SUMMARY1. Intracellular recordings were made from guinea-pig myenteric neurones in vitro.2. From one to sixty action potentials were followed by an afterhyperpolarization, the amplitude and duration of which increased with the number of preceding action potentials.3

Intracellular recordings were made from rat locus coeruleus neurons in vitro, and membrane currents were measured at potentials from -50 to -130 mV. In the absence of any applied agonists, the slope conductance of the cells increased 3-fold when the cell was hyperpolarized from -60 to -120 mV. This conductance increase was complete within 5 msec of the onset of a hyperpolarizing command and was subsequently independent of time for several seconds. The conductance increase was blocked by cesium chloride (1-2 mM), rubidium chloride (1-2 mM), or barium chloride (1-100 microM). The membrane potential range over which the conductance increased was centered at the potassium equilibrium potential (EK; extracellular potassium concentration, 2.5-10.5 mM): the current/voltage (I/V) relation of the cell could be well described by supposing that there were 2 potassium conductances, one voltage independent (G1) and the other (inward rectifier, Gir) activated according to the expression Gir = Gir,max/(1 + exp[(V - EK)/k]), where k ranged from 15 mV in 2.5 mM potassium to 6 mV in 10.5 mM potassium. The additional membrane potassium conductance that developed when agonists at mu-opioid and alpha 2-adrenoceptors were applied also became larger with membrane hyperpolarization, and this voltage dependence was also reduced or blocked by rubidium, cesium, and barium; in the presence of these agonists the current also reached its final value within 5 msec. However, the conductance increased by the agonists (Gag) was not well expressed by simply increasing the values of G1 and Gir,max. It was best described by a potassium conductance that increased according to Gag,max/(1 + exp[(V - Vm)/k]), where Vm (the potential at which the conductance was half-maximum) was close to the resting potential of the cell.(ABSTRACT TRUNCATED AT 400 WORDS)

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SUMMARY1. Bull-frog sympathetic neurones in primary culture were voltage clamped in the whole-cell configuration. The pipette solution contained ATP (5 mM).2. A hyperpolarization-activated sodium-potassium current (H-current: IH) was separated from other membrane currents in a nominally calcium-free solution containing cobalt (2 mM), magnesium (4 mM), barium (2 mm), tetraethylammonium (20 mM), tetrodotoxin (3 /,M), apamin (30 nM) and 4-aminopyridine (1 mm). IH was selectively blocked by caesium (10-300 ,UM).3. The steady-state activation Of IH occurred between -60 and -130 mV. The H-conductance was 4-1-6-6 nS at the half-activation voltage of -90 mV. With the concentrations of potassium and sodium ions in the superfusate at 20 and 70 mm, respectively, the reversal potential of IH was about -20 mV. IH was activated with a time constant of 2-8 s at -90 mV and 22 'C. The Q10 between 16 and 26 'C was 4-3. 4. A non-hydrolysable ATP analogue in the pipette solution did not support IH activation. Intracellular 'loading' of GTP-y-S (30-500,M) led to a progressive activation of IH-5. Forskolin (10 ,UM) increased the maximum conductance ofIH by 70 %. This was associated with a depolarizing shift in the half-activation voltage (5-10 mV) and in the voltage dependence of the activation/deactivation time constant ofIH.6. Essentially the same results as with forskolin were obtained by intracellular 'loading' with cyclic AMP (3-10 /LM) or bath application of 8-bromo cyclic AMP (0-1-1 mM), dibutyryl cyclic AMP (1 mM) and 3-isobutyl-1-methylxanthine