Chronic Treatment with 1,2,3,4-Tetrahydroiso-Quinoline (TIQ), an Environmental and Endogenous Substance, Induces Parkinsonian like Muscle Rigidity in Young and Old Rats
Specific factors causing selective death of nigral dopamine neurons, which lie at the root of Parkinson’s disease, are still unknown. Recently attention has been focused on TIQ and its derivatives which are both endogenous and environmental substances. It has been shown that these substances evoke certain behavioural and biochemical symptoms in monkeys and rats, similar to those found in parkinsonian patients. The aim of the present study was to find out whether TIQ evoked muscle rigidity, and caused degeneration of dopamine cells in the SN and mitochondrial abnormalities in muscles. The muscle tone was measured as mechanical resistance (MMG) of a rat’s hind foot, developed in response to passive extension and flexion at the ankle joint. The reflex EMG activity of the gastrocnemius and tibialis anterior muscles was simultaneously recorded. Degeneration of catecholamine cells was assessed by immunostaining of frontal brain sections for tyrosine hydroxylase (TH) and mitochondrial activity using a histochemical reaction for succinic dehydrogenase (SDH) in the gastrocnemius and tibialis anterior muscles. TIQ was administered in drinking water (20 mg/kg/day) for 115 days to young, middle-aged and old rats. That compound produced an increase in muscle resistance (MMG) and in late EMG reflex responses to movements in old and middle-aged rats. An immunohistochemical analysis showed that long-term treatment with TIQ produced some decrease in the TH-immunoreactivity staining in neurons of the substantia nigra (SN). In an SDH reaction, a patchy loss of the enzyme activity and subsarcolemmal deposits of the dark stained material was observed in a number of muscle fibers in TIQ-treated rats. The latter changes were less frequent in control groups. The present results suggest that TIQ may play a role in inducing Parkinson’s disease.