No abstract

Observational methods and the recording of nonspecific jaw movements or masticatory muscle activity have been used to evaluate oral parafunctional movements in animal models of bruxism. In this study, we have used a new approach in which the non-functional masticatory activity in the rat was assessed by the measurement of incisal attrition, with the aim of investigating the role of diverse factors involved in the etiology of bruxism. We quantified the attrition rate weekly by making superficial notches in the lower incisors and measuring the distances to the incisor edges. Repeated stimulation of the dopaminergic system with apomorphine led to an enhancement of the non-functional masticatory activity (p< 0.0001). The severity of the apomorphine-induced oral behavior was positively correlated (r(s) = 0.69, p < 0.01) with an increase in the incisal attrition rate (20.9%, p < 0.0001). Apomorphine-induced non-functional masticatory activity was strongly enhanced by the placement of an acrylic cap on both lower incisors (306%, p < 0.0001), but not by the cutting of a lower incisor. Repeated cocaine administration also increased the attrition rate (22.5%, p < 0.0001). However, neither chronic blockade of dopaminergic receptors with haloperidol, nor its withdrawal, modified attrition. In addition, since emotional disturbances are considered to be causal factors of bruxism, we tested whether experimental stress might accelerate tooth wear. Exposure to two different chronic stress regimes did not induce significant changes in incisal attrition. Moreover, exposure to chronic stress after the withdrawal of chronic haloperidol treatment did not alter attrition either. These results partially support the role of the central dopaminergic system in bruxism and suggest that stress, in general, may not be a relevant factor in tooth wear.

No abstract

The sensitivity of α₂-adrenoceptors which regulate synthesis and release of noradrenaline was investigated in hippocampus, parietal cortex, and hypothalamus of rats treated with clorgyline. After administering a DOPA decarboxylase inhibitor, the in vivo tyrosine hydroxylase activity and the noradrenaline content were evaluated. Acute and chronic treatment with clorgyline led to both increases of noradrenaline levels and decreases of tyrosine hydroxylase activity, determined as the accumulation of DOPA. Whereas the α₂-adrenoceptor agonist clonidine induced a similar reduction in tyrosine hydroxylase activity in the group subjected to the acute treatment and in the control group, it failed to do so after chronic clorgyline treatment. In hippocampal and cortical synaptosomes, a reduction in the sensitivity of α₂-adrenoceptors which regulate [³H]noradrenaline release, reflected by the shift to the right of the concentration-effect curves for oxymetazoline, was also found after the repeated treatment. These results indicate a desensitization of α₂-adrenoceptors after chronic treatment with clorgyline.

No abstract