The effects of food reward on circadian system function were investigated in the hypothalamic nuclei, prefrontal cortex and liver. Food rewards of small hedonic and caloric value were provided for 16 days 3 h after light phase onset to male Wistar rats. The daily pattern of locomotor activity was monitored. Gene expression profiling performed in the dorsomedial hypothalamus (DMH) and liver at the time of reward delivery indicated transcriptional factors egr1 and npas2 as possible mediators of food reward effects. Candidate genes were measured in the suprachiasmatic nuclei (SCN), DMH, arcuate nucleus (ARC), prefrontal cortex (PFC) and liver along with per2 expression. A daily pattern in glycemia and per2 expression in the SCN was emphasized by food reward. The expression of egr1 was rhythmic in the SCN, DMH, PFC and liver and food reward
weakened or diminished this rhythm. The expression of npas2 was rhythmic in all tissues except for the PFC where food reward induced rhythm in npas2 expression. Food reward induced npas2 and egr1 expression in the DMH at the time of reward delivery. We suppose that the DMH and PFC participate in the adjustment of the circadian system to utilize food reward-induced input via egr1 and npas2 expression.
Catecholamine (dopamine, norepinephrine and epinephrine) synthesizing neurons are widely distributed in the brain, sympathetic ganglia and throughout peripheral organs. Results of several recent experiments clearly suggest that many of these neurons can also contain 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), a derivate of dopamine. However, direct proof of salsolinol synthesis in those neurons is still missing. The data obtained with administration of exogenous salsolinol strongly indicate that it may play an important role in catecholaminergic regulatory processes, such as the regulation of prolactin release and/or neuronal transmission in sympathetic ganglia. Several recent data have also indicated a relationship between salsolinol or its metabolites and the etiology of Parkinson's disease or neuropathology of chronic alcoholism. These seemingly different roles of salsolinol will be discussed separately, but some common features will also be highlighted. Based on all of the discussed data the existence of a “salsolinolergic” system using salsolinol as a neuromodulator, which may be present in catecholamine synthesizing neurons, is postulated.