Effects of Neonatal Methamphetamine and Stress on Brain Monoamines and Corticosterone in Preweanling Rats

Abstract

Neonatal exposure to methamphetamine (MA) and developmental chronic stress significantly alter neurodevelopmental profiles that show a variety of long-term physiological and behavioral effects. In the current experiment, Sprague-Dawley rats were exposed to one of two housing conditions along with MA. Rats were given 0 (saline), 5, or 7.5 mg/kg MA, four times per day from postnatal day (P)11 to 15 or P11 to 20. Half of the litters were reared in cages with standard bedding and half with no bedding. Separate litters were assessed at P15 or P20 for organ weights (adrenals, spleen, thymus); corticosterone; and monoamine assessments (dopamine, serotonin, norepinephrine) and their metabolites within the neostriatum, hippocampus, and prefrontal cortex. Findings show neonatal MA altered mono-amines, corticosterone, and organ characteristics alone, and as a function of developmental age and stress compared with controls. These alterations may in part be responsible for MA and early life stress-induced long-term learning and memory deficits.

Dopaminergic cell protection and alleviation of neuropsychiatric disease symptoms by VMAT2 expression through the class I HDAC inhibitor TC‐H 106

“…Many previous studies have reported the relationship between cortisol and dopamine, and Pruessner et al 53 reported that cortisol‐dopamine plays an important role in the relationship between mother and infant. And some previous reports provide direct evidence that prenatal or early stress induces the cortisol elevation and monoaminergic dysregulation including dopamine system, disrupting neurodevelopment via neuroendocrine dysfunction 54‐57 . Our findings of the behavioral experiments clearly demonstrated that pretreatment with TC H‐106 suppressed the ADHD‐like behaviors of Corti.Pups, indicating the possible involvement of VMAT2 in restoring dopaminergic regulation during the neurodevelopment of Corti.Pups.…”

“…And some previous reports provide direct evidence that prenatal or early stress induces the cortisol elevation and monoaminergic dysregulation including dopamine system, disrupting neurodevelopment via neuroendocrine dysfunction. [54][55][56][57] Our findings of the be- The prefrontal cortex plays an important role in regulating attention and impulsivity; hence, dysregulation of endogenous neurochemicals and neuromodulators are seemingly correlated with the pathogenesis of neuropsychiatric disorders Dysregulation of catecholamine neurotransmitters such as dopamine, norepinephrine, and serotonin in the prefrontal cortex has been reported as an important trigger in the pathogenesis of ADHD. 6 Dysregulation of amines is frequently observed not only in the prefrontal cortex but also in the midbrain region, including the cerebral cortex, cerebellum, and basal ganglia.…”

Postnatal Fluoxetine Treatment Alters Perineuronal Net Formation and Maintenance in the Hippocampus

“…Exposure to juvenile stress is linked to a decrease in the intensity of PNN staining in the CA1 hippocampal subfield, the dorsal anterior Cg cortex, the IL cortex and the motor cortex, immediately following the cessation of the stress ( Ueno et al, 2018 ). Interestingly, MS, LNB, MIA and juvenile stress are all reported to evoke a perturbation of serotonergic signaling ( Benekareddy et al, 2010 ; Luo et al, 2015 ; Goeden et al, 2016 ; Jablonski et al, 2017 ). These results raise the intriguing possibility that both a perturbation of serotonergic signaling, as well as an altered trajectory of PNN development in key limbic circuits, may be associated with the development of anxiogenic and depressive-like behavioral phenotypes noted in adulthood in these models of early adversity.…”

Postnatal fluoxetine treatment alters perineuronal net formation and maintenance in the hippocampus

“…Exposure to juvenile stress is linked to a decrease in the intensity of PNN staining in the CA1 hippocampal subfield, the dorsal anterior cingulate cortex, the infralimbic cortex and the motor cortex, immediately following the cessation of the stress (Ueno et al, 2018). Interestingly, MS, LNB, MIA and juvenile stress are all reported to evoke a perturbation of serotonergic signaling (Benekareddy et al, 2010; Goeden et al, 2016; Jablonski et al, 2017; Luo et al, 2015). These results raise the intriguing possibility that both a perturbation of serotonergic signaling, as well as an altered trajectory of PNN development in key limbic circuits, may be associated with the development of anxiogenic and depressive-like behavioral phenotypes noted in adulthood in these models of early adversity.…”