Vasopressin-containing neurons of the hypothalamic parvocellular paraventricular nucleus of the jerboa: plasticity related to immobilization stress.
The corticotropin-releasing hormone (CRH) neurons of the hypothalamic parvocellular paraventricular nucleus (PVN) have a high potential for phenotypical plasticity, allowing them to rapidly modify their neuroendocrine output, depending upon the type of stressors. Indeed, these neurons coexpress other neuropeptides, such as cholecystokinin (CCK), vasopressin (VP), and neurotensin, subserving an eventual complementary function to CRH in the regulation of the pituitary. Unlike in rats, our previous data showed that in jerboas, CCK is not coexpressed within CRH neurons in control as well as stressed animals. The present study explored an eventual VP participation in the phenotypic plasticity of CRH neurons in the jerboa. We analyzed the VP expression within the PVN by immunocytochemistry in male jerboas submitted to acute stress. Our results showed that, contrary to CRH and CCK, no significant change concerned the number of VP-immunoreactive neurons following a 30-min immobilization. The VP/CRH coexpression within PVN and median eminence was investigated by double immunocytochemistry. In control as well as stressed animals, the CRH-immunopositive neurons coexpressed VP within cell bodies and terminals. No significant difference in the number of VP/CRH double-labeled cells was found between both groups. However, such coexpression was quantitatively more important into the posterior PVN as compared with the anterior PVN. This suggests an eventual autocrine/paracrine or endocrine role for jerboa parvocellular VP which is not correlated with acute immobilization stress. VP-immunoreactive neurons also coexpressed CCK within PVN and median eminence of control and stressed jerboas. Such coexpression was more important into the anterior PVN as compared with the posterior PVN. These results showed the occurrence of at least two VP neuronal populations within the jerboa PVN. In addition, the VP expression did not depend upon acute immobilization stress. These data highlight differences in the neuroendocrine regulatory mechanisms of the stress response involving CRH/CCK or VP. They also underline that adaptative physiological mechanisms to stress might vary from one mammal species to another.
Barakat
Y
Y
Laboratory of Neuroendocrinology and Nutritional and Climatic Environment, Faculty of Sciences Dhar-El Mahraz, University Sidi Mohamed Ben Abdellah, Fez, Morocco.
Pape
J R
JR
Boutahricht
M
M
El Ouezzani
S
S
Alaoui
A
A
Chaigniau
M
M
Barakat
L
L
Tramu
G
G
Mâgoul
R
R
D000818:Animals; D002766:Cholecystokinin / Q000235:genetics / Q000378:metabolism; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D005260:Female; D008297:Male; D008473:Median Eminence / Q000166:cytology / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology / Q000378:metabolism*; D012149:Restraint, Physical; D012377:Rodentia; D013315:Stress, Psychological / Q000378:metabolism / Q000503:physiopathology*; D014667:Vasopressins / Q000235:genetics / Q000378:metabolism*
D014667:Vasopressins; D002766:Cholecystokinin; D003346:Corticotropin-Releasing Hormone