These results indicate that in vivo ELF-MF induce reversible brain DNA damage while they do not elicit the stress response.

Since mild thermal stress seems to exert neuroprotection via induction of heat-shock protein 70 kDa (hsp70), we tested whether hsp70 would preserve striatal bioelectrical activity under conditions of mitochondrial impairment. Corticostriatal slices from rats that had undergone mild thermal stress were exposed to either rotenone or 3-nitropropionic acid (3-NP), that selectively inhibits mitochondrial complex I and complex II, respectively. Rotenone is utilized to obtain an experimental model of Parkinson's disease while 3-NP replicates Huntington's disease phenotype in experimental animals. The cerebral hsp70 increase did not alter field potential amplitude of the slices but partially protected them against rotenone-induced neurotoxicity. Similarly, induction of hsp70 had also a partial neuroprotective effect on the neurotoxicity caused by 3-NP on striatal field potential. Since rotenone and 3-NP treatments mimic the mitochondrial impairment and oxidative stress that contribute to development of Parkinson's disease and Huntington's disease, these data suggest that induction of hsp70 might represent a possible neuroprotective mechanism against the pathophysiological chain of events implicated in these neurodegenerative disorders.

It has been suggested that the GAbAergic striatonigral projection may form part of the efferent pathway responsible for the expression of dopamine-related oral behaviour. Consistent with this suggestion are reports that bilateral injection of the GABA agonist muscimol can produce stereotyped gnawing and biting. We report here two experiments on this effect: (1) A dose of the dopamine receptor blocker haloperidol (0.4 mg/kg), which effectively antagonised oral stereotypy induced by systemically administered apomorphine or intranigral carbachol, had no effect on either the latency or the intensity of the gnawing produced by intranigral muscimol (1 nM); (2) large lesions involving the superior colliculus which effectively suppressed the oral stereotypy induced by 8 mg/kg apomorphine completely abolished the gnawing induced by intranigral injection of muscimol. Collicular lesions suppressed both the gnawing which occurred spontaneously and that elicited by a perioral probe. These findings are consistent with the view that the substantia nigra is a relay station between the caudate nucleus and the superior colliculus in an efferent pathway mediating dopamine-related oral behaviour. In addition, they raise the possibility that such behaviour is produced by the sensitisation of a collicular-mediated perioral reflex.

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