Long-term protection of axotomized neurons in the dorsal lateral geniculate nucleus in the rat following a single administration of basic fibroblast growth factor or ciliary neurotrophic factor.

PubMed ID: 9512273

Author(s): Agarwala S, Kalil RE. Long-term protection of axotomized neurons in the dorsal lateral geniculate nucleus in the rat following a single administration of basic fibroblast growth factor or ciliary neurotrophic factor. J Comp Neurol. 1998 Mar 9;392(2):264-72. PMID 9512273

Journal: The Journal Of Comparative Neurology, Volume 392, Issue 2, Mar 1998

We have studied the long-term effects of basic fibroblast growth factor (bFGF) and ciliary neurotrophic factor (CNTF) on axotomy-induced cell death in the dorsal lateral geniculate nucleus (LGN) of adult rats. LGN neurons were axotomized by a visual cortex lesion in 31 adult rats. A gelatin sponge soaked in a solution of bFGF, CNTF, or saline (control) was placed on the surface of the lesion, and the animals were allowed to survive for 1-12 weeks. Compared with controls, no major improvement was noted in the mean cross-sectional area of surviving LGN neurons in rats treated with bFGF or CNTF at any survival time. However, treatment with either factor significantly increased the number of surviving neurons at each survival time. At 1 week, the survival of LGN neurons in rats treated with bFGF or CNTF was 136% and 131% greater, respectively, than in controls. At 12 weeks, the number of surviving LGN neurons in bFGF- and CNTF-treated rats exceeded that seen in controls by 114% and 58%, respectively. Thus, a single administration of bFGF or CNTF following axotomy reduced neuronal death for long periods of time, but could not prevent atrophy. A single treatment with bFGF or CNTF, therefore, may block the full execution of a cell death program, but cannot prevent its initiation. Alternatively, the transduction pathways for maintaining cell size and preventing cell death may not be identical, and bFGF and CNTF applied as described above may be effective in activating one pathway but not the other.