Prenatal restraint stress impairs learning and memory and hippocampal PKCbeta1 expression and translocation in offspring rats

Wu, Jie; Song, Tianbao; Li, Yuan-Jie; He, Kan-Sheng; Ge, Liang; Wang, Lirong

doi:10.1016/j.brainres.2007.01.024

Cited by 86 publications

(54 citation statements)

References 40 publications

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“…Likewise, in the learned helplessness rat model, repeated inescapable shock significantly attenuated PLC activity and PLCγ 1 and PLCβ 1 protein and mRNA levels, both in the frontal cortex and hippocampus [70]. Moreover, PKCβI expression and translocation were reduced in the hippocampus of adult rats exposed to prenatal stress [71]. In other chronic stress paradigms, namely restrained stress and rats subjected to 4 weeks of forced swimming, decreases of hippocampal PKCα mRNA expression or PKC activity were found [72,73].…”

Section: Depression-like Behaviorsmentioning

confidence: 99%

A Role for the PKC Signaling System in the Pathophysiology and Treatment of Mood Disorders: Involvement of a Functional Imbalance?

et al. 2011

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Mood disorders, such as bipolar and major depressive disorders, are frequent, severe, and often disabling neuropsychiatric diseases affecting millions of individuals worldwide. Available mood stabilizers and antidepressants remain unsatisfactory because of their delayed and partial therapeutic efficacy. Therefore, the development of targeted therapies, working more rapidly and being fully effective, is urgently needed. In this context, the protein kinase C (PKC) signaling system, which regulates multiple neuronal processes implicated in mood regulation, can constitute a novel therapeutic target. This paper reviews the currently available knowledge regarding the role of the PKC signaling pathway in the pathophysiology of mood disorders and the therapeutic potential of PKC modulators. Current antidepressants and mood stabilizers have been shown to modulate the PKC pathway, and the inhibition of this intracellular signaling cascade results in antimanic-like properties in animal models. Disrupted PKC activity has been found both in postmortem brains and platelet from patients with mood disorders. Finally, the PKC inhibitor tamoxifen has recently demonstrated potent antimanic properties in several clinical trials. Overall, emerging data from preclinical and clinical research suggest an imbalance of the PKC signaling system in mood disorders. Thus, PKC may be a critical molecular target for the development of innovative therapeutics.

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Section: Depression-like Behaviorsmentioning

confidence: 99%

A Role for the PKC Signaling System in the Pathophysiology and Treatment of Mood Disorders: Involvement of a Functional Imbalance?

et al. 2011

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“…Prenatally stressed rats show depressive-like behaviors including increased immobility in the Porsolt swim test (Alonso et al, 1991;Frye and Wawrzycki, 2003) and increased anxiety in the elevated plus maze (Fride and Weinstock, 1988). Spatial learning deficits are also observed in adolescent mice (Bustamante et al, 2010) and adult rats (Hosseini-Sharifabad and Hadinedoushan, 2007;Wu et al, 2007) of prenatally restrained mothers.…”

Section: Effects Of Maternal Stressmentioning

confidence: 99%

Maternal influences on epigenetic programming of the developing hypothalamic‐pituitary‐adrenal axis

Grace

Kim

Rogers

2011

Birth Defects Research

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Parental and environmental factors during the prenatal and postnatal periods permanently affect the physiology and metabolism of offspring, potentially increasing disease risk later in life. Underlying mechanisms are being elucidated, and effects on a number of organs and metabolic pathways are likely involved. In this review, we consider effects on the developing hypothalamic-pituitary-adrenal (HPA) axis, which may represent a common pathway for developmental programming. The focus is on prenatal and early postnatal development, during which the HPA axis may be programmed in a manner that affects health for a lifetime. Programming of the HPA axis involves, at least in part, epigenetic remodeling of chromatin, leading to alterations in the expression of genes in many organs and tissues involved in HPA activation and response, including the hippocampus and peripheral tissues.

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“…In particular, brain PRKCB1 is expressed in hippocampus, striatum, suprachiasmatic nucleus and cerebellar granule cells, where PKCbI influences circadian rhythms, learning and memory, whereas PKCbII is involved in fear conditioning. [15][16][17][18][19] In the immune system, PKCb isoenzymes play a critical role in B-cell receptor-mediated responses, T-cell migration and cytokine secretion, dendritic cell differentiation and monocyte and macrophage functioning. [20][21][22][23][24][25] In the gut, PKCbI and bII are expressed by epithelial cells, where they regulate intestinal permeability and cell proliferation, respectively.…”

Section: Introductionmentioning

confidence: 99%

Involvement of the PRKCB1 gene in autistic disorder: significant genetic association and reduced neocortical gene expression

et al. 2008

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Protein kinase C enzymes play an important role in signal transduction, regulation of gene expression and control of cell division and differentiation. The fsI and bII isoenzymes result from the alternative splicing of the PKCb gene (PRKCB1), previously found to be associated with autism. We performed a family-based association study in 229 simplex and 5 multiplex families, and a postmortem study of PRKCB1 gene expression in temporocortical gray matter (BA41/42) of 11 autistic patients and controls. PRKCB1 gene haplotypes are significantly associated with autism (P < 0.05) and have the autistic endophenotype of enhanced oligopeptiduria (P < 0.05). Temporocortical PRKCB1 gene expression was reduced on average by 35 and 31% for the PRKCB1-1 and PRKCB1-2 isoforms (P < 0.01 and < 0.05, respectively) according to qPCR. Protein amounts measured for the PKCbII isoform were similarly decreased by 35% (P = 0.05). Decreased gene expression characterized patients carrying the 'normal' PRKCB1 alleles, whereas patients homozygous for the autism-associated alleles displayed mRNA levels comparable to those of controls. Whole genome expression analysis unveiled a partial disruption in the coordinated expression of PKCb-driven genes, including several cytokines. These results confirm the association between autism and PRKCB1 gene variants, point toward PKCb roles in altered epithelial permeability, demonstrate a significant downregulation of brain PRKCB1 gene expression in autism and suggest that it could represent a compensatory adjustment aimed at limiting an ongoing dysreactive immune process. Altogether, these data underscore potential PKCb roles in autism pathogenesis and spur interest in the identification and functional characterization of PRKCB1 gene variants conferring autism vulnerability.

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Prenatal restraint stress impairs learning and memory and hippocampal PKCbeta1 expression and translocation in offspring rats

Cited by 86 publications

References 40 publications

A Role for the PKC Signaling System in the Pathophysiology and Treatment of Mood Disorders: Involvement of a Functional Imbalance?

A Role for the PKC Signaling System in the Pathophysiology and Treatment of Mood Disorders: Involvement of a Functional Imbalance?

Maternal influences on epigenetic programming of the developing hypothalamic‐pituitary‐adrenal axis

Involvement of the PRKCB1 gene in autistic disorder: significant genetic association and reduced neocortical gene expression

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