PortalPublikationenDecreased anxiety, altered place learning, and increased CA1...

Decreased anxiety, altered place learning, and increased CA1 basal excitatory synaptic transmission in mice with conditional ablation of the neural cell adhesion molecule L1

Standard

Decreased anxiety, altered place learning, and increased CA1 basal excitatory synaptic transmission in mice with conditional ablation of the neural cell adhesion molecule L1. / Law, Janice W S; Lee, Alan Y W; Sun, Mu; Nikonenko, Alexander G; Chung, Sookja K; Dityatev, Alexander; Schachner, Melitta; Morellini, Fabio.

in: J NEUROSCI, Jahrgang 23, Nr. 32, 12.11.2003, S. 10419-32.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Law, JWS, Lee, AYW, Sun, M, Nikonenko, AG, Chung, SK, Dityatev, A, Schachner, M & Morellini, F 2003, 'Decreased anxiety, altered place learning, and increased CA1 basal excitatory synaptic transmission in mice with conditional ablation of the neural cell adhesion molecule L1', J NEUROSCI, Jg. 23, Nr. 32, S. 10419-32.

APA

Law, J. W. S., Lee, A. Y. W., Sun, M., Nikonenko, A. G., Chung, S. K., Dityatev, A., Schachner, M., & Morellini, F. (2003). Decreased anxiety, altered place learning, and increased CA1 basal excitatory synaptic transmission in mice with conditional ablation of the neural cell adhesion molecule L1. J NEUROSCI, 23(32), 10419-32.

Vancouver

Law JWS, Lee AYW, Sun M, Nikonenko AG, Chung SK, Dityatev A et al. Decreased anxiety, altered place learning, and increased CA1 basal excitatory synaptic transmission in mice with conditional ablation of the neural cell adhesion molecule L1. J NEUROSCI. 2003 Nov 12;23(32):10419-32.

Bibtex

@article{249b165545514445967e5a4d40de12e2,
title = "Decreased anxiety, altered place learning, and increased CA1 basal excitatory synaptic transmission in mice with conditional ablation of the neural cell adhesion molecule L1",
abstract = "L1, a neural cell adhesion molecule of the immunoglobulin superfamily, is involved in neuronal migration and differentiation and axon outgrowth and guidance. Mutations in the human and mouse L1 gene result in similarly severe neurological abnormalities. To dissociate the functional roles of L1 in the adult brain from developmental abnormalities, we have generated a mutant in which the L1 gene is inactivated by cre-recombinase under the control of the calcium/calmodulin-dependent kinase II promoter. This mutant (L1fy+) did not show the overt morphological and behavioral abnormalities observed previously in constitutive L1-deficient (L1-/-) mice; however, there was an increase in basal excitatory synaptic transmission that was not apparent in L1-/- mice. Similar to L1-/- mice, no defects in short- and long-term potentiation in the CA1 region of the hippocampus were observed. Interestingly, L1fy+ mice showed decreased anxiety in the open field and elevated plus-maze, contrary to L1-/- mice, and altered place learning in the water maze, similar to L1-/- mice. Thus, mice conditionally deficient in L1 expression in the adult brain share some abnormalities, but also display different ones, as compared with L1-/- mice, highlighting the role of L1 in the regulation of synaptic transmission and behavior in adulthood.",
keywords = "Animals, Anxiety, Behavior, Animal, Chimera, Electrophysiology, Gene Targeting, Hippocampus, Immunohistochemistry, Integrases, Learning, Long-Term Potentiation, Male, Maze Learning, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Mice, Transgenic, Motor Activity, Neural Cell Adhesion Molecule L1, Neuronal Plasticity, Prosencephalon, Spatial Behavior, Synaptic Transmission, Viral Proteins",
author = "Law, {Janice W S} and Lee, {Alan Y W} and Mu Sun and Nikonenko, {Alexander G} and Chung, {Sookja K} and Alexander Dityatev and Melitta Schachner and Fabio Morellini",
year = "2003",
month = nov,
day = "12",
language = "English",
volume = "23",
pages = "10419--32",
journal = "J NEUROSCI",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "32",

