurons in the spinal dorsal horn are reported to be glutamatergic (5). Xu and colleagues report that TRPV1 agonists capsaicin and resiniferatoxin facilitate LTP but suppress LTD (6). Soluble Aβ has been found to inhibit LTP and enhance LTD of glutamatergic transmission (7). Might we expect that altered TRPV1 function as a result of reduced PIP2 in AD may cause memory deficit? Might it also explain the taste deficit in AD (8,9)?

    See also:

    1. PIP2 at the Core of Aβ Oligomers’ Synaptic Attack?

    2. Beyond γ-Secretase: FAD Mutations Affect Calcium Channel via Lipid Messenger

    View all comments by Mary Reid

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