Depletion of brain noradrenaline and dopamine by 6‐hydroxydopamine

Abstract

Summary1. After intracisternal administration, 6-hydroxydopamine had a greater effect on brain noradrenaline than on dopamine. 2. Administration of two doses of 6-hydroxydopamine increased the depletion of noradrenaline but not of dopamine.3. Small doses of 6-hydroxydopamine decreased the concentration of noradrenaline with little or no effect on dopamine. Tyrosine hydroxylase activity was not reduced with these treatments.4. While pargyline pretreatment offered no advantage in the depletion of brain noradrenaline after 6-hydroxydopamine, depletion of brain dopamine was greatly potentiated by this treatment. The reduction of striatal tyrosine hydroxylase activity observed after 6-hydroxydopamine was also potentiated by pargyline pretreatment. 5. The amounts of labelled noradrenaline and dopamine formed from 3H-tyrosine were greatly reduced by 6-hydroxydopamine treatment. After 3H-DOPA, formation of noradrenaline was greatly reduced while formation of labelled dopamine was only moderately reduced suggesting that decarboxylation of DOPA can occur in other than catecholamine containing neurones. 6. Desmethylimipramine and imipramine inhibited depletion of noradrenaline produced by 6-hydroxydopamine but did not alter depletion of dopamine.Reserpine did not inhibit depletion of catecholamines produced by 6-hydroxydopamine. 7. Administration of 6-hydroxydopamine to developing rats lowered both noradrenaline and dopamine concentrations as well as the tyrosine hydroxylase activity in the brains of these animals.

In Vivo Measurement of Density and Affinity of the Monoamine Vesicular Transporter in a Unilateral 6-Hydroxydopamine Rat Model of PD

“…Approximately 30 mins before the 6-OHDA infusion the subjects were given desipramine (25 mg/kg i.p.) to protect noradrenergic fibers (Breese and Traylor, 1971;Kelly and Iversen, 1976;Whishaw et al, 1994). The 6-OHDA solution was delivered at a rate of 1 mL/min using a 50 ml Hamilton syringe through a 26-gauge needle.…”

6-Hydroxydopamine lesion of the rat prefrontal cortex impairs motor initiation but not motor execution

“…One hour before surgery, rats received 40 mg/kg desipramine (Serva, Heidelberg, Germany) per os in order to protect noradrenergic terminals in the PFC from 6-OHDA neurotoxicity (Breese and Traylor 1971). Thirty minutes afterwards, the rats were injected intraperitoneally (i.p.)…”

Attenuation of amphetamine‐induced motor stimulation and stereotypy by 6‐hydroxydopamine in the rat

“…When administered into the cerebrospinal fluid the drug generally has a greater toxic action on noradrenergic than on dopaminergic neurones but if monoamine oxidase is inhibited an equally profound effect can be obtained on dopamine-containing neurones (Breese & Traylor, 1971;Fibiger, Lonsbury, Cooper & Lytle, 1972). In theory, 6-OHDA should be of considerable use in defining the role of catecholaminergic neurones in amphetamine mediated behaviour.…”

“…In the present experiments therefore the effects of 6-OHDA on amphetamine-induced locomotor stimulation and stereotyped behaviour were re-examined. In addition, as MAO inhibition tends to increase the effect of 6-OHDA on dopaminergic neurones (Breese & Traylor, 1971), an attempt was made to evaluate the role of the dopaminergic nigro-striatal system in these behavioural effects.…”