Activated microglia are implicated in cognitive deficits, neuronal death, and successful recovery following intermittent ethanol exposure

2013 ◽  
Vol 236 ◽  
pp. 270-282 ◽  
Author(s):  
Ya-Nan Zhao ◽  
Fang Wang ◽  
Yan-Xia Fan ◽  
Guan-Fang Ping ◽  
Jing-Yu Yang ◽  
...  
Keyword(s):  
Cognitive Deficits ◽  
Neuronal Death ◽  
Ethanol Exposure ◽  
Activated Microglia ◽  
Successful Recovery

BAX is necessary for neuronal death following exposure to isoflurane during the neonatal period

2020 ◽  
Author(s):  
Andrew M. Slupe ◽  
Laura Villasana ◽  
Kevin M. Wright
Keyword(s):  
Cognitive Deficits ◽  
Neuronal Death ◽  
Neuronal Apoptosis ◽  
Neonatal Period ◽  
Volatile Anesthetics ◽  
Acute Injury ◽  
Seizure Threshold ◽  
Apoptotic Pathway ◽  
Neuroinflammatory Response ◽  
Human Primate

AbstractExposure to volatile anesthetics during the neonatal period results in acute neuronal death in rodent and non-human primate models, potentially leading to lasting cognitive deficits. We used Bax-/- mice to show that neuronal death following neonatal exposure to isoflurane is mediated by the apoptotic pathway, and that GABAergic interneurons are selectively vulnerable. Neonatal Bax-/- mice also showed attenuated microglial activation after exposure to isoflurane, indicating that neuroinflammatory response is secondary to neuronal apoptosis. Isoflurane-induced neuronal apoptosis in neonates appeared to have little effect on seizure threshold or cognitive function later in life. Collectively, these findings define the acute injury mechanism of volatile anesthetics during the neonatal period.

scholarly journals Reciprocal modulation of C/EBP-α and C/EBP-β by IL-13 in activated microglia prevents neuronal death

2013 ◽  
Vol 43 (11) ◽  
pp. 2854-2865 ◽  
Author(s):  
Hung Chuan Pan ◽  
Cheng Ning Yang ◽  
Yi Wen Hung ◽  
Wen Jane Lee ◽  
Hsing Ru Tien ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Activated Microglia

scholarly journals Alcohol Exposure during the Developmental Period Induces β-Endorphin Neuronal Death and Causes Alteration in the Opioid Control of Stress Axis Function

Endocrinology ◽  
2007 ◽  
Vol 148 (6) ◽  
pp. 2828-2834 ◽  
Author(s):  
Dipak K. Sarkar ◽  
Peter Kuhn ◽  
Jasson Marano ◽  
Cuiping Chen ◽  
Nadka Boyadjieva
Keyword(s):  
Neuronal Death ◽  
Arcuate Nucleus ◽  
Alcohol Exposure ◽  
Ethanol Exposure ◽  
Developmental Period ◽  
Stress Axis ◽  
Mrna Levels ◽  
Arcuate Nuclei ◽  
Tgf Β1

Proopiomelanocortin-producing neurons in the arcuate nucleus of the hypothalamus secrete β-endorphin (β-EP), which controls varieties of body functions including the feedback regulation of the CRH neuronal activity in the paraventricular nucleus of the hypothalamus. Whether ethanol exposure in developing rats induces β-EP neuronal death and alters their influence on CRH neurons in vivo has not been determined. We report here that binge-like ethanol exposures in newborn rats increased the number of apoptotic β-EP neurons in the arcuate nucleus of the hypothalamus. We also found that immediately after ethanol treatments there was a significant reduction in the expression of proopiomelanocortin and adenylyl cyclases mRNA and an increased expression of several TGF-β1-linked apoptotic genes in β-EP neurons isolated by laser-captured microdissection from arcuate nuclei of young rats. Several weeks after the ethanol treatment, we detected a reduction in the number of β-EP neuronal perikarya in arcuate nuclei and in the number of β-EP neuronal terminals in paraventricular nuclei of the hypothalamus in the treated rats. Additionally, these rats showed increased response of the hypothalamic CRH mRNA to the lipopolysaccharide challenge. The ethanol-treated animals also showed incompetent ability to respond to exogenous β-EP to alter the lipopolysaccharide-induced CRH mRNA levels. These data suggest that ethanol exposure during the developmental period causes β-EP neuronal death by cellular mechanisms involving the suppression of cyclic AMP production and activation of TGF-β1-linked apoptotic signaling and produces long-term structural and functional deficiency of β-EP neurons in the hypothalamus.

