Delayed pituitary adenylate cyclase-activating polypeptide delivery after brain stroke improves functional recovery by inducing m2 microglia/macrophage polarization.

Background And Purpose: Until now, except thrombolysis, the therapeutical strategies targeting the acute phase of cerebral ischemia have been proven ineffective, and no approach is available to attenuate the delayed cell death mechanisms and the resulting functional deficits in the late phase. Then, we investigated whether a targeted and delayed delivery of pituitary adenylate cyclase-activating polypeptide (PACAP), a peptide known to exert neuroprotective activities, may dampen delayed pathophysiological processes improving functional recovery.

Methods: Three days after permanent focal ischemia, PACAP-producing stem cells were transplanted intracerebro ventricularly in nonimmunosuppressed mice.

Effects of corticosterone synthesis inhibitor metyrapone on anxiety-related behaviors in Lurcher mutant mice.

Beyond their motor impairments, the cerebellar Lurcher mutant mice show an alteration of the anxiety-related behaviors we called "behavioral disinhibition". This is characterized by a low avoidance towards the open arms of the elevated plus-maze device paradoxically combined with a dramatic blood corticosterone level rise induced by the exposure to the experimental conditions. The present study was aimed at determining if the disinhibition of the mutants could be caused by their stress-induced high corticosterone rate.

The N-terminal neurotensin fragment, NT1-11, inhibits cortisol secretion by human adrenocortical cells.

Context: Neurotensin (NT) modulates corticosteroid secretion from the mammalian adrenal gland.

Objective: The objective of this study was to investigate the possible involvement of NT in the control of cortisol secretion in the human adrenal gland.

Design: In vitro studies were conducted on cultured human adrenocortical cells.

Activation of endothelinA receptors in frog adrenocortical cells stimulates both calcium mobilization from intracellular stores and calcium influx through L-type calcium channels.

We have previously shown that endothelin (ET)-1 stimulates corticosterone and aldosterone secretion by the frog adrenal gland through activation of ETA receptors positively coupled to both the adenylyl cyclase and phospholipase C (PLC) pathways. The purpose of the present study was to investigate the involvement of calcium in ET-1-induced stimulation of corticosteroid secretion. Cytoautoradiographic labeling using [125I]ET-1 as a tracer revealed the presence of ET-1 binding sites on adrenocortical cells.