k.p.collins at worldnet.att.net
Sun Nov 3 01:45:45 EST 2002
Since I was on PubMed:
A novel mechanism of dendritic spine plasticity involving estradiol
induction of prostaglandin-E2.
Amateau SK, McCarthy MM.
Program in Neuroscience, University of Maryland at Baltimore, School
of Medicine, Baltimore, Maryland 21201, USA. samat001 at umaryland.edu
The mechanisms establishing and maintaining dendritic spines in the
mammalian CNS remain primarily unknown. We report a novel mechanism
of neuronal spine plasticity in the developing preoptic area in which
estradiol induces prostaglandin-E2 (PGE2) synthesis that in turn
increases the density of spine-like processes. Estradiol requires
PGE2 synthesis, in vivo and in vitro, and upregulates the dendritic
spine protein spinophilin, an effect attenuated by antagonism of the
AMPA-kainate receptor. This signaling pathway may involve cross talk
between neighboring neurons and astrocytes and appears specific to
the preoptic area in that hippocampal neurons responded with an
increase in spinophilin to estradiol but not PGE2. Regionally
specific mechanisms of estradiol-mediated synaptic plasticity allow
for epigenetic control of complex sex-typic behaviors.
PMID: 12351732 [PubMed - indexed for MEDLINE]
© by someone other than me.
"Functional multiplexing", AoK, Ap9, and ['maybe'] glial-neuron
"cross talk", AoK, Ap5.
Functionally-multiplexed TD E/I-minimization at the cellular level
There's more than one form of backward propagation.
Hey! This's fun!
K. P. Collins
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