Abstract WP329: The Role of miR-34b/c in Global Ischemic Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Hyae-Ran Byun ◽  
Morgan Porch ◽  
Fabrizio Pontarelli ◽  
Brenda L Court Vazquez ◽  
R.Suzanne Zukin ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Deficits ◽  
Neuronal Death ◽  
Target Genes ◽  
Pyramidal Neurons ◽  
Unmet Need ◽  
Global Ischemia ◽  
Hippocampal Ca1

Transient global ischemia arising as a consequence of cardiac arrest in humans causes selective, delayed death of hippocampal CA1 pyramidal neurons and cognitive impairment. Effective treatments to ameliorate the neurodegeneration and cognitive dysfunction associated with global ischemia are an unmet need. Emerging evidence points to a widespread role for microRNAs (miRNAs) as key modulators of target gene expression in neurons. Accordingly, dysregulation of miRNAs are implicated in the pathophysiology of neurodegenerative disease and neurological disorders. Our findings, derived via miRNA-seq, indicate that expression of a subset of microRNAs are altered in postischemic CA1 including miR-34b/c, miR-21, miR-331, miR-181 and miR-29. Ingenuity pathway analysis reveals that miR-34b/c is the leading miR candidate implicated in cell death and survival. A role for miR-34 in the pathogenesis of global ischemia is, as yet, unclear. Here we show ischemia induces p53-dependent activation of miR-34b/c and downregulation of its target genes Bcl-2 and Sirt1, which together promote neuronal death in selectively vulnerable hippocampal CA1 in vivo . Consistent with this, inhibition of miR-34b/c affords neuroprotection, rescues impaired synaptic plasticity and reduces memory deficits in global ischemia. These findings document a causal role for p53-dependent activation of miR-34b/c in neuronal death and identify a novel therapeutic target for amelioration of the neurodegeneration and cognitive deficits associated with ischemic stroke.

scholarly journals Aster ageratoides Turcz. extract attenuates Alzheimer’s disease-associated cognitive deficits and vascular dementia-associated neuronal death

2020 ◽  
Vol 53 (2) ◽  
pp. 216-227 ◽  
Author(s):  
Ji Heun Jeong ◽  
Seung Eun Lee ◽  
Jeong Hoon Lee ◽  
Hyung Don Kim ◽  
Kyung-Hae Seo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Cognitive Deficits ◽  
Neuronal Death

scholarly journals Mechanisms Underlying Neuronal Death Induced by Chromogranin A-activated Microglia

2000 ◽  
Vol 276 (16) ◽  
pp. 13113-13120 ◽  
Author(s):  
Jaroslava Ciesielski-Treska ◽  
Gabrielle Ulrich ◽  
Sylvette Chasserot-Golaz ◽  
Jean Zwiller ◽  
Marie-Odile Revel ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Chromogranin A ◽  
Activated Microglia

Cognitive deficits and CNS damage after a 4-day binge ethanol exposure in rats

2002 ◽  
Vol 72 (3) ◽  
pp. 521-532 ◽  
Author(s):  
Jennifer A. Obernier ◽  
Aaron M. White ◽  
H.Scott Swartzwelder ◽  
Fulton T. Crews
Keyword(s):  
Cognitive Deficits ◽  
Ethanol Exposure ◽  
Binge Ethanol Exposure ◽  
Binge Ethanol

Proinflammatory mediators released by activated microglia induces neuronal death in Japanese encephalitis

Glia ◽  
2007 ◽  
Vol 55 (5) ◽  
pp. 483-496 ◽  
Author(s):  
Ayan Ghoshal ◽  
Sulagna Das ◽  
Soumya Ghosh ◽  
Manoj Kumar Mishra ◽  
Vivek Sharma ◽  
...  
Keyword(s):  
Japanese Encephalitis ◽  
Neuronal Death ◽  
Activated Microglia ◽  
Proinflammatory Mediators
Sign in / Sign up

Export Citation Format

Share Document