Psychiatry related information on TRPC2

• TRPC2-deficient mice exhibit striking behavioral defects in the regulation of sexual and social behaviors [1].

High impact information on TRPC2

• While encoding an active channel in the mouse, the human TRPC2 appears to be a pseudogene [2].
• Here we analyzed total RNA samples from brain and testis for presence of TRPC2 a and b and describe the splicing patterns responsible for their formation, as well as those leading to the alpha and beta forms of TRPC2 [2].
• Co-expression of TRPC2 with other TRPCs did not restore plasma-membrane trafficking [3].
• We report the molecular cloning of two novel murine TRPC2 splice variants, mTRPC2alpha and mTRPC2beta. mTRPC2alpha RNA is expressed at low levels in many tissues and cell systems, while mTRPC2beta is exclusively and abundantly expressed in the vomeronasal organ (VNO) [3].
• Furthermore, field potential and single-cell patch-clamp recordings showed that TRPC2 is dispensable for the transduction of MHC peptide ligands by sensory neurons in the basal zone of the VNO [4].

Biological context of TRPC2

• Additionally for TRPC1, a larger species, and for TRPC2, a smaller species was detected in all three cell lines with sequencing revealing the fragments to contain TRPC sequence, suggesting that they were either products of alternative splicing events or from closely related genes [5].
• Neurobiology of TRPC2: from gene to behavior [6].
• The mammalian genome codes for seven TRPCs of which TRPC2 is the largest with the most restricted pattern of expression and has several alternatively spliced variants [7].
• TRPC2: molecular biology and functional importance [7].
• This indicates that a previously unrecognized TRPC2-independent signal transduction mechanism in the VNO underlies the sensing of cues required for the formation of this pheromonal recognition memory [4].

Anatomical context of TRPC2

• TRPC2, a member of the canonical TRPC subfamily, is highly localized to the dendritic tip of vomeronasal sensory neurons [1].
• In sperm, TRPC2 is activated by the sperm's interaction with the oocyte's zona pellucida, leading to entry of Ca2+ and activation of the acrosome reaction [7].
• The expression and localisation of caspase-12, an enzyme that has been involved in the apoptosis triggered by a stress on the endoplasmic reticulum, was not different in TRPC2(+) and TRPC2(-) cells [8].

Associations of TRPC2 with chemical compounds

• PLC activation results in the production of inositol 1,4,5-trisphosphate (IP(3)), and TRPC2 has IP(3) receptor (IP(3)R) binding sites [9].
• When stimulated with thapsigargin (TG), apoptosis occurred in both TRPC2(+) and TRPC2(-) cells but 12h earlier in TRPC2(+) cells, suggesting that store-dependent entry of Ca(2+) can accelerate the process [8].
• Epo-induced Ca(2+) influx through TRPC2 was inhibited by pretreatment with U-73122 or by downregulation of PLCgamma1 by RNA interference [9].

Other interactions of TRPC2

• TRPC2 coassociated with Epo-R, PLCgamma, and IP(3)R, and the association between TRPC2 and IP(3)R was disrupted in these mutants [9].

References