Glucocorticoids increase extracellular [3H]d-aspartate overflow in hippocampal cultures during cyanide-induced ischemia

Chou, Yun-Chia; Lin, Walter J.; Sapolsky, Robert M.

doi:10.1016/0006-8993(94)91565-2

Cited by 31 publications

(10 citation statements)

References 53 publications

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“…Stress itself can increase glutamate release in both regions and inhibit its uptake by glial transporters (Chou et al, 1994). Glutamate-induced NMDA activation has been shown to induce NF-B activation in several brain structures (Guerrini et al, 1995;Kaltschmidt et al, 1995;Glezer et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Chronic Unpredictable Stress Exacerbates Lipopolysaccharide-Induced Activation of Nuclear Factor-κB in the Frontal Cortex and Hippocampus via Glucocorticoid Secretion

Munhoz¹,

Lepsch²,

Kawamoto³

et al. 2006

J. Neurosci.

252

232

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Although the anti-inflammatory actions of glucocorticoids (GCs) are well established in the periphery, these stress hormones can increase inflammation under some circumstances in the brain. The transcription factor nuclear factor-B (NF-B), which is inhibited by GCs, regulates numerous genes central to inflammation. In this study, the effects of stress, GCs, and NMDA receptors on lipopolysaccharide (

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Section: Discussionmentioning

confidence: 99%

Chronic Unpredictable Stress Exacerbates Lipopolysaccharide-Induced Activation of Nuclear Factor-κB in the Frontal Cortex and Hippocampus via Glucocorticoid Secretion

Munhoz¹,

Lepsch²,

Kawamoto³

et al. 2006

J. Neurosci.

252

232

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“…Some of these factors also may be related to the specific hippocampal damage observed in this study of humans. It is also possible that hypercortisolemia (high blood level of glucocorticoids) which is known to occur after cardiac arrest [26, 27]has neurotoxic effects on the hippocampus [28, 29]. Experimental studies suggest that direct glucocorticoid exposure leads to neuronal loss and a decrease in dendritic branching in the hippocampus [30]associated with memory deficits [31].…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Damage in the Human Brain after Cardiac Arrest

et al. 2000

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Background and Purpose: Very few reports are available on changes in the human hippocampus after cardiac arrest. The objective of this study was to investigate if specific hippocampal volume losses can be demonstrated in the human brain following reperfusion after cardiac arrest. Methods: We assessed the volumes of the hippocampal formation (HF) and temporal lobe excluding HF (TL) as the contrast using magnetic resonance (MR)-imaging-based volumetry in 11 vegetative patients after cardiac arrest and in 22 healthy controls of similar age, sex and body size distribution. The measured volumes were normalized for differences in the head size among subjects by dividing by the total intracranial volume (TICV). The MR images of the 11 patients were obtained between days 8 and 21 after cardiac arrest. Results: The observed volumes of HFs and TLs of both patient and control groups were as follows: right HF volume (HFV): 2.67 ± 0.19 (mean ± SD, cm³) in patients versus 3.89 ± 0.44 in controls; left HFV: 2.72 ± 0.17 versus 3.74 ± 0.35; right TL volume (TLV): 73.37 ± 6.54 versus 80.08 ± 7.62, and left TLV: 72.45 ± 6.77 versus 78.59 ± 6.68. The normalized indices (HFV/TICV and TLV/TICV) were as follows: right HF: 0.0021 ± 0.0002 (mean ± SD) in patients versus 0.0031 ± 0.0001 in controls, p < 0.0001, left HF: 0.0022 ± 0.0002 versus 0.0030 ± 0.0001, p < 0.0001, right TL: 0.058 ± 0.002 versus 0.064 ± 0.004, p = 0.0007, and left TL: 0.058 ± 0.002 versus 0.062 ± 0.004, p = 0.0014. The HFV-TLV ratios (HFV/TICV divided by TLV/TICV) of both groups were: right HFV-TLV ratio: 0.037 ± 0.004 in patients versus 0.049 ± 0.004 in controls, p < 0.0001, left HFV-TLV ratio: 0.038 ± 0.004 versus 0.048 ± 0.004, p < 0.0001. Conclusions: The patient group had HFs that were 26.8–30.6% smaller than those of the control group, but in the patient group, the TLs slightly decreased in size by only 7.8–8.2% of the volume of those in the control group within 21 days after cardiac arrest. The volume reductions in the bilateral HFs of patients after cardiac arrest were significantly larger than those in the bilateral TLs. We speculate that this specific rapid hippocampal shrinkage reflects its greater vulnerability to global brain ischemia.

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“…When glucocorticoid levels are raised from the low basal range to the levels triggered by an excitotoxic insult (stroke or seizure) the levels of glutamate at the synapse are increased both in vivo and in vitro (30, 77, 79). In vitro the effect was more because of decreasing glutamate removal from the synapse than to increasing release (79). As noted, this appears to be, at least in part, because of the disruptive energetic effects of the hormone.…”

Section: Effects Of Glucocorticoids Upon Glutamate Accumulationmentioning

confidence: 99%

Stress and depression: possible links to neuron death in the hippocampus

2002

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Recent intriguing reports have shown an association between major depression and selective and persistent loss of hippocampal volume, prompting considerable speculation as to its underlying causes. In this paper we focus on the hypothesis that overt hippocampal neuron death could cause this loss and review current knowledge about how hippocampal neurons die during insults. We discuss (a) the trafficking of glutamate and calcium during insults; (b) oxygen radical generation and programmed cell death occurring during insults; (c) neuronal defenses against insults; (d) the role of energy availability in modulating the extent of neuron loss following such insults. The subtypes of depression associated with hippocampal atrophy typically involve significant hypersecretion of glucocorticoids, the adrenal steroids secreted during stress. These steroids have a variety of adverse affects, direct and indirect, in the hippocampus. Thus glucocorticoids may play a contributing role toward neuron death. We further discuss how glucocorticoids cause or exacerbate cellular changes associated with hippocampal neuron loss in the context of the events listed above.

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Glucocorticoids increase extracellular [3H]d-aspartate overflow in hippocampal cultures during cyanide-induced ischemia

Cited by 31 publications

References 53 publications

Chronic Unpredictable Stress Exacerbates Lipopolysaccharide-Induced Activation of Nuclear Factor-κB in the Frontal Cortex and Hippocampus via Glucocorticoid Secretion

Chronic Unpredictable Stress Exacerbates Lipopolysaccharide-Induced Activation of Nuclear Factor-κB in the Frontal Cortex and Hippocampus via Glucocorticoid Secretion

Hippocampal Damage in the Human Brain after Cardiac Arrest

Stress and depression: possible links to neuron death in the hippocampus

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