Abstract
Early life adversities leave long-lasting structural and functional consequences on the brain, which may persist later in life. Dopamine is a neurotransmitter that is extremely important in mood and motor control. The aim of this study was to investigate the effect of maternal deprivation during the ninth postnatal day on the volume of dopaminergic nuclei and the number of dopaminergic neurons in adolescence and adulthood. Maternally deprived and control Wistar rats were sacrificed on postnatal day 35 or 60, and the dopaminergic neurons were stained in coronal histological sections of ventral midbrain with the tyrosine hydroxylase antibody. The volume of dopaminergic nuclei and the number of dopaminergic neurons in the substantia nigra (SN) and ventral tegmental area (VTA) were analyzed in three representative coordinates. Maternal deprivation caused weight loss on postnatal day 21 (weaning) and corticosterone blood level elevation on postnatal days 35 and 60 in stressed compared to control rats. In maternally deprived animals, the volumes of SN and VTA were increased compared to the controls. This increase was accompanied by an elevation in the number of dopaminergic neurons in both nuclei. Altogether, based on somatic and corticosterone level measurements, maternal deprivation represents a substantial adversity, and the phenotype it causes in adulthood includes increased volume of the dopaminergic nuclei and number of dopaminergic neurons.
Highlights
Development of the nervous system plays a pivotal role in the establishment of healthy adult brain, while stressful events in critical neurodevelopmental periods may cause abberations and maladaptive phenotypes, such as schizophrenia and other neurocognitive disorders (Murray et al, 1992; Waddington et al, 1997)
Early life stress caused by maternal deprivation of pups during a critical period of development is known as the stress hyporesponsive period (SHRP) (Chocyk et al, 2011)
Our results have shown an increase in the density of tyrosine hydroxylase (TH) + neurons on P60 in both the examined stereotaxic range of substantia nigra pars reticulata (SNpr) as well as substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA) in the anterior/posterior (A/P) coordinate
Summary
Development of the nervous system plays a pivotal role in the establishment of healthy adult brain, while stressful events in critical neurodevelopmental periods may cause abberations and maladaptive phenotypes, such as schizophrenia and other neurocognitive disorders (Murray et al, 1992; Waddington et al, 1997). Ellenbroek and Cools (2002) have shown that early maternal deprivation induces schizophrenia-like phenotypes. Early life stress caused by maternal deprivation of pups during a critical period of development is known as the stress hyporesponsive period (SHRP) (Chocyk et al, 2011). The SHRP for rats occurs between postnatal days 4 and 14, and it is a period of time during which pup–mother interactions, such as licking, grooming, and arched-back nursing, suppress the basal and stress-induced levels of glucocorticoids (de Kloet et al, 2005). It has been previously shown that early maternal deprivation can disrupt normal salience in adult rats and that this phenotype is dependent on the day of deprivation (Ellenbroek and Cools, 2002). Prepulse inhibition was disrupted when deprivation took place on postnatal day 9 (P9), but it remained intact when the rats were deprived on P13 (Ellenbroek et al, 1998; Ellenbroek and Cools, 2002), meaning that prepulse inhibition was most severely affected when deprivation took place around P6–P9, right in the middle of SHRP (Ellenbroek and Cools, 2002)
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