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.

EM66 is a secretogranin II-derived peptide strongly expressed within hypothalamic neuroendocrine areas such as the parvocellular aspect of the paraventricular nucleus (pPVN) as well as the median eminence (ME), suggesting a hypophysiotropic role for this neuropeptide. The aim of the present study was to explore such a role in the corticotrope and thyrotrope axes. We analyzed EM66 occurrence respectively in CRH and TRH neurosecretory cells of the rat pPVN by double immunohistochemistry. Functionally, we studied the effect of acute stress (immobilization for 2 h or cold exposure at 5°C for 4 h) and hypothyroidism (induced by 1-week thyroidectomy) on EM66 immunoreactivity (IR) within the pPVN. Double immunohistochemical labeling revealed that EM66-IR colocalized with CRH or TRH labelings within pPVN hypophysiotropic neurons as well as the axon terminals of the external layer of the ME. Because TRH neuronal population of the pPVN is completely distinct from the CRH neurosecretory system, our data demonstrate the existence of at least two distinct EM66 neuronal populations in the rat pPVN. Acute immobilization or cold exposure stresses did not affect EM66 expression as evaluated by the number of EM66-IR neurons within the pPVN. These results suggest that EM66 does not participate to the phenotypic plasticity of hypothalamic parvocellular neurons in response to acute stress. In addition, short-term hypothyroidism did not provoke any significant variation of the number of intraparaventricular EM66 neurons, indicating that EM66 expression would be insensitive to short-term hypothyroidism despite its occurrence within TRH neurons. Thus, the present data show the occurrence of EM66 in distinct areas of the rat PVN but its expression is not coregulated with those of CRH and TRH during acute stress and hypothyroidism.
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