In cardiac myocytes, the cytoplasmic-free concentration of Mg 2ϩ ([Mg 2ϩ ] i ) is maintained at or slightly lower than 1.0 mM [1][2][3][4], a level several hundred fold lower than that expected from its passive distribution. It follows that Mg 2ϩ must be actively extruded from the cells to counterbalance Mg 2ϩ influx driven by the electrochemical gradient across the cell membrane.As it is such an active extrusion pathway, it has been postulated that a Na ϩ -Mg 2ϩ exchange that utilizes energy from Na ϩ influx plays an important role in cardiac myocytes [5][6][7] as well as in other cell types (for review, see Flatman [8] and Romani and Scarpa [9]).However, experimental evidence of the Na ϩ -Mg 2ϩ exchange in cardiac myocytes is controversial [3,4,10], and detailed properties of the transport still remain largely unknown.The present study was aimed to determine, under control of the membrane potential, if Na ϩ -Mg 2ϩ exchange plays an essential role in cardiac myocytes, and how the membrane potential, over a wide range, modulates the transport of Mg 2ϩ across the cell membrane. This information is one of the important clues to the elucidation of Na ϩ -Mg 2ϩ exchange stoichiometry. Flatman et al. [11] studied, for the first time, Na ϩ -

Whole‐cell patch clamp recordings were made from substantia nigra pars reticulata (SNr) neurones in rat midbrain slices. Monosynaptic IPSCs were evoked by electrical stimulation of the cerebral peduncle in the presence of the glutamate receptor antagonists CNQX (6‐cyano‐7‐nitroquinoxaline‐2,3‐dione) and AP5 (2‐amino‐5‐phosphonopentanoic acid). IPSCs were predominantly outward at −70 mV (in 124/135 cells), with a reversal potential of −83 mV, a time to peak of 2.6 ms and a decay time constant of 6.5 ms. Faster inward IPSCs were also observed in thirty‐five cells, with a time to peak of 1.0 ms, a decay time constant of 2.3 ms, and a reversal potential of −61 mV. Both IPSCs were sensitive to the GABAA receptor antagonists picrotoxin or bicuculline. In cells recorded with Cs+‐filled pipettes, the outward IPSC reversal potential was shifted to −76 mV, closer to the estimated Cl− equilibrium potential of −56 mV, while that of the inward IPSC was unchanged at −64 mV. The outward IPSC was reversibly depressed by up to 100 % by dopamine in a concentration‐dependent manner with an IC50 of 10.5 μm, while the inward IPSC was relatively insensitive. Dopamine was without effect on cell holding current, or on outward IPSC reversal potential, but it increased paired‐pulse IPSC facilitation, consistent with a presynaptic site of action. The D1‐like dopamine receptor agonist SKF 38393 (10 μm) depressed the outward IPSC by 43 %, while the D2‐like dopamine receptor agonist quinpirole (10 μm) was without effect. It is concluded that GABA‐ergic synaptic input onto distal rather than proximal regions of SNr neurones is susceptible to presynaptic inhibition via a D1‐like receptor. These inputs are probably from striato‐nigral fibres, and their inhibition by dopamine is likely to influence the patterning of basal ganglia output.

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