Vasopressin-Containing Neurons of the Hypothalamic Parvocellular Paraventricular Nucleus of the Jerboa: Plasticity Related to Immobilization Stress

Abstract

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.

Immunocytochemical distribution of EM66 within the hypothalamic parvocellular paraventricular nucleus: Colocalization with CRH and TRH but no plasticity related to acute stress and thyroidectomy in the rat

“…Using protocols thoroughly validated previously [21,[40][41][42][43], the present work showed that acute immobilization (2 h) or cold exposure (5°C, 4 h) did not affect the EM66 immunoreactivity evaluated by the number of EM66-IR neurons within the pPVN. Consistent with these results, other paradigms such as acute immune stress induced by an ip injection of LPS, known to increase cytokines in brain and plasma [44,45], or central injection of cytokines as IL-1β known to be associated with HPA axis activation, did not affect the number of EM66-IR neurons of the pPVN [21].…”

The role of oxytocin in regulation of appetitive behaviour, body weight and glucose homeostasis

“…Intragastric administration of nutrients that promote satiety (eg, select amino acids) also triggers OXT gene expression and OXT neuronal activation in mice. Importantly, OXT neurones or terminals co‐express other anorexigens, including corticotrophin‐releasing hormone, nesfatin‐1 and cholecystokinin (CCK), and OXT appears to contribute to and/or potentiate the hypophagic action of nesfatin‐1, CCK and leucine in rats and mice. OXT neuronal activation is modified by feeding regulatory peptides either directly (via synapses formed with OXT cells) or indirectly (as an element of broader circuits).…”

Electroconvulsive seizure-induced changes in gene expression in the mouse hypothalamic paraventricular nucleus

“…Among them, we focused on the gene encoding cholecystokinin (Cck) as a target candidate for trial antidepressant drugs and as a modulator of the stress responses in the PVN. CCK is a neuropeptide that is involved in feeding, memory formation, and anxiety behavior, and it is expressed in both CRH-and AVP-containing neurons of the PVN (Barakat et al, 2006;Beinfeld et al, 1980;Mezey et al, 1986;Vanderhaeghen et al, 1980). It has been reported that the administration of stress or glucocorticosteroids upregulates Cck mRNA expression in the PVN (Cournil et al, 2000;Kim et al, 2003).…”