Stress- and non-stress-mediated mechanisms are involved in pain-induced apoptosis in hippocampus and dorsal lumbar spinal cord in rats

Jalalvand, Elham; Javan, Mohammad; Haeri-Rohani, Ali; Ahmadiani, Abolhasan

doi:10.1016/j.neuroscience.2008.08.052

Cited by 23 publications

(16 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These findings in the hippocampus are in sharp contrast to those uncovered in the spinal cord [25,186] , potentially reflecting varied roles of these neuromodulators in the de- but not acute pain (a single formalin injection), significantly reduced the neurogenesis in the DG area of the HF, measured by bromedeoxyuridine staining [196] , similar to previous observations from various stress models [192,197] . This paininduced decrease in hippocampal cell proliferation was recently confirmed by another immunoblotting study, comparing the apoptotic effects of chronic inflammatory pain and immobilization stress in rats [198] . In this report, repeated exposure to injections of 5% formalin gave rise to an increased ratio of Bax/Bcl-2 and activated caspase-3 in both lumbar spinal cord and hippocampus of both intact and adrenalectomized rats, implicating enhanced apoptosis in these two regions by chronic pain [198] .…”

Section: Egr1 Expression the Zinc Finger Transcription Factorsupporting

confidence: 57%

“…This paininduced decrease in hippocampal cell proliferation was recently confirmed by another immunoblotting study, comparing the apoptotic effects of chronic inflammatory pain and immobilization stress in rats [198] . In this report, repeated exposure to injections of 5% formalin gave rise to an increased ratio of Bax/Bcl-2 and activated caspase-3 in both lumbar spinal cord and hippocampus of both intact and adrenalectomized rats, implicating enhanced apoptosis in these two regions by chronic pain [198] . [199] .…”

Section: Egr1 Expression the Zinc Finger Transcription Factorsupporting

confidence: 57%

See 1 more Smart Citation

Roles of the hippocampal formation in pain information processing

2009

View full text Add to dashboard Cite

Abstract:Pain is a complex experience consisting of sensory-discriminative, affective-motivational, and cognitive-evaluative dimensions. Now it has been gradually known that noxious information is processed by a widely-distributed, hierarchicallyinterconnected neural network, referred to as neuromatrix, in the brain. Thus, identifying the multiple neural networks subserving these functional aspects and harnessing this knowledge to manipulate the pain response in new and beneficial ways are challenging tasks. Albeit with elaborate research efforts on the cortical responses to painful stimuli or clinical pain, involvement of the hippocampal formation (HF) in pain is still a matter of controversy. Here, we integrate previous animal and human studies from the viewpoint of HF and pain, sequentially representing anatomical, behavioral, electrophysiological, molecular/ biochemical and functional imaging evidence supporting the role of HF in pain processing. At last, we further expound on the relationship between pain and memory and present some unresolved issues.

show abstract

Section: Egr1 Expression the Zinc Finger Transcription Factorsupporting

confidence: 57%

Section: Egr1 Expression the Zinc Finger Transcription Factorsupporting

confidence: 57%

Roles of the hippocampal formation in pain information processing

2009

View full text Add to dashboard Cite

show abstract

“…Western Blot analysis was performed to investigate changes of COX-1, COX-2, HSP70 and cleaved Caspase-3 protein expression on the lumbar spinal cord tissue of all the animals, using protocol published by Jalalvand et al [29]. Briefly, tissues samples were homogenized on ice in cold lysis buffer containing 50 mM Tris-HCl (pH = 8.0), 150 mM Sodium chloride (NaCl), 0.1% Triton X-100, 0.25% sodium deoxycholate, 0.1% sodium dodecyl sulfate (SDS), 1 mM Ethylene diamine tetracetic acid (EDTA), 1% protease inhibitor cocktail (Roche Diagnostics, Mannheim, Germany).…”

