Characterization of two pathological gating-charge substitutions in Cav1.4 L-type calcium channels.

Cav1.4 L-type calcium channels are predominantly expressed at the photoreceptor terminals and in bipolar cells, mediating neurotransmitter release. Mutations in its gene, , can cause congenital stationary night-blindness type 2 (CSNB2).

A novel calcium channel Cavβ splice variant with unique properties predominates in the retina.

Cavβ subunits are essential for surface expression of voltage-gated calcium channel complexes and crucially modulate biophysical properties like voltage-dependent inactivation. Here, we describe the discovery and characterization of a novel Cavβ variant with distinct features that predominates in the retina. We determined spliced exons in retinal transcripts of the Cacnb2 gene, coding for Cavβ, by RNA-Seq data analysis and quantitative PCR.

Charge-Converting Nanoemulsions as Promising Retinal Drug and Gene Delivery Systems.

Aim: This study aimed to develop phosphatase-responsive ζ potential converting nanocarriers utilizing polyphosphate-coated cell-penetrating peptide (CPP)-decorated nanoemulsions (NEs) as a novel gene delivery system to retinal cells.

Methods: Poly-l-lysine (PLL) was first conjugated with oleylamine (OA) only at its carboxylic end to form the amphiphilic PLL-oleylamine (PLOA) conjugate. Afterward, NEs were loaded with PLOA prior to being coated with tripolyphosphate (TPP) to generate PLOA/TPP NEs.

Knockout of Ca1.3 L-type calcium channels in a mouse model of retinitis pigmentosa.

Retinitis Pigmentosa is a genetically heterogeneous, degenerative retinal disorder characterized by gradual dysfunction and death of photoreceptors, first rods and later cones, and progressive blindness. Studies suggested that application of L-type calcium channel blockers rescues photoreceptors in paradigms related to Ca overflow. To investigate whether Cav1.

Cav1.4 dysfunction and congenital stationary night blindness type 2.

Cav1.4 L-type Ca channels are predominantly expressed in retinal neurons, particularly at the photoreceptor terminals where they mediate sustained Ca entry needed for continuous neurotransmitter release at their ribbon synapses. Cav1.