Some Behavioural Interactions between 5-Hydroxytryptamine and Dopamine

Selective adjustment of the speed of internal clock and memory processes.

“…To date, the notion of reciprocally antagonistic neurotransmitter systems has faired well in accounting for the mechanisms of various drug interactions (e.g., McGeer, Grewaal, & McGeer, 1974) and time-dependent variations in aversively motivated behaviors (e.g., Anisman, 1975). In regard to neurochemical changes produced by footshock stress, the role of serotonin as the opponent to dopamine action has been implicated by a number of studies (e.g., Curzon, 1981;Gabay, 198.1;Harvey & Simansky, 1981). It remains to be determined if this opponent relation between serotonin and dopamine is important for determining clock speed and variability, but the observation of an opponent process in time perception seems worth emphasizing.…”

Pharmacological Evidence that Serotonergic Stimulation of Prolactin Secretion is Mediated via the Dorsal Raphe Nucleus

“…Ad ministration of saline also caused a significant increase in plasma prolactin at 30 min which we believe to be an acute effect from the injection stress. Interestingly, PCA prevent ed this acute rise in prolactin secretion and induced the later elevation which was significantly higher than control levels at I h. The prevention of the acute rise in prolactin in the PCA-treated group may be due to an initial amphetamine like effect of PCA on dopamine turnover [10,11,15,21,37,38,40], Experiment 2. The increase in serum prolactin concen trations following injection of PCA was dose-dependent as shown in table II.…”

“…In contrast, median raphe lesions did not prevent the effect of PCA on plasma prolactin levels. In summary, these data support the hypothesis that release of serotonin increases prolactin secretion, in addition, these data suggest that serotonergic neurons in the dorsal raphe nucleus are part of a neural pathway which can mediate increases in prolactin se cretion.There is considerable pharmacological evidence sup porting the hypothesis that activation of the serotonergic pathways in the central nervous system results in increased prolactin secretion [1,[6][7][8][9][25][26][27][28], The majority of central serotonergic neurons originate in the dorsal and median raphe nuclei in the hindbrain [2][3][4][5]12] and project rostrally, innervating hypothalamic and rostral limbic and cortical areas [2,33,36.42.43].Since serotonin (5-HT) does not cross the blood-brain barrier [14], various pharmacological agents have been uti lized to examine the regulatory functions of the serotoner gic projections.DT-p-chloroamphetamine (PCA) is a drug which affects catecholamine neurotransmission [11,15,21,37,38,40] and has a biphasic effect on brain serotonin. In the initial few hours it causes a substantial release [18,30,41] followed by long-term inhibition of tryptophan hydroxylase, serotonin uptake, monoamine oxidase and depletion of serotonin stores [37,38].…”

Modulatory role of serotonin in neural information processing: Implications for human psychopathology.

“…The role of 5-HT in LA is controversial because manipulations of 5-HT, when considered alone, have yielded inconsistent results. For example, although facilitation of 5-HT functional activity is primarily inhibitory in spontaneous LA (Applegate, 1980; Gerson & Baldessarini, 1980; Jones et al, 1981), very high levels of activity are associated with a state of hyperactivity called the serotonin syndrome (Curzon, 1981; Gerson & Baldessarini, 1980; Green, 1981; Jacobs, 1986; Ogren, 1985b; Siever, Guttmacher, & Murphy, 1984). These disparate results seen with 5-HT activation may be due, in part, to the effects of 5-HT on different neurobiologic systems.…”

“…The serotonin syndrome is thought to result primarily from excitation of the descending 5-HT raphe fibers (Gerson & Baldessarini, 1980; Ogren, 1985b). Moreover, the forward locomotion (and partially the backward locomotion) component of this syndrome is due to the action of central dopaminergic neurons (Curzon, 1981; Dickinson, Andrews, & Curzon, 1984; Ogren, 1985b). On the other hand, inhibition of spontaneous LA is achieved by activation of ascending 5-HT pathways, most probably those arising from the dorsal raphe nucleus (DR; Applegate, 1980; Gerson & Baldessarini, 1980; Jones et al, 1981).…”