A single brain-derived neurotrophic factor injection modifies hypothalamo–pituitary–adrenocortical axis activity in adult male rats

Givalois, Laurent; Naert, Gaëlle; Rage, Florence; Ixart, G.; Arancibia, Sandor; Tapia‐Arancibia, Lucía

doi:10.1016/j.mcn.2004.07.002

Cited by 124 publications

(141 citation statements)

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“…Shading indicates the A␤ [25][26][27][28][29][30][31][32][33][34][35] sequence; the intramembrane domain is indicated by a dashed box. B: Electron microscopy of scrambled A␤ [25][26][27][28][29][30][31][32][33][34][35] , A␤ , and A␤ [25][26][27][28][29][30][31][32][33][34][35] peptides before and after in vitro incubation at 37°C for 4 days. A␤ and A␤ [25][26][27][28][29][30][31][32][33][34][35] formed an extensive network of fibrils after 4 days at 37°C, but scrambled peptide did not; the image at the far right presents a higher-magnification view for the A␤ [25][26][27][28]…”

Section: Amyloid ␤ Peptidementioning

confidence: 99%

“…4 Structure-activity studies revealed that peptides containing the highly hydrophobic 25-35 region formed stable aggregates and mediated neuronal death by necrosis or apoptosis. 5,6,7 The truncated A␤ [25][26][27][28][29][30][31][32][33][34][35] fragment includes extracellular and intramembrane residues that have been reported to represent an active region of A␤. 8 In vivo, two nontransgenic rodent models of AD have been studied to analyze the molecular, morphological, and behavioral consequences of amyloid toxicity: the infusion of A␤ 1-40/42 protein and the injection of preaggregated A␤ [25][26][27][28][29][30][31][32][33][34][35] peptide.…”

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confidence: 99%

“…These models have led to highly pertinent pathomimetic observations and provide complementary approaches to the numerous transgenic mouse lines developed as AD models. In particular, at 1 week after A␤ [25][26][27][28][29][30][31][32][33][34][35] injection, reactive gliosis was observed in the rat hippocampus, 9 caspase-3 activity was induced in the hippocampus and cortex, 9 a reduction in the number of neurons was measured in the CA1 or CA3 hippocampal area, 9 -11 and significant oxidative stress was observed. [11][12][13] Nonetheless, this amyloid toxicity model remains controversial with respect to AD.…”

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confidence: 99%

“…First, although the presence of A␤ [25][26][27][28][29][30][31][32][33][34][35] has been repeatedly demonstrated in brains of AD patients, 14,15 this fragment appears to be a minor peptide in plaques and its contribution to the toxicity induced by all amyloid-related species remains unclear. Second, the intracerebroventricular injection of A␤ [25][26][27][28][29][30][31][32][33][34][35] induces marked toxicity within days or weeks, which is not in accord with the long-term progression of AD in humans (an argument that is unrelated to the nature of the toxicity). Third, it is possible that peptide injection mimics only the amyloid toxicity observed in AD physiopathology, but not the processes involved in A␤ formation or Tau protein hyperphosphorylation.…”

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confidence: 99%

“…Klementiev et al 16 recently documented some evidence that contradicts this latter reservation. Moreover, very recently, Chavant et al 17 reported that, at 2 weeks after injection, A␤ [25][26][27][28][29][30][31][32][33][34][35] significantly increased APP processing in the hippocampus of mice.…”

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confidence: 99%

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Time-Course and Regional Analyses of the Physiopathological Changes Induced after Cerebral Injection of an Amyloid β Fragment in Rats

Zussy

Brureau

Delair

et al. 2011

The American Journal of Pathology

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Alzheimer's disease (AD) is a neurodegenerative pathology characterized by the presence of senile plaques and neurofibrillary tangles, accompanied by synaptic and neuronal loss. The major component of senile plaques is an amyloid ␤ protein (A␤) formed by pathological processing of the A␤ precursor protein. We assessed the time-course and regional effects of a single intracerebroventricular injection of aggregated A␤ fragment 25-35 (A␤ 25-35 ) in rats. Using a combined biochemical, behavioral, and morphological approach, we analyzed the peptide effects after 1, 2, and 3 weeks in the hippocampus, cortex, amygdala, and hypothalamus. The scrambled A␤ 25-35 peptide was used as negative control. The aggregated forms of A␤ peptides were first characterized using electron microscopy, infrared spectroscopy, and Congo Red staining. Intracerebroventricular injection of A␤ 25-35 decreased body weight, induced short-and long-term memory impairments, increased endocrine stress, cerebral oxidative and cellular stress, neuroinflammation, and neuroprotective reactions, and modified endogenous amyloid processing, with specific time-course and regional responses. Moreover, A␤ 25-35 , the presence of which was shown in the different brain structures and over 3 weeks, provoked a rapid glial activation, acetylcholine homeostasis perturbation, and hippocampal morphological alterations. Alzheimer's disease (AD) is a chronic neurodegenerative pathology characterized by the presence of senile plaques and neurofibrillary tangles, accompanied by synaptic and neuronal loss in brain areas responsible for learning and memory impairments. 1 The major component of senile plaques is an amyloid ␤ protein (A␤) derived from amyloid precursor protein (APP). Genetic, cell biological, and postmortem studies on AD brain, together with A␤ neurotoxicity findings, gave rise to the amyloid cascade hypothesis to explain A␤-associated neurodegenerative processes. 2 In normal healthy individuals, A␤ peptides are present only in small quantities, as soluble monomers that circulate in cerebrospinal fluid and blood. In AD patients, A␤ peptides, which vary in length from 40 to 43 amino acids, accumulate as insoluble fibrillar deposits. 3 When cultured rat hippocampal neurons are exposed to aggregated A␤ peptides, their neurites adopt a dystrophic appearance and become comparable to those observed surrounding and infiltrating senile plaques. This observation suggested that A␤ is responsible for the neuritic abnormalities in AD pathology. 4 Structure-activity studies revealed that peptides containing the highly hydrophobic 25-35 region formed stable aggregates and mediated neuronal death by necrosis or apoptosis. 5,6,7 The truncated A␤ 25-35 fragment includes extracellular and intramembrane residues that have been reported to represent an active region of A␤. 8

