Clinical studies indicate that early life adversity increases the risk for psychiatric disorders, like e.g., depression, schizophrenia and addiction. Moreover, behavioral data imply that early life stress has enduring impact on dopaminergic neurotransmission. The mechanisms engaged in the above effects are poorly understood. Our recent study has revealed that maternal separation (MS) in rats, a model of early life stress, affects the number of midbrain neurons expressing tyrosine hydroxylase (TH), a rate-limiting enzyme in dopamine synthesis. In the present work, we investigated the impact of MS on TH expression in brain regions containing dopaminergic axonal terminals, i.e., in the prelimbic cortex (PLC), dorsal striatum (caudate-putamen, CPu) and nucleus accumbens (NAc) of juvenile, adolescent and adult rats of both sexes. Specifically, we applied immunohistochemical method and quantified the length density of TH-immunoreactive (IR) terminals in the PLC (by stereological estimation) and TH expression in the CPu and NAc, using optical densitometry. It was found that MS affected the length density of TH-IR terminals in the PLC in males only. MS increased the length density of TH-IR terminals (in layers I and II-VI) in adolescent male rats, however the opposite effect (a decrease) was observed in a layer I of the PLC in adults. Optical densitometry revealed that, in juvenile male rats, MS reduced TH expression in the CPu, NAc shell and core. Interestingly, in juvenile females an increase in TH level was observed as an effect of MS. In adolescence, MS did not affect optical density of TH immunoractivity in the CPu and NAc. Though, in adulthood, MS selectively increased TH expression in the NAc core in males only. Our results indicate that early life stress, sex- and age-dependently, disturbs density of dopaminergic innervation of the PLC, CPu and NAc. Moreover, they imply how early adversity affects synaptic plasticity and evokes dysfunction of dopaminergic systems.
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