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2014 ; 307
(12
): R1405-12
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Sensitization of sodium appetite: evidence for sustained molecular changes in the
lamina terminalis
#MMPMID25354727
Hurley SW
; Zhang Z
; Beltz TG
; Xue B
; Johnson AK
Am J Physiol Regul Integr Comp Physiol
2014[Dec]; 307
(12
): R1405-12
PMID25354727
show ga
Animals with a history of sodium depletions exhibit increases in salt intake, a
phenomenon described as the sensitization of sodium appetite. Using a novel
experimental design, the present experiments investigated whether putative
molecular markers of neural plasticity and changes in the message for components
of the brain renin-angiotensin-aldosterone-system (RAAS) accompany the
sensitization of sodium appetite. An initial set of experiments examined whether
the glutamatergic N-methyl-d-aspartate receptor antagonist MK-801 would attenuate
sodium appetite sensitization and prevent changes in mRNA expression associated
with sensitization. Rats with repeated sodium depletions exhibited enhanced
sodium appetite and mRNA expression for components of the RAAS in areas along the
lamina terminalis (LT), a region of the brain that is important for the
regulation of body fluid homeostasis, and these effects were significantly
attenuated by MK-801 pretreatment. A second set of experiments investigated
whether successive sodium depletions would elevate sodium intake and induce a
pattern of fos-B staining consistent with the ?fos-B isoform in areas along the
LT. The pattern of fos-B staining in the subfornical organ was consistent with
the characteristics of ?fos-B expression. Specifically, fos-B/?fos-B expression
was increased 4 days after the last of a series of sodium depletions,
fos-B/?fos-B expression was nearly absent in control rats, and the quantity of
fos-B/?fos-B staining was directly associated with a history of sodium
depletions. These findings demonstrate that the sensitization of sodium appetite
is associated with sustained molecular alterations in the LT that are indicative
of neural plasticity and upregulation of the central RAAS.