Modulation of glutamatergic transmission by sulfated steroids: role in fetal alcohol spectrum disorder.

Details

Serval ID
serval:BIB_116878C6C989
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Modulation of glutamatergic transmission by sulfated steroids: role in fetal alcohol spectrum disorder.
Journal
Brain research reviews
Author(s)
Valenzuela C.F., Partridge L.D., Mameli M., Meyer D.A.
ISSN
0165-0173 (Print)
ISSN-L
0165-0173
Publication state
Published
Issued date
03/2008
Volume
57
Number
2
Pages
506-519
Language
english
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Review
Publication Status: ppublish
Abstract
It is well established that sulfated steroids regulate synaptic transmission by altering the function of postsynaptic neurotransmitter receptors. In recent years, evidence from several laboratories indicates that these agents also regulate glutamatergic synaptic transmission at the presynaptic level in an age-dependent manner. In developing neurons, pregnenolone sulfate (PREGS) increases the probability of glutamate release, as evidenced by an increase in the frequency of AMPA receptor-mediated miniature excitatory postsynaptic currents and a decrease in paired-pulse facilitation. In hippocampal slices from postnatal day 3-5 rats, this effect is mediated by an increase in Ca(2+) levels in the axonal terminal that depends on presynaptic NMDA receptors. This is followed by delayed potentiation of postsynaptic AMPA receptor currents. Importantly, depolarization of postsynaptic neurons, inhibition of hydroxysteroid sulfatase activity and acute exposure to ethanol mimics the effect of exogenous PREGS application. This developmental form of synaptic plasticity cannot be observed in slices from rats older than postnatal day 6, when presynaptic NMDA receptors are no longer expressed in CA1 hippocampal region. Both in the CA1 hippocampal region and the dentate gyrus of more mature rats, PREGS, dehydroepiandrosterone sulfate and hydroxysteroid sulfatase inhibitors increase paired-pulse facilitation, without affecting basal glutamate release probability. This effect depends on activation of sigma(1)-like receptors and G(i/o) and involves a target in the release machinery that is downstream of residual Ca(2+). These presynaptic actions of sulfated steroids could play important roles in physiological processes ranging from synapse maturation to learning and memory, as well as pathophysiological conditions such as fetal alcohol spectrum disorder.

Keywords
Animals, Brain/drug effects, Brain/embryology, Brain/metabolism, Dehydroepiandrosterone Sulfate/metabolism, Ethanol/adverse effects, Female, Fetal Alcohol Spectrum Disorders/metabolism, Glutamine/metabolism, Humans, Neurons/drug effects, Neurons/metabolism, Pregnancy, Pregnenolone/metabolism, Receptors, N-Methyl-D-Aspartate/metabolism, Steroids/metabolism, Synaptic Transmission/drug effects, Synaptic Transmission/physiology
Pubmed
Create date
31/01/2017 15:49
Last modification date
20/08/2019 12:39
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