Section: Measurement Of Glutathione (Gsh) Levelsmentioning

confidence: 99%

Acute 17β-Estradiol Pretreatment Protects Against Abdominal Aortic Occlusion Induced Spinal Cord Ischemic-Reperfusion Injury

et al. 2010

View full text Add to dashboard Cite

Postoperative neurologic deficit due to spinal cord ischemia-reperfusion (I/R) injury is the most devastating complication following thoracoabdominal aortic aneurysm repairs. The protective potential for 17β-Estradiol has not been yet studied in such injury. In this study, ischemia induction for 18 min in male New Zealand White rabbits resulted in the highest percentage (80%) of biphasic paraplegic outcome assessed by Tarlov's score. Acute Estradiol pretreatment (1 mg/kg, i.p., 30 min before I/R induction) altered this outcome and significantly prevented the worsening pattern of neurologic deficits over 48 h of observation. Histopathologic and oxidative stress evaluations of lumbar spinal cords taken in delayed permanent paraplegic phase (48 h after ischemia induction), further confirmed protective efficacy of Estradiol in such context. In western blot analysis, the expression of cleaved caspase-3 and heat shock protein 70 declined in Estradiol pretreated group compared to ischemic control group. TUNEL assay also showed the efficacy of Estradiol to abate motor neuron apoptosis. Interestingly, Estradiol respectively increased and decreased the expression of Cyclooxygenase (COX)-1 and COX-2, to a significant extent. Estradiol, exerting its protection through affecting one or a combination of involved biochemical factors can constitute a potential candidate to protect against thoracoabdominal aortic aneurysm repairs induced spinal cord I/R injury.

show abstract

“…Stressors of different types [25][26][27][28] or treatments with glucocorticoids [29][30][31][32] induce apoptosis in different tissues, including testicular germ cells [33]. Fluid from follicles of women whose oocytes were not fertilized contained cortisol levels significantly higher than in the fluid from follicles containing successfully fertilized oocytes [34].…”

Section: Introductionmentioning

confidence: 99%

Restraint Stress Impairs Oocyte Developmental Potential in Mice: Role of CRH-Induced Apoptosis of Ovarian Cells1

Liang

Wei

Cheng

et al. 2013

Biology of Reproduction

View full text Add to dashboard Cite

This study examined the role of CRH-induced ovarian cell apoptosis in the restraint stress (RS)-induced impairment of oocyte competence. Oocyte percentages of apoptotic cumulus cells (CCs) did not differ between stressed and control mice before in vitro maturation (IVM) but became significantly higher in stressed mice after IVM without serum, growth factor, and hormone. The level of Bcl2 mRNA decreased significantly in mural granulosa cells (MGCs) and ovarian homogenates after RS. Whereas ovarian estradiol, testosterone, and IGF1 decreased, cortisol and progesterone increased significantly following RS. RS increased the level of CRH in serum, ovary, and oocyte while enhancing the expression of CRHR1 in CCs, MGCs, and thecal cells. RS down-regulated ovarian expression of glucocorticoid receptor and brain-derived neurotrophic factor. Furthermore, CRH supplementation to IVM medium impaired oocyte developmental potential while increasing apoptotic CCs, an effect that was completely overcome by addition of the CRHR1 antagonist antalarmin. Results suggest that RS impaired oocyte competence by increasing CRH but not glucocorticoids. Increased CRH initiated a latent apoptotic program in CCs and oocytes during their intraovarian development, which was executed later during IVM to impair oocyte competence. Thus, elevated CRH interacted with increased CRHR1 on thecal cells and MGCs, reducing the production of testosterone, estrogen, and IGF1 while increasing the level of progesterone. The imbalance between estrogen and progesterone and the decreased availability of growth factors triggered apoptosis of MGCs and facilitated CC expression of CRHR1, which interacted with the oocyte-derived CRH later during IVM to induce CC apoptosis and reduce oocyte competence.

show abstract

Stress- and non-stress-mediated mechanisms are involved in pain-induced apoptosis in hippocampus and dorsal lumbar spinal cord in rats

Cited by 23 publications

References 51 publications

Roles of the hippocampal formation in pain information processing

Roles of the hippocampal formation in pain information processing

Acute 17β-Estradiol Pretreatment Protects Against Abdominal Aortic Occlusion Induced Spinal Cord Ischemic-Reperfusion Injury

Restraint Stress Impairs Oocyte Developmental Potential in Mice: Role of CRH-Induced Apoptosis of Ovarian Cells1

Contact Info

Product

Resources

About