Organum Vasculosum Lamina Terminalis Neurons Research Articles

Human recombinant tumor necrosis factor and interferon affect the activity of neurons in the organum vasculosum laminae terminalis

It is generally thought that fever is induced by blood-borne cytokines via an action on hypothalamic thermosensitive neurons. Recent studies suggest that the organum vasculosum laminae terminalis (OVLT), which lacks the blood-brain barrier, may be necessary for fever induction by systemic pyrogens. We have examined the responses of neurons in the OVLT to the pyrogenic cytokines, human recombinant tumor necrosis factor α (TNF) and interferon α2 (IFN), by recording extracellular single-units in brain slice preparations from guinea pigs. Of all the OVLT neurons tested with TNF (900–5000 ng/ml perfusate/min) and IFN (1200–8500 units/ml perfusate/min), administered for 2.5 min, 44% increased their firing rates (FR) for 30.6–57.5 min (average, 47.4 min) with onset latencies of 6.1–9.8 min (average, 7.9 min). The remaining 56% of the neurons did not change their FR after TNF or IFN. Carrier vehicles for these cytokines produced no FR change. The results suggest the possibility that the OVLT may be a site where chemical signals of blood-borne cytokines are transduced into neuronal signals.

Altered angiotensin II sensitivity of neurons in the organum vasculosum lamina terminalis region of the spontaneously hypertensive rat

Using in vitro hypothalamic brain slices, differences in angiotensin II (AII) sensitivity of neurons in the organum vasculosum lamina terminalis (OVLT) region were compared between spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY). AIIm the AII competitive antagonist saralasin, and l-glutamate were micropressure-applied onto OVLT neurons. AII excitation of SHR neurons was blocked or antagonized by simultaneous application of saralasin, evoked at significantly lower thresholds and displayed exaggerated periods of postactivity compared to OVLT neurons in preparations taken from WKY controls. Neuronal responses to l-glutamate were similar between the two rat strains. Differences in neuronal sensitivity to AII may be causally linked to hypertension in SHR.

Development of angiotensin II-sensitive OVLT neurons in SHR and WKY rats

Angiotensin II (AII) sensitivity of neurons in the region of the organum vasculosum laminae terminalis (OVLT) was examined electrophysiologically using in vitro hypothalamic brain slices taken from 4-, 9- and 14-week-old spontaneously hypertensive (SHR) and normotensive Wintar-Kyoto (WKY) rats. Micropressure application of AII, its competitive antagonist saralasin, and l-glutamate revealed that neurons in this region of SHR were significantly more sensitive to AII than cells in age-matched WKY preparations. Neuronal sensitivity to l-glutamate was similar between SHR and WKY rats at all ages. Following electrophysiological study, hypothalamic and cortical brain slices were assayed for 125I-labelled AII binding. AII receptor binding in the hypothalamic slices from SHR was elevated significantly above binding in WKY hypothalamic slices at 4, 9, and weeks of age. In contrast. AII binding in cortical slices taken from SHR and WKY rats was similar. These data suggest that altered neuronal AII-sensitivity is not a consequence of hypertension development in SHR and may contribute to its development.