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Characteristics of taurine release in slices from adult and developing mouse brain stem

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Summary.

Taurine has been thought to function as a regulator of neuronal activity, neuromodulator and osmoregulator. Moreover, it is essential for the development and survival of neural cells and protects them under cell-damaging conditions. Taurine is also involved in many vital functions regulated by the brain stem, including cardiovascular control and arterial blood pressure. The release of taurine has been studied both in vivo and in vitro in higher brain areas, whereas the mechanisms of release have not been systematically characterized in the brain stem. The properties of release of preloaded [3H]taurine were now characterized in slices prepared from the mouse brain stem from developing (7-day-old) and young adult (3-month-old) mice, using a superfusion system. In general, taurine release was found to be similar to that in other brain areas, consisting of both Ca2+-dependent and Ca2+-independent components. Moreover, the release was mediated by Na+-, Cl−-dependent transporters operating outwards, as both Na+-free and Cl− -free conditions greatly enhanced it. Cl− channel antagonists and a Cl− transport inhibitor reduced the release at both ages, indicating that a part of the release occurs through ion channels. Protein kinases appeared not to be involved in taurine release in the brain stem, since substances affecting the activity of protein kinase C or tyrosine kinase had no significant effects. The release was modulated by cAMP second messenger systems and phospholipases at both ages. Furthermore, the metabotropic glutamate receptor agonists likewise suppressed the K+-stimulated release at both ages. In the immature brain stem, the ionotropic glutamate receptor agonists N-methyl-D-aspartate (NMDA) and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) potentiated taurine release in a receptor-mediated manner. This could constitute an important mechanism against excitotoxicity, protecting the brain stem under cell-damaging conditions.

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Abbreviations

9-AC:

9-antracenecarboxylate

AIDA:

(RS)-1-aminoindan-1,5-dicarboxylate

AMPA:

2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate

2R,4R-APDC:

(2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate

cAMP:

cyclic adenosine monophosphate

ATPase:

adenosine triphosphatase

cGMP:

cyclic guanosine monophosphate

DHPG:

(S)-3,5-dihydroxyphenylglycine

DIDS:

diisothiocyanostilbene-2,2′-disulphonate

EDTA:

ethylenediaminetetra-acetate

EGLU:

(2S)-2-cyclopropyl-4-phosphonophenylglycine

GABA:

γ-aminobutyrate

GAT:

GABA transporter

Hepes:

N-2-hydroxyethylpiperazine-N′-2-ethanesulphonic acid

IBMX:

3-isobutyl-1-methylxanthine

L-AP4:

L(+)-2-amino-4-phosphonobutyrate

L-SOP:

O-phospho-L-serine

MK-801 (dizocilpine):

(5S,10R)-(+)-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-amine

NBQX:

2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide

NMDA:

N-methyl-D-aspartate

ODQ:

1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one

PDE:

phosphodiesterase

PMA:

4β-phorbol 12-myristate 13-acetate

PKC:

protein kinase C

RO 20-1724:

4-(3-butoxy-4-methoxyphenyl)-2-imidazolidone

SITS:

4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonate

trans-ACPD:

(±)-1-aminocyclopentane-trans-1,3-dicarboxylate

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  1. Tampere Brain Research Center, Medical School, University of Tampere, Tampere, Finland

    P. Saransaari

  2. Department of Clinical Physiology and Nuclear Medicine, Tampere University Hospital, Tampere, Finland

    S. S. Oja

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Saransaari, P., Oja, S. Characteristics of taurine release in slices from adult and developing mouse brain stem. Amino Acids 31, 35–43 (2006). https://doi.org/10.1007/s00726-006-0290-5

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