AnnotationVulnerability of developing brain not explained by cell number/cell size hypothesis
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Cited by (24)
Prenatal and postnatal cocaine exposure enhances the induction and expression of locomotor sensitization to cocaine in rats
2020, Reproductive ToxicologyCitation Excerpt :The above data indicate that prenatal exposure to cocaine in both humans and animals induces long-term physiological dysregulation and neural alteration in the reward-related circuitry of offspring [19,20]. Pioneering studies have described that the development of the central nervous system is more vulnerable to different types of insults (malnutrition, drugs, toxins, etc.) during the period of the fastest rate of brain development [21,22]—known as a vulnerable period [23,24]. Insults, during this vulnerable period, produce permanent and irreversible alterations in brain development [25].
Developmental cigarette smoke exposure: Hippocampus proteome and metabolome profiles in low birth weight pups
2014, ToxicologyCitation Excerpt :However in the mouse, both structural and functional development continues postnatally with structural maturation not complete until between 2 and 3 weeks of age (Arnold and Trojanowski, 1996a; Bayer, 1980a,b; Grove and Tole, 1999; Tole et al., 1997; Tole and Grove, 2001; Woodhams et al., 1989; Woodhams and Webb, 1989). The postnatal development period, critical for the mouse to establish neural differentiation and gene expression patterns, corresponds to the third trimester of human fetal brain growth (Dobbing, 1981; Dobbing and Sands, 1981; Morgane et al., 2002; Romijn et al., 1991). Cigarette smoke is a strong oxidizing agent that induces a state of systemic oxidative stress.
Mechanical-tactile stimulation (MTS) intervention in a neonatal stress model alters adult adipose tissue deposition and prevents hyperinsulinemia in male rats
2013, Early Human DevelopmentCitation Excerpt :Neonatal rats (postnatal days 5–10) are developmentally less mature than human infants in several ways. For example, neurodevelopment at birth in neonatal rats is estimated to be similar to human infants in the third trimester [16–18]. The neonatal stress model attempts to evaluate the potential impact stressors like those encountered in the NICU might have on adipose tissue deposition in a growing neonatal animal.
Delayed increase of astrocytic aquaporin 4 after juvenile traumatic brain injury: Possible role in edema resolution?
2012, NeuroscienceCitation Excerpt :Two mechanisms may account for these age-related differences: (i) increased post-injury cerebral blood flow in the young and (ii) developmental and mechanical properties of the brain and skull (Kochanek, 2006). Experimental studies suggest that post-traumatic edema in the immature brain may also be related to enhanced diffusion of excitotoxic neurotransmitters, an intensified inflammatory response (Kochanek, 2006), and higher brain water content in the young rat compared to the adult rat (Dobbing and Sands, 1981). Developmental differences in water homeostasis between children and adults may also account for the observed greater risk of post-traumatic edema in the younger population.
Estimation of neuronal numbers in rat hippocampus following neonatal amphetamine exposure: A stereology study
2008, Neurotoxicology and TeratologyCitation Excerpt :One important stage of central nervous system development is the brain growth spurt. During this stage, as defined by Dobbing and Sands [13], the brain undergoes a rapid, transient period of growth by increasing the rate of proliferation [14], which renders the developing brain extremely sensitive to insult from teratogens [12,18,19,39]. While neurodegeneration during the brain growth spurt is important for the elimination of non-functioning or redundant neurons [32], drugs such as alcohol [30,41] and phencyclidine (PCP) [29] have been shown to cause excessive levels of cell loss within different regions of the developing brain.