Increase of thyrotropin-releasing hormone immunoreactivity in the nucleus of the solitary tract following bilateral lesions of the hypothalamic paraventricular nuclei.
The effects of bilateral electrolytic lesions of hypothalamic paraventricular nucleus on thyrotropin-releasing hormone (TRH)-immunoreactive fibers of the nucleus of the solitary tract were studied by both immunocytochemistry and radioimmunoassay. Contrasting with a near disappearance of TRH immunoreactivity in the median eminence, both morphological and biochemical approaches demonstrate that such hypothalamic lesions induced significant increase of TRH immunoreactivity in the nucleus of solitary tract. These results confirm that TRH fibers of the nucleus of the solitary tract do not originate in the hypothalamic paraventricular nucleus (PVN). They further indicate that these TRH neurons projecting to the nucleus of the solitary tract are strongly influenced by neurons located within the PVN area.
D000818:Animals; D006651:Histocytochemistry; D007124:Immunoenzyme Techniques; D008297:Male; D008526:Medulla Oblongata / Q000033:anatomy & histology / Q000378:metabolism*; D009434:Neural Pathways / Q000033:anatomy & histology / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000033:anatomy & histology / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism*; D013997:Time Factors
D013973:Thyrotropin-Releasing Hormone