Characterization of neuronal migration disorders in neocortical structures: quantitative receptor autoradiography of ionotropic glutamate, GABA<sub>A</sub> and GABA<sub>B</sub> receptors

European Journal of Neuroscience - Tập 10 Số 10 - Trang 3095-3106 - 1998
Karl Zilles1, M Qü, Axel Schleicher, Heiko J. Luhmann
1C. & O. Vogt Institute of Brain Research, University of Düsseldorf, Germany. [email protected]

Tóm tắt

AbstractEpileptiform activity was previously described [Luhmann et al. (1998) Eur.J. Neurosci., 10, 3085–3094] in the neocortex of the adult rat following freeze lesioning of the newborn neocortex. After a survival time of 3 months, a small area of dysplastic cortex surrounded by histologically normal (exofocal) neocortex was observed. The dysplastic cortex is characterized by the formation of a small sulcus and a three‐ to four‐layered architecture. Two questions are addressed here: (i) is the hyperexcitability associated with changes in binding to major excitatory and inhibitory transmitter receptors in the dysplastic cortex?; and (ii) do such changes also occur in the exofocal cortex?  Alterations in binding to glutamatergic N‐methyl‐d‐aspartate (NMDA), (±)‐α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA), kainate and GABAA and GABAB (γ‐aminobutyric acid) receptors are demonstrated with quantitative in vitro receptor autoradiography by using the ligands [3H]MK‐801, [3H]AMPA, [3H]kainate, [3H]muscimol and [3H]baclofen, respectively. In the dysplastic cortex, the binding to NMDA, AMPA and kainate receptors is significantly increased, whereas the binding to GABAA and GABAB receptors is reduced. Exofocal areas of the lesioned hemisphere show an imbalance between excitatory and inhibitory receptor binding with an up‐regulation of the binding to AMPA and kainate, and a down‐regulation to GABAA receptors. The binding to GABAB and NMDA receptors is not significantly changed in the exofocal areas.  The imbalance between excitatory and inhibitory receptors may cause the hyperexcitability, as previously found in the identical experimental model, and may also induce epileptiform activity in the human cortex with migration disorders.

Từ khóa


Tài liệu tham khảo

10.1111/j.1460-9568.1995.tb01117.x

10.1046/j.1471-4159.1995.65062808.x

Barkovich J.A., 1992, Schizencephaly: correlation of clinical findings with MR characteristics, Am. J. Neuroradiol., 13, 104

10.1017/S031716710002610X

Bayer S.A.&Altman J.1991Neocortical Development. Raven New York.

10.1038/203591b0

10.1016/0165-3806(92)90007-J

10.1016/0006-8993(95)01033-X

10.1111/j.1600-0404.1992.tb08049.x

Burgard E., 1993, Developmental changes in NMDA and non‐NMDA receptor‐mediated synaptic potentials in rat neocortex, J. Neurophysiol., 69, 230, 10.1152/jn.1993.69.1.230

Chagnac‐Amitai Y., 1989, Horizontal spread of synchronized activity in neocortex and its control by GABA‐mediated inhibition, J. Neuroscience, 61, 747

10.1002/cne.902960407

10.1016/0166-2236(91)90003-D

10.1016/0306-4522(90)90144-S

Dvorak K., 1978, Experimentally induced focal microgyria and Status verrucosus deformis in rats—Pathogenesis and interrelation. Histological and autoradiographical study. Acta Neuropathol. (, Berl.), 44, 121

10.1152/jn.1996.76.5.3471

10.1007/BF00230294

10.1016/0022-510X(94)90198-8

10.1073/pnas.93.11.5584

10.1002/cne.903590111

10.1523/JNEUROSCI.14-09-05302.1994

10.1016/0306-4522(95)00130-B

10.1016/0736-5748(95)00051-H

10.1038/351568a0

10.1523/JNEUROSCI.11-02-00428.1991

10.1097/00005072-199103000-00006

10.1155/NP.1991.1

10.1155/NP.1991.29

10.1093/cercor/6.3.514

Johnson T.D., 1996, Modulation of channel function by polyamines, Trends Neurosci., 17, 22

10.1038/325529a0

10.1212/WNL.44.12.2407

10.1126/science.2841759

10.1126/science.8096653

10.1016/0896-6273(95)90002-0

10.1093/acprof:oso/9780195083309.003.0014

10.1016/0301-0082(95)00042-9

10.1002/(SICI)1097-4695(19990615)39:4<558::AID-NEU9>3.0.CO;2-5

10.1016/S0920-1211(96)00041-1

10.1046/j.1460-9568.1998.00311.x

10.1007/BF00305396

10.1002/cne.903170107

10.1016/0165-0270(83)90086-9

10.1097/00001756-199505090-00011

10.1002/ana.410300603

10.1126/science.283.5400.401

10.1002/cne.903500110

Piggott M.A., 1994, Modulation of [3H]MK‐801 binding by polyamines in human development and aging, Neurosci. Res. Commun., 15, 49

10.1016/S0306-4522(97)00656-8

Qü M., 1994, Modulation des glutamatergen NMDA‐Rezeptors im Hippocampus der Ratte während der postnatalen Ontogenese, Ann. Anat., 176, 55

10.1002/cne.901450105

Reynolds I.J., 1988, Multiple sites for the regulation of the NMDA receptor, Mol. Pharmacol., 33, 581

10.1073/pnas.84.21.7744

10.1046/j.1471-4159.1995.65041674.x

10.1002/ana.410400210

Rickmann M., 1981, Differentiation of ‘preplate’ neurons in the pallium of the rat, Bibl. Anat., 19, 142

10.1016/0165-3806(94)90155-4

10.1016/0006-8993(96)00351-4

10.1016/0306-4522(95)00262-H

10.1016/0306-4522(94)90405-7

10.1097/00004647-199609000-00014

Sieghart W., 1995, Structure and pharmacology of γ‐aminobutyric acidA receptor subtypes, Pharmacol. Rev., 47, 181

10.1016/0091-3057(95)00200-6

10.1038/326698a0

Sutor B., 1995, Development of excitatory and inhibitory postsynaptic potentials in the rat neocortex, Perspect. Dev. Neurobiol., 2, 409

10.1007/BF00293950

10.1126/science.7973662

10.1136/jnnp.34.4.369

10.1212/WNL.33.3.257

Traub R.D., 1985, Neuronal interactions during epileptic events in vitro, Fed. Proc., 44, 2953

10.1016/0006-8993(95)00652-7

10.1093/cercor/5.6.483

10.1002/cne.902900108

Williams K., 1991, Developmental changes in the sensitivity of the N‐methyl‐d‐aspartate receptor to polyamines, Mol. Pharmacol., 40, 774

10.1016/0024-3205(91)90463-L

Witte O.W., 1997, Lesion‐induced network plasticity in remote brain areas, Trends Neurosci., 20, 348

Wong R.K., 1984, Local circuit interactions in synchronization of cortical neurones, J. Exp. Biol., 112, 169, 10.1242/jeb.112.1.169

10.1007/978-3-642-70573-1

Zilles K., 1995, Autoradiography and Correlative Imaging., 277

Thông tin
Thông tin xuất bản

European Journal of Neuroscience

Tập 10 Số 10

3095-3106

Thông tin tác giả