IBYME   02675
INSTITUTO DE BIOLOGIA Y MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
artículos
Título:
Estradiol increases dendritic length and spine density in CA1 neurons of the hippocampus of spontaneously hypertensive rats: A Golgi impregnation study.
Autor/es:
BROCCA, M. ELVIRA; PIETRANERA, LUCIANA; BEAUQUIS, JUAN; DE NICOLA, ALEJANDRO F.
Revista:
EXPERIMENTAL NEUROLOGY
Editorial:
ACADEMIC PRESS INC ELSEVIER SCIENCE
Referencias:
Lugar: Amsterdam; Año: 2013 vol. 247 p. 158 - 164
ISSN:
0014-4886
Resumen:
Increased neuronal vulnerability has been described in the brain of
spontaneously hypertensive rats (SHR), models of primary hypertension.
Previous data indicate that estradiol treatment corrects several
dysfunctions of the hippocampus and hypothalamus of SHR. Considering
this evidence we analyzed the dendritic arborization and spine density
of the CA1 subfield in SHR and Wistar-Kyoto (WKY) normotensive rats with
and without estradiol treatment. Five month old male SHR and WKY rats
received single estradiol or cholesterol pellets (sham treatment) for 2
weeks. A substantial rise of circulating estradiol (>25 fold) and
testicular atrophy was present in all estradiol-receiving rats. In both
SHR and WKY rats, estradiol decreased blood pressure by ~20 mm Hg;
however, a moderate hypertension persisted in SHR (164 mm Hg). Using a
modified Golgi impregnation technique, apical and basal dendrites of the
CA1 subfield were subjected to Sholl analysis. Spine density was also
statistically analyzed. Apical dendritic length was significantly lower
in SHR compared to WKY rats (p<0.01), whereas estradiol treatment
increased dendritic length in the SHR group only (SHR vs SHR+estradiol;
p<0.01). Apical dendritic length plotted against the shell distances
20-100, 120-200 and 220-300 μm, revealed that changes were more
pronounced in the range 120-200 μm between SHR vs. WKY rats (p<0.05)
and SHR vs. SHR+estradiol (p<0.05). Instead, basal dendrites were not
significantly modified by hypertension or steroid treatment. Spine
density of apical dendrites was lower in SHR than WKY (p<0.05) and
was up-regulated in the SHR+estradiol group compared to the SHR group
(p<0.001). Similar changes were obtained for basal dendritic spines.
These data suggest that changes of neuronal processes in SHR are plastic
events restorable by estradiol treatment. In conjunction with previous
results, the present data reveal new targets of estradiol
neuroprotection in the brain of hypertensive rats.