Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release.

Dec 24, 1997Journal of neuroscience research

Loss of a key hormone in the brain's internal clock affects hormone levels in stress-control neurons and increases stress hormone release

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Abstract

AVP content in the suprachiasmatic nucleus (SCN) was reduced by 24% following targeted microinjection of a toxin.

A significant decrease in AVP expression in the SCN was observed, as indicated by reduced AVP immunoreactive content and mRNA levels.
Decreased AVP content in the parvocellular subdivision of the paraventricular nucleus (pPVN) aligns with the observed depletion in the SCN.
Increased AVP content and mRNA were found in the magnocellular subdivision of the paraventricular nucleus (mPVN), suggesting differential regulation of AVP synthesis.
Plasma ACTH levels were double following AVP depletion, indicating potential stimulation of the hypothalamo-pituitary-adrenal system.
Concurrently, corticotrophin-releasing hormone (CRH) mRNA increased by 24% in the PVN, while CRH content in the median eminence decreased by 26%.

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Arginine vasopressin (AVP) produced in the hypothalamic suprachiasmatic nuclei (SCN) plays a role in establishing neuroendocrine rhythms and, in particular, in regulating the corticotrope axis rhythm. It has recently been shown that AVP from SCN inhibits corticosteroid release. In order to investigate the influence of suprachiasmatic AVP on the different peptidergic systems through the hypothalamus, SCN neurons containing AVP were functionally lesioned by using toxins associated with a cytotoxic monoclonal antibody (MAb) raised against AVP. Six days later, the AVP contents and AVP mRNA were measured in different hypothalamic and extrahypothalamic sites. Adrenocorticotrophic hormone (ACTH) concentration was also measured in plasma. Microinjection of the AVP-MAb/toxin mixture into SCN brought about a significant decrease in the AVP expression in SCN. This is demonstrated by the decrease in the AVP immunoreactive content (24%, P < 0.01) and the decrease of AVP hybridized mRNA (33%, P < 0.01). This points to the efficiency of the microinjection in decreasing the production of AVP in the injection area. Modifications of the AVP contents in the two subdivisions of the hypothalamic paraventricular nucleus (PVN) were also observed. AVP contents decreased in the parvocellular subdivision (pPVN); this is coherent with the AVP depletion in SCN since pPVN is the major site of the SCN hypothalamic efferences. AVP content and AVP mRNA increased in the magnocellular subdivision (mPVN); this also confirms the difference in AVP synthesis regulation according to the PVN subdivisions. The microinjection did not modify AVP expression in supraoptic nuclei or oxytocin (OT) immunoreactive content in the main hypothalamic OT containing sites. Plasma ACTH values were double (P < 0.02) the values measured under non-specific IgG treatment 10 hr after lights on. This probably resulted from the stimulation of the hypothalamo-pituitary-adrenal system since corticotrophin-releasing hormone (CRH) mRNA increased simultaneously by 24% (P < 0.05) in the PVN and the immunoreactive CRH content of the median eminence significantly decreased (26%, P < 0.05). Overall, our data confirm that AVP produced in the SCN inhibits the CRH-adrenocorticotrope axis in normal conditions, probably because of SCN projections of AVP neurons on the PVN.

Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release.

Abstract

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