Alterations in hyperpolarization-activated cyclic nucleotidegated cation channel (HCN) expression in the hippocampus following pilocarpine-induced status epilepticus
2
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
To understand the effects of HCN as potential mediators in the pathogenesis of epilepsy that evoke long-term impaired excitability; the present study was designed to elucidate whether the alterations of HCN expression induced by status epilepticus (SE) is responsible for epileptogenesis. Although HCN1 immunoreactivity was observed in the hippocampus, its immunoreactivities were enhanced at 12 hrs following SE. Although, HCN1immunoreactivities were reduced in all the hippocampi at 2weeks, a re-increase in the expression at 2-3 months following SE was observed. In contrast to HCN1, HCN 4 expressions were un-changed, although HCN2 immunoreactive neurons exhibited some changes following SE. Taken together, our findings suggest that altered expressions of HCN1 following SE may be mainly involved in the imbalances of neurotransmissions to hippocampal circuits; thus, it is proposed that HCN1 may play an important role in the epileptogenic period as a compensatory response. [BMB Reports 2012; 45(11): 635-640]
Abstract
To understand the effects of HCN as potential mediators in the pathogenesis of epilepsy that evoke long-term impaired excitability; the present study was designed to elucidate whether the alterations of HCN expression induced by status epilepticus (SE) is responsible for epileptogenesis. Although HCN1 immunoreactivity was observed in the hippocampus, its immunoreactivities were enhanced at 12 hrs following SE. Although, HCN1immunoreactivities were reduced in all the hippocampi at 2weeks, a re-increase in the expression at 2-3 months following SE was observed. In contrast to HCN1, HCN 4 expressions were un-changed, although HCN2 immunoreactive neurons exhibited some changes following SE. Taken together, our findings suggest that altered expressions of HCN1 following SE may be mainly involved in the imbalances of neurotransmissions to hippocampal circuits; thus, it is proposed that HCN1 may play an important role in the epileptogenic period as a compensatory response. [BMB Reports 2012; 45(11): 635-640]
참고문헌 (34)
- Dalby, N. O., "The process of epileptogenesis; a pathophysiological approach", Curr. Opin. Neurol., 14, pp.187~192 (2001)
- Margerison, J. H., "Epilepsy and the temporal lobes. A clinical, electroencephalographic and neuropathological study of the brain in epilepsy, with particular reference to the temporal lobes", Brain, 89, pp.499~530 (1966)
- De Lanerolle, N. C., "Hippocampal interneuron loss and plasticity in human temporal lobe epilepsy", Brain Res., 495, pp.389~395 (1989)
- Mathern, G. W., "The pathophysiologic relationships between lesion pathology, intracranial ictal EEG onsets, and hippocampal neuron losses in temporal lobe epilepsy", Epilepsy Res., 21, pp.133~147 (1995)
- Wittner, L., "Preservation of perisomatic inhibitory input of granule cells in the pileptic human dentate gyrus", Neuroscience, 108, pp.587~600 (2001)
- DiFrancesco, D., "Pacemaker mechanisms in cardiac tissue", Annu. Rev. Physiol., 55, pp.455~472 (1993)
- Pape, H. C., "Queer current and pacemaker: the hyperpolarization- activated cation current in neurons", Annu. Rev. Physiol., 58, pp.299~327 (1996)
- Maccaferri, G., "Properties of the hyperpolarization-activated current in rat hippocampal CA1 pyramidal cells", J. Neurophysiol., 69, pp.2129~2136 (1993)
- Richter, H., "Hyperpolarization- activated cation currents in stellate and pyramidal neurons of rat entorhinal cortex", Neurosci. Lett., 281, pp.33~36 (2000)
- Dickson, C. T., "Properties and role of I(h) in the pacing of subthreshold oscillations in entorhinal cortex layer II neurons", J. Neurophysiol., 83, pp.2562~2579 (2000)
- Williams, S. R., "Site independence of EPSP time course is mediated by dendritic I(h) in neocortical pyramidal neurons", J. Neurophysiol., 83, pp.3177~3182 (2000)
