Compensatory increase in tyrosine hydroxylase activity in rat brain after intraventricular injections of 6-hydroxydopamine.
The neurotoxin 6-hydroxydopamine produced a permanent loss of endogenous norepinephrine and of 3H-labeled norepinephrine uptake sites in the hippocampus within 5 days. These losses were initially accompanied by parallel decreases in tyrosine hydroxylase activity and synaptosomal norepinephrine synthesis. Within 21 days, however, hippocampal tyrosine hydroxylase activity and norepinephrine synthesis rate increased three- to fivefold. These data suggest a novel form of plasticity in brain-damaged animals characterized by an increase in the capacity for transmitter biosynthesis in residual neurons.
D000818:Animals; D005728:Ganglia, Sympathetic / Q000201:enzymology; D006624:Hippocampus / Q000201:enzymology*; D006892:Hydroxydopamines / Q000494:pharmacology*; D008125:Locus Coeruleus / Q000201:enzymology*; D008297:Male; D009410:Nerve Degeneration; D009411:Nerve Endings / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism*
D006892:Hydroxydopamines; D014446:Tyrosine 3-Monooxygenase; D009638:Norepinephrine