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in response to THC has also been related to an increase of slow-wave activity on EEG (Domino 1981). In vitro THC (1-100 nM) inhibited muscarinic receptor binding, which also ocurred with two nonpsychoactive cannabinoids (cannabidiol and cannabinol) (Ali et al. 1991). However, these effects were not observed in vivo. Monoamines

Cannabinoid agonists produce dose-related activation of meso-prefrontal dopaminergic transmission, which depends upon the CB1 receptor (Diana et al. 1998a). Conversely, withdrawal from chronic cannabinoid administration produces a reduction in mesolimbic dopaminergic transmission. Although THC stimulates the presynaptic activity of mesolimbic dopaminergic neurons, there is a decrease in postsynaptic sensitivity (Bonnin et al. 1993). Further, this effect is modulated by estrogen, but not estradiol. THC increases the firing rate and burst-pattern firing in the ventral tegmental area and substantia nigra, although the ventral tegmental area is more sensitive in this respect (French et al. 1997). In contrast, cannabidiol failed to have this effect. In vivo microdialysis, on the other hand, showed that THC has no effect on extracellular dopamine or 5-HT concentrations in the striatum or nucleus accumbens (Castaneda et al. 1991). However, this study also failed to show behavioral differences between drug and vehicle groups. Cannabinoids also induce increases in norepinephrine, but not 5-HT turnover in the prefrontal cortex (Jentsch et al. 1997). Opioids

Cannabinoids are known to interact with opioid systems. This is particularly relevant to their analgesic effects and is discussed at length in chapter 8.


Cannabis compounds interact with the endocrine system. THC reduces testicular production of testosterone, even though it enhances respon-

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