Functional ectopic neural lobe increases GAP-43 expression via PI3K/AKT pathways to alleviate central diabetes insipidus after pituitary stalk lesion in rats.

Abstract:

:Central diabetes insipidus can occur after hypothalamic-hypophyseal tract injury. This injury is linked with a deficit in circulating vasopressin and oxytocin, which are produced in the supraoptic nuclei and the hypothalamic paraventricular nuclei. Previous studies indicate that an ectopic neural lobe forms after pituitary stalk lesion in rats, and while the relationship between an ectopic neural lobe and CDI outcomes is unclear, the underlying mechanisms are also unknown. Here, we report that two different CDI characteristics are shown in rats that underwent pituitary stalk electric lesion and are defined by two different groups classified as the recovery group and the no-recovery group. Rats showed an enlarged functional ectopic neural lobe at the lesion site with a low CDI index. Moreover, growth associated protein-43, p-PI3K and p-AKT were up-regulated in the unmyelinated fibers of the ectopic neural lobe. Our findings suggest that the enlarged structure formed a functional ectopic neural lobe after the pituitary stalk lesion, and its regeneration might influence the CDI outcome. This regeneration might be due to an increase in GAP-43 expression through the PI3K/AKT pathway.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Feng Z,Ou Y,Zhou M,Wu G,Ma L,Zhang Y,Liu Y,Qi S

doi

10.1016/j.neulet.2018.02.038

subject

Has Abstract

pub_date

2018-04-23 00:00:00

pages

1-6

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(18)30120-4

journal_volume

673

pub_type

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