Deficits in locomotor behaviour and thermoregulation produced by intrahypothalamic dopamine injections

When nigrostriatal dopamine neurones degenerate, a loss of functional dopamine in the striatum occurs and is accompanied by increased dopamine in the degenerating axons which traverse the hypothalamus. While the behavioural deficits which occur after nigrostriatal degeneration have been attributed to the loss of functional dopamine neurotransmission, evidence produced by us suggests that the increased levels of amines in the degenerating axons may be neuroactive and participate in the production of these behavioural deficits. To test this hypothesis further, albino rats were injected bilaterally with 200 nmol of dopamine in a location just rostral to the diencephalon/mesencephalon border, where amine accumulation is commonly observed following lateral hypothalamic damage. The effect of these injections upon open field performance, thermoregulation and motor reflex control was determined 40 min after dopamine injection. In a second study, pargyline (15 mg/kg. i.p.) was administered 30 min before intracerebral dopamine to determine whether this treatment would increase the severity of motor and thermoregulatory deficits which occurred after dopamine injections alone. Deficits in locomotion, rearing and the ability to regulate body temperature were seen after the dopamine injections while motor reflex control in these animals was similar to that seen in vehicle-injected controls. The behavioural deficits displayed by pargyline pretreated, dopamine injected animals were slightly but not significantly more severe than those displayed by animals receiving dopamine injections alone. Fluorescent histochemical assessment of injection sites revealed that dopamine injection produced an increase in fluorescence or "amine accumulation" at the site of injection but this was considerably less than that seen after catecholamine degeneration.(ABSTRACT TRUNCATED AT 250 WORDS)