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Section: Amyloid ␤ Peptidementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Time-Course and Regional Analyses of the Physiopathological Changes Induced after Cerebral Injection of an Amyloid β Fragment in Rats

Zussy

Brureau

Delair

et al. 2011

The American Journal of Pathology

Self Cite

121

129

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Effects of negative stressors on DNA methylation in the brain: Implications for mood and anxiety disorders

Hing

Gardner

Potash

2014

American J of Med Genetics Pt B

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Stress is a major contributor to anxiety and mood disorders. The recent discovery of epigenetic changes in the brain resulting from stress has enhanced our understanding of the mechanism by which stress is able to promote these disorders. Although epigenetics encompasses chemical modifications that occur at both DNA and histones, much attention has been focused on stress-induced DNA methylation changes on behavior. Here, we review the effect of stress-induced DNA methylation changes on physiological mechanisms that govern behavior and cognition, dysregulation of which can be harmful to mental health. A literature review was performed in the areas of DNA methylation, stress, and their impact on the brain and psychiatric illness. Key findings center on genes involved in the hypothalamic-pituitary-adrenal axis, neurotransmission and neuroplasticity. Using animal models of different stress paradigms and clinical studies, we detail how DNA methylation changes to these genes can alter physiological mechanisms that influence behavior. Appropriate levels of gene expression in the brain play an important role in mental health. This dynamic control can be disrupted by stress-induced changes to DNA methylation patterns. Advancement in other areas of epigenetics, such as histone modifications and the discovery of the novel DNA epigenetic mark, 5-hydroxymethylcytosine, could provide additional avenues to consider when determining the epigenetic effects of stress on the brain.

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Roles for γ‐aminobutyric acid in the development of the paraventricular nucleus of the hypothalamus

McClellan

Stratton

Tobet

2010

J of Comparative Neurology

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The development of the hypothalamic paraventricular nucleus (PVN) involves several factors that work together to establish a cell group that regulates neuroendocrine functions and behaviors. A number of molecular markers were noted within the developing PVN, including estrogen receptors (ER), neuronal nitric oxide synthase (nNOS) and brain derived neurotrophic factor (BDNF). By contrast, immunoreactive gamma-aminobutyric acid (GABA) was found in cells and fibers surrounding the PVN. Two animal models were used to test the hypothesis that GABA works through GABAA and GABAB receptors to influence the development of the PVN. Treatment with bicuculline to decrease GABAA receptor signaling from embryonic day (E)10 to 17 resulted in fewer cells containing immunoreactive (ir)-ERα in the region of the PVN versus control. GABABR1 receptor subunit knockout mice were used to examine the PVN at P0 without GABAB signaling. In female but not male GABABR1 subunit knockout mice, the positions of cells containing ir-ERα shifted from medial to lateral compared to wildtype controls, while the total number of ir-ERα containing cells was unchanged. In E17 knockout mice, ir-nNOS cells and fibers were spread over a greater area. There was also a significant decrease in ir-BDNF in the knockout mice in a region dependent manner. Changes in cell position and protein expression subsequent to disruption of GABA signaling may be due, in part, to changes in nNOS and BDNF signaling. Based on the current study, the PVN can be added as another site where GABA exerts morphogenetic actions in development.

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A single brain-derived neurotrophic factor injection modifies hypothalamo–pituitary–adrenocortical axis activity in adult male rats

Cited by 124 publications

References 68 publications

Time-Course and Regional Analyses of the Physiopathological Changes Induced after Cerebral Injection of an Amyloid β Fragment in Rats

Time-Course and Regional Analyses of the Physiopathological Changes Induced after Cerebral Injection of an Amyloid β Fragment in Rats

Effects of negative stressors on DNA methylation in the brain: Implications for mood and anxiety disorders

Roles for γ‐aminobutyric acid in the development of the paraventricular nucleus of the hypothalamus

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