| First Author | Park SJ | Year | 2008 |
| Journal | Neurosci Lett | Volume | 439 |
| Issue | 2 | Pages | 165-9 |
| PubMed ID | 18514403 | Mgi Jnum | J:137049 |
| Mgi Id | MGI:3797687 | Doi | 10.1016/j.neulet.2008.05.013 |
| Citation | Park SJ, et al. (2008) The absence of the clathrin-dependent endocytosis in rod bipolar cells of the FVB/N mouse retina. Neurosci Lett 439(2):165-9 |
| abstractText | The high rate of exocytosis at the ribbon synapses is balanced by following compensatory endocytosis. Unlike conventional synaptic terminals where clathrin-mediated endocytosis (CME) is a predominant mechanism for membrane retrieval, CME is thought to be only a minor mechanism of endocytosis at the retinal ribbon synapses, but CME is present there and it works. We examined the clathrin expression in the FVB/N rd1 mouse, which is an animal model of retinitis pigmentosa. The broadly distributed pattern of clathrin immunoreactivity in the inner plexiform layer was similar in both the control and FVB/N mouse retinas, but the immunoreactive punta within the rod bipolar axon terminals located in the proximal IPL were decreased in number and reduced in size at postnatal days 14 and they came to disappear at postnatal days 21. This preferential decrease of the clathrin expression at ribbon synapses in the rod bipolar cell axon terminals of the FVB/N mouse retina demonstrates another plastic change after photoreceptor degeneration and this suggests that clathrin may be important for normal synaptic function at the rod bipolar ribbon synapses in the mammalian retina. |
