Neutrinoless double-beta decay and seesaw mechanism

From the standard seesaw mechanism of neutrino mass generation, which is based on the assumption that the lepton number is violated at a large (~10exp(+15) GeV) scale, follows that the neutrinoless double-beta decay is ruled by the Majorana neutrino mass mechanism. Within this notion, for the inverted neutrino-mass hierarchy we derive allowed ranges of half-lives of the neutrinoless double-beta decay for nuclei of experimental interest with different sets of nuclear matrix elements. The present-day results of the calculation of the neutrinoless double-beta decay nuclear matrix elements are briefly discussed. We argue that if neutrinoless double-beta decay will be observed in future experiments sensitive to the effective Majorana mass in the inverted mass hierarchy region, a comparison of the derived ranges with measured half-lives will allow us to probe the standard seesaw mechanism assuming that future cosmological data will establish the sum of neutrino masses to be about 0.2 eV.Comment: Some changes in sections I, II, IV, and V; two new figures; additional reference

Modulation of Neurally Mediated Vasodepression and Bradycardia by Electroacupuncture through Opioids in Nucleus Tractus Solitarius

Abstract Stimulation of vagal afferent endings with intravenous phenylbiguanide (PBG) causes both bradycardia and vasodepression, simulating neurally mediated syncope. Activation of µ-opioid receptors in the nucleus tractus solitarius (NTS) increases blood pressure. Electroacupuncture (EA) stimulation of somatosensory nerves underneath acupoints P5–6, ST36–37, LI6–7 or G37–39 selectively but differentially modulates sympathoexcitatory responses. We therefore hypothesized that EA-stimulation at P5–6 or ST36–37, but not LI6–7 or G37–39 acupoints, inhibits the bradycardia and vasodepression through a µ-opioid receptor mechanism in the NTS. We observed that stimulation at acupoints P5–6 and ST36–37 overlying the deep somatosensory nerves and LI6–7 and G37–39 overlying cutaneous nerves differentially evoked NTS neural activity in anesthetized and ventilated animals. Thirty-min of EA-stimulation at P5–6 or ST36–37 reduced the depressor and bradycardia responses to PBG while EA at LI6–7 or G37–39 did not. Congruent with the hemodynamic responses, EA at P5–6 and ST36–37, but not at LI6–7 and G37–39, reduced vagally evoked activity of cardiovascular NTS cells. Finally, opioid receptor blockade in the NTS with naloxone or a specific μ-receptor antagonist reversed P5–6 EA-inhibition of the depressor, bradycardia and vagally evoked NTS activity. These data suggest that point specific EA stimulation inhibits PBG-induced vasodepression and bradycardia responses through a μ-opioid mechanism in the NTS