Development of synaptic inhibition in glycine transporter 2 deficient mice

Latal, A. T.; Kremer, T.; Gomeza, J.; Eulenburg, V.; Hülsmann, S.

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Development of synaptic inhibition in glycine transporter 2 deficient mice

MPS-Authors

Latal, A. T.
Max Planck Society;

/persons/resource/persons208057

Kremer, T.
Neurochemistry Department, Max Planck Institute for Brain Research, Max Planck Society;

/persons/resource/persons207980

Gomeza, J.
Neurochemistry Department, Max Planck Institute for Brain Research, Max Planck Society;

/persons/resource/persons207950

Eulenburg, V.
Neurochemistry Department, Max Planck Institute for Brain Research, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Latal, A. T., Kremer, T., Gomeza, J., Eulenburg, V., & Hülsmann, S. (2010). Development of synaptic inhibition in glycine transporter 2 deficient mice. Molecular and Cellular Neuroscience, 44(4), 342-352.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002E-1D2A-F

Abstract

Mice deficient for the neuronal glycine transporter subtype 2 (GlyT2) die during the second postnatal week after developing neuromotor deficiencies, which resembles severe forms of human hyperekplexia. This phenotype has been attributed to a dramatic reduction in glycinergic neurotransmission. In the present study we analyzed the development of GABAergic and glycinergic synaptic transmission in GlyT2-knockout mice during early postnatal life. Anti-glycine immunohistochemistry in spinal cord and brainstem slices and whole-cell voltage-clamp recordings of glycinergic inhibitory postsynaptic currents (IPSCs) from hypoglossal motoneurons revealed strikingly reduced levels of synaptic glycine already at birth. Since GABA and glycine use the same vesicular inhibitory amino acid transporter (VIAAT or VGAT) we also analysed GABAergic neurotransmission. No increase of GABA immunoreactivity was observed in the spinal cord and brainstem of GlyT2(-/-) mice at any stage of postnatal development. Correspondingly no up-regulation of GABAergic IPSCs was detected in GlyT2(-/-) hypoglossal motoneurons. These data suggest that in the first postnatal week, loss of the glycine transporter 2 is neither compensated by glycine de-novo synthesis nor by up-regulation of the GABAergic transmission in GlyT2(-/-) mice. (C) 2010 Elsevier Inc. All rights reserved.