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Mice with previously implanted electrodes for recording the cortical electroencephalogram and electromyograms underwent all-day baseline videopolysomnography with a 12/12 light cycle, after which animals received doses of 24 or 48 mg/kg of the neurotoxin precursor MPTP (1-methyl-4-phenyl-1.2.3.7-tetrahydropyridine) or physiological saline (controls) and recording was continued for 14 days. At the end of the experiments, morphological monitoring of the extent of lesions to the dopaminergic system was performed. Increases in motor activity and the total duration of waking during the dark part of the night were seen after administration of MPTP, as compared with controls. These changes were accompanied by decreases in the durations of rapid and (at the level of a tendency) slow-wave sleep. These changes were apparent by recording day 7 and were significant by day 14; they were more marked after treatment at a dose of 48 mg/kg than after the smaller dose. No changes were seen during the light period of the day. Morphological monitoring demonstrated a 70% reduction in the number of dopamine-containing neurons in the compact zone of the substantia nigra after administration of MPTP (48 mg/kg) and a 35% drop after MPTP (24 mg/kg).

One of the most important functions of the neuroendocrine system is that of regulating reproduction, particularly the inhibition of prolactin secretion in the hypophysis by dopamine (DA) synthesized in the arcuate nucleus. Apart from DA, noradrenaline (NA) also has a role in controlling prolactin secretion. While the role of DA in this regulation is known, that of NA remains incompletely understood. Previous studies have suggested that in conditions of functional insufficiency of the dopaminergic system, NA suppresses compensatory DA synthesis in the dopamine-producing neurons of the arcuate nucleus. The aim of the present work was to clarify the role of NA in the control of dopamine-producing neurons in the arcuate nucleus. This was addressed using two pharmacological models: 1) exclusion of dopaminergic and noradrenergic neurons and/or their axons in the arcuate nucleus, and b) exclusion of dopaminergic neurons only, to allow the role of the noradrenergic component to the catecholaminergic regulation of prolactin secretion to be assessed. In conditions of functional insufficiency of dopaminergic neurons, retention of the noradrenergic innervation of the arcuate nucleus was found to lead to decreased expression of the first enzyme in DA synthesis – tyrosine hydroxylase – and exacerbation of DA deficiency. This is evidence for noradrenergic inhibitory control of the expression of tyrosine hydroxylase in arcuate nucleus neurons.