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Expression of functional GABA_A receptors in cholecystokinin-secreting gut neuroendocrine murine STC-1 cells

G. Glassmeier, K.-H. Herzig *, M. Höpfner, K. Lemmer, A. Jansen and H. Scherübl

1. Gastrointestinal neuroendocrine (NE) cells synthesize, store and secrete -aminobutyric acid (GABA). Recently, an autocrine-paracrine function of GABA has been proposed for secretion from NE cells.

2. To search for functional GABA_A receptors in NE gut cells, we performed whole-cell and perforated-patch-clamp studies in the intestinal cholecystokinin (CCK)-secreting NE cell line STC-1.

3. Application of GABA evoked currents in STC-1 cells. These effects were mimicked by muscimol, an agonist of GABA_A receptors, and blocked by picrotoxin or bicuculline, antagonists of GABA_A receptors. The GABA- or muscimol-activated currents reversed near 0 mV, which under the recording conditions used was consistent with the activation of the GABA_A receptor-Cl^- channel complex.

4. In contrast to the effect on most neurons, GABA as well as muscimol led to a (reversible) depolarization of the membrane potential of STC-1 cells. Membrane depolarization in turn activated voltage-gated Ca²⁺ channels and increased intracellular Ca²⁺ concentrations in STC-1 cells.

5. In accordance with the observed membrane depolarization and activation of voltage-gated Ca²⁺ channels, both GABA and muscimol stimulated Ca²⁺-dependent CCK release. In contrast, bicuculline inhibited the GABA-induced secretion of CCK.

6. Using the reverse transcription-polymerase chain reaction (RT-PCR), mRNA of the GABA_A receptor subunits 2, 3, 5, 1, 3 and could be detected in STC-1 cells.

7. In summary, we have shown that the CCK-secreting gut NE cell line STC-1 expresses functional GABA_A receptors and that GABA stimulates CCK release. Thus, GABA is involved in the fine tuning of CCK secretion from the gut NE cell line STC-1.

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