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NMDA preconditioning and neuroprotection in vivo: delayed onset of kainic acid-induced neurodegeneration and c-Fos attenuation in CA3a neurons.
Brain Res. 2009 Feb 23; 1256:162-72.BR

Abstract

Intraventricular (i.c.v.) kainic acid (KA) causes an acute excitotoxic lesion to the CA3 region of rodent hippocampus. Recent evidence implicated c-fos gene in regulating neuron survival and death following an excitotoxic insult. In this study we attempted to prevent KA-induced damage in CA3 neurons with NMDA preconditioning, which produced a marked expression of c-fos in the hippocampus. NMDA (0.6-6 microg, i.c.v.) was injected to anesthetized rats alone or 1 h before KA (0.15 microg, i.c.v.). Following KA injection, vibratome sections were processed for immunohistochemistry/electron microscopy. c-Fos and Nissl staining were used to estimate the extent of neuronal excitation and damage, respectively. Quantitative evaluation of c-Fos-labeled cells showed significantly less c-Fos in CA3a than in neighboring CA3b and CA2 from 1 to 4 h after KA alone. Attenuation of expressed c-Fos in CA3a was accompanied by damage of neurons with more apoptotic than necrotic signs. NMDA preconditioning elevated CA3a c-Fos expression and at 1 and 2 h exceeded markedly that after KA alone. However, at 4 h after KA, NMDA-preconditioned c-Fos induction in CA3a diminished to the same level as that seen after KA alone. The onset of neuronal degeneration was delayed in similar way. While NMDA-induced c-Fos expression in CA3a could be blocked by MK-801 completely, MK-801 and CNQX were both without significant effect on KA-induced c-Fos expression and neuronal damage. In conclusion, inhibition of c-Fos expression and onset of neuronal damage in CA3a following icv KA injection might be transiently delayed by i.c.v. NMDA preconditioning.

Authors+Show Affiliations

Department of Physiology, Faculty of Medicine, Kuwait University, P.O.Box 24923, 131 10 Safat, Kuwait.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19118538

Citation

Mohammadi, Shirin, et al. "NMDA Preconditioning and Neuroprotection in Vivo: Delayed Onset of Kainic Acid-induced Neurodegeneration and c-Fos Attenuation in CA3a Neurons." Brain Research, vol. 1256, 2009, pp. 162-72.
Mohammadi S, Pavlik A, Krajci D, et al. NMDA preconditioning and neuroprotection in vivo: delayed onset of kainic acid-induced neurodegeneration and c-Fos attenuation in CA3a neurons. Brain Res. 2009;1256:162-72.
Mohammadi, S., Pavlik, A., Krajci, D., & Al-Sarraf, H. (2009). NMDA preconditioning and neuroprotection in vivo: delayed onset of kainic acid-induced neurodegeneration and c-Fos attenuation in CA3a neurons. Brain Research, 1256, 162-72. https://doi.org/10.1016/j.brainres.2008.12.019
Mohammadi S, et al. NMDA Preconditioning and Neuroprotection in Vivo: Delayed Onset of Kainic Acid-induced Neurodegeneration and c-Fos Attenuation in CA3a Neurons. Brain Res. 2009 Feb 23;1256:162-72. PubMed PMID: 19118538.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - NMDA preconditioning and neuroprotection in vivo: delayed onset of kainic acid-induced neurodegeneration and c-Fos attenuation in CA3a neurons. AU - Mohammadi,Shirin, AU - Pavlik,Alfred, AU - Krajci,Dimitrolos, AU - Al-Sarraf,Hameed, Y1 - 2008/12/16/ PY - 2008/06/18/received PY - 2008/12/04/revised PY - 2008/12/05/accepted PY - 2009/1/3/entrez PY - 2009/1/3/pubmed PY - 2009/3/17/medline SP - 162 EP - 72 JF - Brain research JO - Brain Res VL - 1256 N2 - Intraventricular (i.c.v.) kainic acid (KA) causes an acute excitotoxic lesion to the CA3 region of rodent hippocampus. Recent evidence implicated c-fos gene in regulating neuron survival and death following an excitotoxic insult. In this study we attempted to prevent KA-induced damage in CA3 neurons with NMDA preconditioning, which produced a marked expression of c-fos in the hippocampus. NMDA (0.6-6 microg, i.c.v.) was injected to anesthetized rats alone or 1 h before KA (0.15 microg, i.c.v.). Following KA injection, vibratome sections were processed for immunohistochemistry/electron microscopy. c-Fos and Nissl staining were used to estimate the extent of neuronal excitation and damage, respectively. Quantitative evaluation of c-Fos-labeled cells showed significantly less c-Fos in CA3a than in neighboring CA3b and CA2 from 1 to 4 h after KA alone. Attenuation of expressed c-Fos in CA3a was accompanied by damage of neurons with more apoptotic than necrotic signs. NMDA preconditioning elevated CA3a c-Fos expression and at 1 and 2 h exceeded markedly that after KA alone. However, at 4 h after KA, NMDA-preconditioned c-Fos induction in CA3a diminished to the same level as that seen after KA alone. The onset of neuronal degeneration was delayed in similar way. While NMDA-induced c-Fos expression in CA3a could be blocked by MK-801 completely, MK-801 and CNQX were both without significant effect on KA-induced c-Fos expression and neuronal damage. In conclusion, inhibition of c-Fos expression and onset of neuronal damage in CA3a following icv KA injection might be transiently delayed by i.c.v. NMDA preconditioning. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/19118538/NMDA_preconditioning_and_neuroprotection_in_vivo:_delayed_onset_of_kainic_acid_induced_neurodegeneration_and_c_Fos_attenuation_in_CA3a_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(08)03005-9 DB - PRIME DP - Unbound Medicine ER -