Neonatal 6-OHDA and recovery of function

The toxin 6-OHDA does not cross the blood brain barrier after peripheral administration in the adult animal, and so must be administered centrally in order to yield effective lesions. This restriction does not apply in neonates. Thus, 6-OHDA can produce profound depletions of central catecholamines when administered subcutaneously or intracisternally to neonatal rats or mice (Breese and Traylor, 1971). Moreover, greater selectivity for individual amine pathways can be achieved by refinements of the route of delivery or by pharmacological manipulation, and different protocols of administration can allow relatively selective depletions. For example, several small repeated injections of 6-OHDA spare dopamine and preferentially deplete dopamine, whereas dopamine toxicity after a single large injection can be enhanced by pargyline treatment, in particular if the noradrenaline depletion is concurrently blocked with pargyline (Breese and Traylor, 1971 Cooper et al., 1973 Smith et al., 1973 Luthman et al., 1989). 

Rather, similar to the compensation observed with adult lesions, residual populations of dopamine neurones (which may be as little as 1 or 2%) spared by the lesion appear to underlie the remarkable compensation seen after neonatal 6-OHDA lesions also. Evidence 

---