Immunohistochemical localization of taurine-synthesizing enzyme in the rat olfactory bulb

The mammalian brain is rich in the amino acid taurine that is synthesized via cysteine sulfinate decarboxylase (CSD). Taurine has been shown to be an inhibitory neuromodulator as well as a trophic factor essential for neuronal differentiation. Brain taurine has uneven regional distribution, being particularly concentrated in the main olfactory bulb, where it is the most abundant neuroactive amino acid, exceeding glutamate and GABA in concentration. A group of researchers has employed antiserum against CSD purified from rat liver to study the nature of taurineproducing cells in some brain regions. These studies localized CSD to astrocytes in the cerebellum and hippocampus, implying that brain synthesis of taurine is solely associated with glial cells. In the present study, immunohistochemical localization of CSD in the rat olfactory bulb was examined using polyclonal antibodies that we developed to a synthetic fragment of the CSD protein. With these antibodies, CSD immunoreactivity was found in primary olfactory afferents, various neurons in the glomerular and external plexiform layers, and in mitral cells. These elements also showed taurine immunoreactivity. Granule cells were immunonegative for CSD but contained taurine. The results demonstrate potential sites of taurine production in the main olfactory bulb and suggest that neuronal cells are involved in brain biosynthesis of taurine

Anatomy and neurochemistry of the olfactory bulb

This chapter focuses on anatomical organization and neurotransmitters of the olfactory bulb, with an emphasis on afferent projections from brain sources. An overview of neuronal and molecular mechanisms underlying odor coding in the olfactory bulb is also provided. Most of the information comes from rodents; human data are presented, whenever possible. A number of original papers could not be cited due to space limitations

Direct inhibitory effect of taurine on relay neurones of the rat olfactory bulb in vitro.

none3Whole-cell recordings in rat olfactory bulb slices showed that bath application of 5 mM taurine produces a potent and reversible inhibition of identified mitral and tufted cells. Under current-clamp conditions, a shift of the membrane potential toward the chloride equilibrium potential and a 75% reduction in the membrane resistance were observed. These effects were strongly blocked by bicuculline (10 microM), but not by GABA(B) antagonist and strychnine, and completely maintained under the blockage of synaptic transmission. The results suggest that inhibition of bulbar relay neurons produced by taurine is primarily due to direct activation of somatic GABA(A) receptors and initiation of chloride conductance. This study demonstrates for the first time the actions of taurine in the olfactory system.nonePuopolo M; Kratskin I; Belluzzi O.Puopolo, M; Kratskin, I; Belluzzi, Ottorin

Neuroinhibitory actions of taurine in the main olfactory bulb

The amino acid taurine is abundant in the olfactory bulb (OB), exceeding glutamate and GABA in concentration. In whole-cell patch-clamp recordings in slices of rat OB, we studied the actions of taurine on the principal neurons (PNs), mitral and tufted cells, and the local interneurons, periglomerular (PG) cells. Taurine decreased, in a dose-dependent manner (EC50 = 2.2 mM), the input resistance of PNs and shifted membrane potential towards ECl. The GABAA receptor antagonists, bicuculline and picrotoxin, but not GABAB receptor antagonists, CGP 35348 and CGP 55845A, blocked the taurine effects. This implies that taurine inhibits PNs by increasing GABAA receptor Cl– conductance. PG cells, which also express GABAA receptors, were insensitive to taurine. Olfactory nerve stimulation evoked monosynaptic excitatory responses in PNs and PG cells voltage clamped at ECl or treated with picrotoxin. Taurine (5 mM) and the GABAB receptor agonist baclofen suppressed PNs responses. CGP 55845A, but not bicuculline and the postsynaptic GABAB receptor antagonist CGP 35348, abolished this suppression. The taurine action most likely was due to GABAB receptor-mediated inhibition of presynaptic glutamate release. Neither taurine nor baclofen affected PG cell responses. The results suggest that taurine reduces the excitability of PNs and their sensory input without influencing PG cells. Selective inhibitory actions of taurine in the OB may represent a physiologic mechanism protecting PNs from hyperexcitation. Supported by NIH grant DC04083 (I.K.) and Fondazione Caricento (O.B.)

Selective neuroinhibitory effects of taurine in slices of rat main olfactory bulb

Taurine is abundant in the main olfactory bulb, exceeding glutamate and GABA in concentration. In whole-cell patch-clamp recordings in rat olfactory bulb slices, taurine inhibited principal neurons, mitral and tufted cells. In these cells, taurine decreased the input resistance and caused a shift of the membrane potential toward the chloride equilibrium potential. The taurine actions were sustained under the blockade of transmitter release and were reversible and dose-dependent. At a concentration of 5 mM, typically used in this study, taurine showed 90% of its maximal effect. GABAA antagonists, bicuculline and picrotoxin, blocked the taurine actions, whereas the glycine receptor antagonist strychnine and GABAB antagonists, CGP 55845A and CGP 35348, were ineffective. These findings are consistent with taurine directly activating GABAA receptors and inducing chloride conductance. Taurine had no effect on periglomerular and granule interneurons. The subunit composition of GABAA receptors in these cells, differing from those in mitral and tufted cells, may account for taurine insensitivity of the interneurons. Taurine suppressed olfactory nerve-evoked monosynaptic responses of mitral and tufted cells while chloride conductance was blocked. This action was mimicked by the GABAB agonist baclofen and abolished by CGP 55845A; CGP 35348, which primarily blocks postsynaptic GABAB receptors, was ineffective. The taurine effect most likely was due to GABAB receptor-mediated inhibition of presynaptic glutamate release. Neither taurine nor baclofen affected responses of periglomerular cells. The lack of a baclofen effect implies that functional GABAB receptors are absent from olfactory nerve terminals that contact periglomerular cells. These results indicate that taurine decreases the excitability of mitral and tufted cells and their responses to olfactory nerve stimulation without influencing periglomerular and granule cells. Selective effects of taurine in the olfactory bulb may represent a physiologic mechanism that is involved in the inhibitory shaping of the activation pattern of principal neurons