Zusammenfassung
Glial cells in the diseased nervous system undergo a process known as reactive gliosis. Gliosis of retinal Muller glial cells is characterized by an upregulation of glial fibrillary acidic protein and frequently by a reduction of inward K+ current amplitudes. Purinergic signaling is assumed to be involved in gliotic processes. As previously shown, lack of the nucleotide receptor P2Y(1) leads to ...
Zusammenfassung
Glial cells in the diseased nervous system undergo a process known as reactive gliosis. Gliosis of retinal Muller glial cells is characterized by an upregulation of glial fibrillary acidic protein and frequently by a reduction of inward K+ current amplitudes. Purinergic signaling is assumed to be involved in gliotic processes. As previously shown, lack of the nucleotide receptor P2Y(1) leads to an altered regulation of K+ currents in Muller cells of the ischemic retina. Here, we asked first whether this effect is mediated by the IP3 receptor subtype 2 (IP(3)R2) known as the major downstream signaling target of P2Y(1) in Muller cells. The second question was whether lack of IP(3)R2 affects neuronal survival in the control and ischemic retina. Ischemia was induced in wild type and IP(3)R2-deficient (IP (3) R2 (-/-)) mice by transient elevation of the intraocular pressure. Immunostaining and TUNEL labelling were used to quantify neuronal cell loss. The downregulation of inward K+ currents in Muller cells from ischemic IP (3) R2 (-/-) retinae was less strong than in wild type animals. The reduction of the number of cells in the ganglion cell layer and of calretinin- and calbindin-positive cells 7 days after ischemia was similar in wild type and IP (3) R2 (-/-) mice. However, IP(3)R2 deficiency led to an increased number of TUNEL-positive cells in the outer nuclear layer at 1 day and to an enhanced postischemic loss of photoreceptors 7 days after ischemia. This implies that IP(3)R2 is involved in some but not all aspects of signaling in Muller cells after an ischemic insult.
Altmetric