Damage to the NBM leads to a sustained lesion-induced increase in functional NGF in the cortex.
Bilateral infusions of colchicine or vehicle were made in the nucleus basalis magnocellularis of rats. Cortical homogenates were assessed in a choline acetyltransferase (ChAT) activity assay and a PC12 cell neurite outgrowth assay 3, 7, 14, 28, 35 or 84 days post-lesion. Cortical ChAT activity was initially decreased by 30%, followed by recovery to control levels at 84 days post-lesion. Cortical nerve growth factor (NGF) activity was increased 35% above control levels at all time points following colchicine infusion, while addition of a NGF antibody blocking all activity. The data show an increase in functional NGF in the target area of the lesioned neurons preceding and coinciding with regional recovery of a cholinergic marker, suggesting that NGF has a role in the cholinergic recovery.
Shaughnessy
L W
LW
Curriculum in Neurobiology, University of North Carolina, Chapel Hill 27599, USA.
Barone
S
S
D000818:Animals; D000970:Antineoplastic Agents; D001370:Axonal Transport / Q000187:drug effects*; D001681:Biological Assay; D002795:Choline O-Acetyltransferase / Q000378:metabolism*; D003078:Colchicine; D004797:Enzyme-Linked Immunosorbent Assay; D008297:Male; D009414:Nerve Growth Factors / Q000378:metabolism*; D016716:PC12 Cells; D010296:Parietal Lobe / Q000502:physiology; D051381:Rats; D013377:Substantia Innominata / Q000502:physiology*
D000970:Antineoplastic Agents; D009414:Nerve Growth Factors; D002795:Choline O-Acetyltransferase; D003078:Colchicine