}

RIS

TY - JOUR

T1 - Decreased anxiety, altered place learning, and increased CA1 basal excitatory synaptic transmission in mice with conditional ablation of the neural cell adhesion molecule L1

AU - Law, Janice W S

AU - Lee, Alan Y W

AU - Sun, Mu

AU - Nikonenko, Alexander G

AU - Chung, Sookja K

AU - Dityatev, Alexander

AU - Schachner, Melitta

AU - Morellini, Fabio

PY - 2003/11/12

Y1 - 2003/11/12

N2 - L1, a neural cell adhesion molecule of the immunoglobulin superfamily, is involved in neuronal migration and differentiation and axon outgrowth and guidance. Mutations in the human and mouse L1 gene result in similarly severe neurological abnormalities. To dissociate the functional roles of L1 in the adult brain from developmental abnormalities, we have generated a mutant in which the L1 gene is inactivated by cre-recombinase under the control of the calcium/calmodulin-dependent kinase II promoter. This mutant (L1fy+) did not show the overt morphological and behavioral abnormalities observed previously in constitutive L1-deficient (L1-/-) mice; however, there was an increase in basal excitatory synaptic transmission that was not apparent in L1-/- mice. Similar to L1-/- mice, no defects in short- and long-term potentiation in the CA1 region of the hippocampus were observed. Interestingly, L1fy+ mice showed decreased anxiety in the open field and elevated plus-maze, contrary to L1-/- mice, and altered place learning in the water maze, similar to L1-/- mice. Thus, mice conditionally deficient in L1 expression in the adult brain share some abnormalities, but also display different ones, as compared with L1-/- mice, highlighting the role of L1 in the regulation of synaptic transmission and behavior in adulthood.

AB - L1, a neural cell adhesion molecule of the immunoglobulin superfamily, is involved in neuronal migration and differentiation and axon outgrowth and guidance. Mutations in the human and mouse L1 gene result in similarly severe neurological abnormalities. To dissociate the functional roles of L1 in the adult brain from developmental abnormalities, we have generated a mutant in which the L1 gene is inactivated by cre-recombinase under the control of the calcium/calmodulin-dependent kinase II promoter. This mutant (L1fy+) did not show the overt morphological and behavioral abnormalities observed previously in constitutive L1-deficient (L1-/-) mice; however, there was an increase in basal excitatory synaptic transmission that was not apparent in L1-/- mice. Similar to L1-/- mice, no defects in short- and long-term potentiation in the CA1 region of the hippocampus were observed. Interestingly, L1fy+ mice showed decreased anxiety in the open field and elevated plus-maze, contrary to L1-/- mice, and altered place learning in the water maze, similar to L1-/- mice. Thus, mice conditionally deficient in L1 expression in the adult brain share some abnormalities, but also display different ones, as compared with L1-/- mice, highlighting the role of L1 in the regulation of synaptic transmission and behavior in adulthood.

KW - Animals

KW - Anxiety

KW - Behavior, Animal

KW - Chimera

KW - Electrophysiology

KW - Gene Targeting

KW - Hippocampus

KW - Immunohistochemistry

KW - Integrases

KW - Learning

KW - Long-Term Potentiation

KW - Male

KW - Maze Learning

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Mutant Strains

KW - Mice, Transgenic

KW - Motor Activity

KW - Neural Cell Adhesion Molecule L1

KW - Neuronal Plasticity

KW - Prosencephalon

KW - Spatial Behavior

KW - Synaptic Transmission

KW - Viral Proteins

M3 - SCORING: Journal article

C2 - 14614101

VL - 23

SP - 10419

EP - 10432

JO - J NEUROSCI

JF - J NEUROSCI

SN - 0270-6474

IS - 32

ER -