EMBRYONIC AND POSTNATAL EXPRESSION OF 4 GAMMA-AMINOBUTYRIC-ACID TRANSPORTER MESSENGER-RNAS IN THE MOUSE-BRAIN AND LEPTOMENINGES

Citation
Je. Evans et al., EMBRYONIC AND POSTNATAL EXPRESSION OF 4 GAMMA-AMINOBUTYRIC-ACID TRANSPORTER MESSENGER-RNAS IN THE MOUSE-BRAIN AND LEPTOMENINGES, Journal of comparative neurology, 376(3), 1996, pp. 431-446
Citations number
64
Categorie Soggetti
Neurosciences
ISSN journal
00219967
Volume
376
Issue
3
Year of publication
1996
Pages
431 - 446
Database
ISI
SICI code
0021-9967(1996)376:3<431:EAPEO4>2.0.ZU;2-H
Abstract
The distribution of gamma-aminobutyric acid (GABA) transporter mRNAs ( mGATs) was studied in mouse brain during embryonic and postnatal devel opment using in situ hybridization with radiolabeled oligonucleotide p robes. Mouse GATs 1 and 4 were present in the ventricular and subventr icular zones of the lateral ventricle from gestational day 13. During postnatal development, mGAT1 mRNA was distributed diffusely throughout the brain and spinal cord, with the highest expression present in the olfactory bulbs, hippocampus, and cerebellar cortex. The mGAT4 messag e was densely distributed throughout the central nervous system during postnatal week 1; however, the hybridization signal in the cerebral c ortex and hippocampus decreased during postnatal weeks 2 and 3, and in adults, mGAT4 labeling was restricted largely to the olfactory bulbs, midbrain, deep cerebellar nuclei, medulla, and spinal cord. Mouse GAT E mRNA was expressed only in proliferating and migrating cerebellar gr anule cells, whereas mGAT3 mRNA was absent from the brain and spinal c ord throughout development. Each of the four mGATs was present to some degree in the leptomeninges. The expression of mGATs 2 and 3 was almo st entirely restricted to the pia-arachnoid, whereas mGATs 1 and 4 wer e present only in specific regions of the membrane. Although mGATs 1 a nd 4 may subserve the classical purpose of terminating inhibitory GABA ergic transmission through neuronal and glial uptake mechanisms, GABA transporters in the pia-arachnoid may help to regulate the amount of G ABA available to proliferating and migrating neurons at the sub-pial s urface during perinatal development. (C) 1996 Wiley-Liss, Inc.