Taurine and β-alanine Sample Clauses

Taurine and β-alanine. Taurine is released from neurons and glia upon hypo-osmotic swelling and is believed to behave chiefly as an osmoregulator. However, in spinal cord, microdialysis experiments reveal that taurine and β-alanine are released following sciatic nerve stimulation in concentrations comparable to glutamate (Paleckova, Xxxxxxx et al. 1992). Taurine and β-alanine are weak agonists at GABAA receptors (Xxxxxx and Xxxxx 0000), though taurine may also be a potent activator of extrasynaptic GABAA receptors (Jia, Yue et al. 2008). Taurine and β-alanine also directly depolarize primary afferents in the in vitro rat spinal cord (Xxxxx 1978). As in frog, responses are blocked by picrotoxin (50 μM) and bicuculline (5 μM). Like GABA and glycine, taurine and β-alanine are transported via Na+-dependent high affinity uptake systems with significant sequence homology to the GABA and glycine transporters systems (Xxxxx, Xxxxxx et al. 1992; Liu, Xxxxx-Xxxxxxxx et al. 1993). More recently, taurine labeling has been demonstrated in spinal cord with greatest density in superficial dorsal horn, but also associated with myelinated axon terminals (Lee, Renno et al. 1992). Additionally, cysteine dioxygenase and sulfinoalanine decarboxylase, two critical enzymes in the taurine synthesis, are expressed in primary afferents (Xxxxxx, Xu et al. 2006) and synaptic vesicles contained within synaptosomes are enriched in taurine (Bonhaus, Lippincott et al. 1984). In sum, primary afferents may co-release substances that act on receptors having GABAA-like pharmacology.