Effect of environmental enrichment on fearful behavior and gastrin‐releasing peptide receptor expression in the amygdala of prenatal stressed rats

Abstract

Prenatal stressed offspring exhibit more fearful behavior in behavioral tests, which can be reversed by environmental enrichment (EE). However, the physiological basis of these phenomena remains unclear. Previous studies revealed that abnormal fearful behavior of prenatally stressed offspring may be a consequence of increased activities of CRFergic systems (corticotropin-releasing factor and its receptors) in the amygdala. Gastrin-releasing peptide receptors (GRPR) also have an important role in regulating amygdala-dependent, fear-related learning. The aim of this study was to examine weather prenatal stress and EE can affect the expression of GRPR in the amygdala. We reported here that prenatal chronic stress (subjected to immobilization and bright light stress for 45 min three times per day) caused increased fearfulness in defensive withdrawal test but had no effect on the expression of GRPR in the amygdala. However, enriched environment housing treatment on postnatal days 21-60 can dramatically increase the expression of GRPR in amygdala and reduce fearfulness in the defensive withdrawal test. Our results demonstrate for the first time that EE can modify the expression of GRPR in the amygdala, which might contribute to our understanding of the physiological effects of environmental enrichment.

Neonatal amygdala lesions alter mother–infant interactions in rhesus monkeys living in a species‐typical social environment

“…Indeed, the subtle behavioral changes described here differ greatly from the reported impact of neonatal amygdalectomy in previous studies carried out in a more restricted social environments, reducing the possibilities that others in the social environment could compensate for social deficits in the lesioned animals (Bachevalier, ; Bauman et al, ; Kling & Green, ; Prather et al, ; Thompson, ). Evidence from the rodent literature has already demonstrated the significant and positive impact of enriched environments have on cognitive functioning in normal, neonatal and adult ischemic, and prenatally stressed animals (Pereira et al, ; Sozda et al, ; Qian et al, ). Therefore, it is possible that the species‐typical environment of a large multigenerational age‐graded social group provides enhanced stimulation that compensates for the effects of early amygdala damage on social cognition.…”

Impaired extinction of fear conditioning after REM deprivation is magnified by rearing in an enriched environment

“…The pronounced deficit in extinction observed in EE-reared animals may have been due to changes in brain structures responsible for the acquisition and extinction of fear conditioning such as the amygdala and PFC. Relevant effects of EE exposure on the amygdala include alterations in expression of corticotropin releasing factor receptors (Sztainberg, Kuperman, Tsoory, Lebow, & Chen, 2010), increased proliferation of progenitor cells and suppressed apoptosis (Okuda et al, 2009), increased brain-derived neurotropic factor levels (Segovia, Del Arco, de Blas, Garrido, & Mora, 2008), and increased gastrin-releasing peptide receptors, which are involved in fear learning (Qian, Zhou, Pan, Liu, & Wang, 2008). EE exposure also produces alterations in the PFC such as increased energy metabolism as assessed by cytochrome c oxidase histochemistry (Sampedro-Piquero et al, 2013), increased FosB immunostaining (Lehmann & Herkenham, 2011), and increased concentrations of serotonin (Brenes, Rodriguez, & Fornaguera, 2008).…”

Adolescent Binge Drinking Alters Adult Brain Neurotransmitter Gene Expression, Behavior, Brain Regional Volumes, and Neurochemistry in Mice

“…GRPR is enriched in amygdala and GRPR deficient mice show enhanced fear conditioning with normal spatial learning and no anxiety-like behavior in the water maze and elevated plus maze, respectively (Shumyatsky et al, 2002). Environmental enrichment during adolescence increases GRPR expression and reduces fearfulness (Qian et al, 2008), suggesting that environmental amygdala plasticity during adolescence is in part reflected in GRPR expression and lifelong sensitivity to amygdala fear conditioning. COMT polymorphisms have been implicated in many disorders including addiction (Enoch, 2006), schizophrenia (Tan et al, 2007), aggression (Volavka et al, 2004), and Alzheimer's disease (Serretti et al, 2007).…”