- Chen, K., "Persistently modified h-channels after complex febrile seizures convert the seizure-induced enhancement of inhibition to hyperexcitability", Nat. Med., 7, pp.331~337 (2001)
- Bender, R. A., "Enhanced expression of a specific hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN) in surviving dentate gyrus granule cells of human and experimental epileptic hippocampus", J. Neurosci., 23, pp.6826~6836 (2003)
- Walker, M. C., "Febrile convulsions; a ‘benign’ condition?", Nat. Med., 5, pp.871~872 (1999)
- Chen, K., "Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits", Nat. Med., 5, pp.888~894 (1999)
- Brewster, A., "Developmental febrile seizures modulate hippocampal gene expression of hyperpolarization-activated channels in an isoform- and cell-specific manner", J. Neurosci., 22, pp.4591~4599 (2002)
- Santoro, B., "Molecular and functional heterogeneity of hyperpolarization- activated pacemaker channels in the mouse CNS", J. Neurosci., 20, pp.5264~5275 (2000)
- Bender, R. A., "Differential and age-dependent expression of hyperpolarization-activated, cyclic nucleotide-gated cation channel isoforms 1-4 suggests evolving roles in the developing rat hippocampus", Neuroscience, 106, pp.689~698 (2001)
- Lupica, C. R., "Contribution of the hyperpolarization-activatedcurrent (Ih) to membrane potential and GABA release inhippocampal interneurons", J. Neurophysiol., 86, pp.261~268 (2001)
- Magee, J. C., "Dendritic Ih normalizes temporal summation in hippocampal CA1 neurons", Nat. Neurosci., 2, pp.508~514 (1999)
- Magee, J. C., "Dendritic hyperpolarization-activated currents modify the integrative properties of hippocampal CA1 pyramidal neurons", J. Neurosci., 18, pp.7613~7624 (1998)
- Poolos, N. P., "Pharmacological upregulation of h-channels reduces the excitability of pyramidal neuron dendrites", Nat. Neurosci., 5, pp.767~774 (2002)
- Okazaki, M. M., "Hippocampal mossy fiber sprouting and synapse formation after status epilepticus in rats; visualization after retrograde transport of biocytin", J. Comp. Neurol., 352, pp.515~534 (1995)
- Wenzel, H. J., "Kainic acid-induced mossy fiber sprouting and synapse formation in the dentate gyrus of rats", Hippocampus, 10, pp.244~260 (2000)
- Buckmaster, P. S., "Axon sprouting in a model of temporal lobe epilepsy creates a predominantly excitatory feedback circuit", J. Neurosci., 22, pp.6650~6658 (2002)
- Buckmaster, P. S., "Axon arbors and symaptic connections of a vulnerable population of interneurons in the dentate gyrus in vivo", J. Comp. Neurol., 445, pp.360~373 (2002)
- Isokawa, M., "Glutamate currents in morphologically identified human dentate granule cells in temporal lobe epilepsy", J. Neurophysiol., 77, pp.3355~3369 (1997)
- Moosmang, S., "Differential distribution of four hyperpolarizationactivatedcation channels in mouse brains", J. Biol. Chem., 380, pp.975~980 (1999)
- Ludwig, A., "Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2", EMBO J., 22, pp.216~224 (2003)
- Kim, D. S., "Seizure activity affects neuroglial Kv1 channel immunoreactivities in the gerbil hippocampus", BRAIN RESEARCH, 1151, pp.172~187 (2007), ELSEVIER SCIENCE BV
- Kim, D. S., "Spatiotemoral characteristics of astroglial death in the rat hippocampo-entorhinal complex following pilocarpine-induced status epilepticus", J. Comp. Neurol., 511, pp.581~598 (2008)
- An, S. J. and Kim, D. S., "Alterations in Serotonin Receptors and Transporter Immunoreactivities in the Hippocampus in the Rat Unilateral Hypoxic-induced Epilepsy Model", CELLULAR AND MOLECULAR NEUROBIOLOGY, 31(8), pp.1245~1255 (2011), SPRINGER[DOI]
- Dae-Kyoon Park, "Alteration in NCX-3 immunoreactivity within the gerbil hippocampus following spontaneous seizures", BMB Reports, 44(5), pp.306~311 (2011), 생화학분자생물학회
- Saet-Byeol Lee, "Altered PLCβ-1 expression in the gerbil hippocampal complex following spontaneous seizure", BMB Reports, 44(9), pp.566~571 (2011), 생화학분자생물학회