Dopamine/dopaminergic system mechanisms

Bruxism mainly occurs in stage 2 sleep and REM sleep (Bader et ah, 1977). A relationship to stress and anxiety has been suggested, but the disorder can be chronic without apparent association with stress (Faulkner, 1990 Pierce et ah, 1995). It has been suggested that the central dopaminergic system may be involved in the modulation of sleep bruxism (Lobbezoo et al., 1997). Case reports indicate that bruxism can be induced by the SSRI paroxetine (Romanelli et al., 1996). The mechanism remains unclear possibilities include sleep disturbance, serotonergic-mediated inhibition of dopamine manifesting as akathisia, and SSRI-induced anxiety. SSRI-induced bruxism may respond to therapy with buspirone (Ellison et al., 1993). 

Reserpine, used as a folk medicine in India, was found to have antipsychotic properties at about the same time as CPZ. Both agents affected the dopaminergic system, albeit in different ways, but the functional results were similar (i.e., lowering dopamine activity). This phenomenon has continued to be an important factor in hypotheses about the mechanism of action of these drugs and for biological theories about the pathophysiology of psychotic disorders. 

Considerable data has been accumulated over the past eight years showing that 5-HTg receptors can modulate the release of dopamine in terminal response of the mesolimbic areas. The mesolimbic dopaminergic system has been involved in the mediation of locomotor activity and has been shown to modulate reward mechanisms. Acute but also chronic in vivo administration of ondansetron failed to modify dopaminergic neuronal activity [140, 141], but an attenuation of dopamine release was evident when dopaminergic pathways were activated first. Thus, 5-HTg receptor antagonists partially reversed the activation of the dopaminergic mesolimbic pathway induced by stress procedures [142], by DiMe-C7... 

Indirect mechanisms Nicotine has indirect effects on monoamine systems. A considerable amount of research has examined the relationships between nicotine and dopamine activity in the brain, in light of dopamine s role in reinforcement and nicotine s addictive properties. Nicotine increases dopamine turnover in the striatum and cerebral cortex (Clarke and Reuben 1996 Tani et al. 1997 Nanri et al. 1998). It also increases burst activity in dopamine neurons of the ventral tegmental area (VTA), a primary source of dopamine to the forebrain (Nisell et al. 1995 Fisher et al. 1998). Such a firing pattern in the VTA is associated with processes of reinforcement, learning, and cognitive activity. Nicotine actions on dopaminergic neurons occur at both somatodendritic sites and synaptic terminals. Further, both systemic nicotine and direct administration into the VTA increase dopamine release in the nucleus ac-... 

Opioids have been shown to increase the release of dopamine in the nucleus accumbens but they also subserve reinforcement in animals by a non-dopaminergic mechanism (Di Chiara 8c North,1992 Koob, 1992). Physiologically the opioid system appears to be largely involved in the con-sumatory rewards of feeding, drinking, sexual and maternal behaviour (Koob, 1992 Di Chiara 8c North, 1992) and certain types of social behaviour (Panksepp, 1981 Bolles 8c Fanselow, 1982). 

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