Submitted on November 29, 2006
Accepted on January 2, 2007
Substantia nigra osmoregulation: Taurine and ATP involvement
Ingrid Morales1, Jose Dopico1, Magdalena Sabate2, Tomas Gonzalez-Hernandez3, and Manuel Rodriguez4*
1 Laboratory of Neurobiology and Experimental Neurology, Department of Physiology, University of La Laguna, La Laguna, Tenerife, Canary Islands, Spain
2 Department of Pharmacology and Physical Medicine, University of La Laguna, La Laguna, Tenerife, Canary Islands, Spain
3 Department of Anatomy, University of La Laguna, La Laguna, Tenerife, Canary Islands, Spain
4 Laboratory of Neurobiology and Experimental Neurology, Department of Physiology, University of La Laguna, Tenerife, Canary Islands, Spain
* To whom correspondence should be addressed. E-mail: mrdiaz{at}ull.es.
An extracellular non-synaptic taurine pool of glial origin was recently reported in the substantia nigra (SN). There is previous evidence showing taurine as an inhibitory neurotransmitter in the substantia nigra (SN) but the physiological role of this non-synaptic pool of taurine has not been explored. By using microdialysis methods, the action of local osmolarity on non-synaptic taurine pool was studied in the SN of the rat. Hypo-osmolar pulses (285-80 mOsm) administered in the SN by the microdialysis probe increased extrasynaptic taurine in a dose-dependent way, a response that was counteracted by compensating osmolarity with choline. The opposite effect (taurine decrease) was observed when osmolarity was increased. Under basal conditions, the blockade of either the AMPA-kainate glutamate receptors with 6-cyano-7-nitroquinoxaline-2,3-dionine disodium or the purinergic receptors with pyridoxalphosphate-6-azophenyl-2`,4`-disulphonic acid modified the taurine concentration, suggesting that both receptors modulate the extrasynaptic pool of taurine. In addition, these drugs decreased the taurine response to hypo-osmolar pulses, suggesting roles for glutamatergic and purinergic receptors on the taurine response to osmolarity. The participation of purinergic receptors was also supported by the fact that ATP (which under basal conditions increased the extrasynaptic taurine in a dose-dependent way) administered in doses saturating purinergic receptors also decreased the taurine response to hypo-osmolarity. Taken together, present data suggest osmoregulation as a role of the non-synaptic taurine pool of the SN, a function which also involves glutamate and ATP, and which could influence the nigral-cell vulnerability in Parkinson`s disease.
