Feasibility study of heavy ion collision physics at NICA JINR

The Nuclotron-based Ion Collider fAcility (NICA) project is under active realization at the Joint Institute for Nuclear Research (JINR, Dubna). The main goal of the project is experimental study of baryon rich QCD matter in heavy ion (up to Au) collisions at centre-of-mass energies up to 11 GeV per nucleon. Two modes of the operation is foreseen, collider mode and extracted beams, with the two detectors, MPD and BM@N. In the collider mode the average luminosity is L = 1027cm2s1 for Au(79+). Extracted beams of various nuclei species with maximum momenta 13 GeV/c (for protons) will be available. The NICA project also foresees a study of spin physics with the detector SPD with extracted and colliding beams of polarized deuterons and protons at centre-of-mass energies up to 27 GeV (for protons). The NICA experimental program allows to search for possible signs of the phase transitions and critical phenomena as well as to shed light on the problem of nucleon spin structure. Hereafter, feasibility studies of the observables, which are most sensitive to such phenomena, are presented

Chemical Synapses without Synaptic Vesicles: Purinergic Neurotransmission through a CALHM1 Channel-mitochondrial Signaling Complex

Conventional chemical synapses in the nervous system involve a presynaptic accumulation of neurotransmitter-containing vesicles, which fuse with the plasma membrane to release neurotransmitters that activate postsynaptic receptors. In taste buds, type II receptor cells do not have conventional synaptic features but nonetheless show regulated release of their afferent neurotransmitter, ATP, through a large-pore, voltage-gated channel, CALHM1. Immunohistochemistry revealed that CALHM1 was localized to points of contact between the receptor cells and sensory nerve fibers. Ultrastructural and super-resolution light microscopy showed that the CALHM1 channels were consistently associated with distinctive, large (1- to 2-μm) mitochondria spaced 20 to 40 nm from the presynaptic membrane. Pharmacological disruption of the mitochondrial respiratory chain limited the ability of taste cells to release ATP, suggesting that the immediate source of released ATP was the mitochondrion rather than a cytoplasmic pool of ATP. These large mitochondria may serve as both a reservoir of releasable ATP and the site of synthesis. The juxtaposition of the large mitochondria to areas of membrane displaying CALHM1 also defines a restricted compartment that limits the influx of Ca2+ upon opening of the nonselective CALHM1 channels. These findings reveal a distinctive organelle signature and functional organization for regulated, focal release of purinergic signals in the absence of synaptic vesicles