Remodeling of retinal ganglion cell dendrites in the absence of action potential activity.
The dendrites of ganglion cells in the retina have an excess number of spines and branches that are normally lost during the first postnatal month of development. We investigated whether this dendritic remodeling can be prevented when the action potential activity of ganglion cells is abolished by chronic intraocular injections of tetrodotoxin (TTX) during the first 4 or 5 postnatal weeks in the cat. Dendritic tree morphologies of alpha and beta ganglion cells from TTX-treated, non-TTX-treated (contralateral eye), and normal control retinae were compared after intracellular filling with Lucifer yellow. Qualitative observations and quantitative measurements indicate that TTX treatment does not prevent the normally occurring loss of spines and dendritic branches. Indeed, the dendritic trees of both alpha and beta cells in TTX injected eyes actually have even fewer spines and branches than normal cells at equivalent ages. However, because the total dendritic lengths of these cells are also reduced after TTX blockade, spine density is indistinguishable from untreated animals at the same age. In addition, although dendritic field areas are not altered with treatment, the complexity of the dendritic trees is reduced. These observations suggest that dendritic remodeling can occur in the absence of ganglion cell action potential activity. Thus, the factors that influence the dendritic and axonal development of retinal ganglion cells must differ, because similar TTX treatment during the period of axonal remodeling does have profound effects on the final pattern of terminal arborizations.
Wong
R O
RO
Department of Neurobiology, Stanford University School of Medicine, California 94305.
Herrmann
K
K
Shatz
C J
CJ
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002415:Cats; D003712:Dendrites / Q000648:ultrastructure*; D005829:Geniculate Bodies / Q000473:pathology; D012160:Retina / Q000187:drug effects / Q000254:growth & development; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D015222:Sodium Channels / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D015222:Sodium Channels; D013779:Tetrodotoxin