(378) Optogenetic inhibition sensory neurons mediating bladder nociception

Mickle, Aaron D.; Samineni, Vijay K.; Park, S.; Shin, Grace; Pullen, Melanie Y.; Grajales-Reyes, José G.; Lake, Thomas P.; Rogers, Joseph G.; Gereau, Robert W.

doi:10.1016/j.jpain.2016.01.285

Cited by 1 publication

(2 citation statements)

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“…This can be quantified physiologically, and anatomically at the ultrastructural level or by counting dendritic spines on excitatory pyramidal cells of the cerebral cortex. Importantly, the extent and direction of experience-induced synaptic changes in cortical areas correlate with time windows of neuronal as well as endocrine development Elston et al, 2009). Repeated brief maternal separation in newborn rats before a stress hyporesponsive period of the hypothalamic-pituitary-adrenal axis significantly reduces dendritic spine density in layer II/III pyramidal neurons of the prefrontal cortex (Fig.…”

Section: Neurobiological Signatures Of Windows Of Vulnerabilitymentioning

confidence: 95%

“…Gene microarrays were used to look for differences in transcript expression in the amygdala (Sabatini et al, 2007). This structure is established as having a clear role in social, anxious, and depressive behaviors in the nonhuman primate (Baron-Cohen et al, 2000;Emery et al, 2001;Drevets et al, 2002;Amaral, 2003;Bauman et al, 2004;Etkin et al, 2004;Lorberbaum et al, 2004). Comparing gene expression in the same monkeys in which behavior was carefully characterized throughout development enables a genes-to-behavior approach to directly examine linkages (Nelson et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Social Origins of Developmental Risk for Mental and Physical Illness

et al. 2017

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Adversity in early childhood exerts an enduring impact on mental and physical health, academic achievement, lifetime productivity, and the probability of interfacing with the criminal justice system. More science is needed to understand how the brain is affected by early life stress (ELS), which produces excessive activation of stress response systems broadly throughout the child's body (toxic stress). Our research examines the importance of sex, timing and type of stress exposure, and critical periods for intervention in various brain systems across species. Neglect (the absence of sensitive and responsive caregiving) or disrupted interaction with offspring induces robust, lasting consequences in mice, monkeys, and humans. Complementary assessment of internalizing disorders and brain imaging in children suggests that early adversity can interfere with white matter development in key brain regions, which may increase risk for emotional difficulties in the long term. Neural circuits that are most plastic during ELS exposure in monkeys sustain the greatest change in gene expression, offering a mechanism whereby stress timing might lead to markedly different long-term behaviors. Rodent models reveal that disrupted maternal-infant interactions yield metabolic and behavioral outcomes often differing by sex. Moreover, ELS may further accelerate or delay critical periods of development, which reflect GABA circuit maturation, BDNF, and circadian Clock genes. Such factors are associated with several mental disorders and may contribute to a premature closure of plastic windows for intervention following ELS. Together, complementary cross-species studies are elucidating principles of adaptation to adversity in early childhood with molecular, cellular, and whole organism resolution.

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Section: Neurobiological Signatures Of Windows Of Vulnerabilitymentioning

confidence: 95%