Repetitive firing properties of medial pontine reticular formation neurones of the rat recorded in vitro.

1. Intracellularly recorded neurones in nucleus reticularis pontis caudalis of the medial pontine reticular formation (mPRF) in the in vitro slice preparation were analysed for repetitive firing properties in response to intracellularly applied constant‐current pulses. 2. Three neuronal classes were defined by this procedure: (1) non‐burst neurones, which had only a non‐burst firing pattern; (2) low‐threshold burst neurones, which had either a low‐threshold burst pattern or a non‐burst pattern; (3) high‐threshold burst neurones, which had either a high‐threshold burst pattern or a non‐burst pattern. 3. Histological characterization of electrophysiologically identified mPRF neurones with carboxyfluorescein showed no definite morphological difference between the first two classes. There was a trend for low‐threshold burst neurones to have larger somata. 4. The low‐threshold burst was generated by a slow calcium‐dependent low‐threshold spike, revealed in the presence of tetrodotoxin. The size of the low‐threshold spike and thus the number of fast action potentials in the low‐threshold burst was controlled by at least five factors including: activation; inactivation; amplitude of low‐threshold conductance available to be activated; delayed outward conductance; and early transient outward conductance. 5. The non‐burst pattern examined in both non‐burst and low‐threshold burst neurones appeared to be controlled primarily by one or more calcium‐dependent potassium conductances sensitive to the removal of calcium and tetraethyl‐ammonium. In the presence of tetrodotoxin (TTX), the addition of antagonists to calcium‐dependent potassium current revealed a slow high‐threshold calcium spike which was distinguished from the low‐threshold spike by its threshold, lack of inactivation (at potentials negative to ‐40 mV) and insensitivity to Mg2+. A long‐duration after‐hyperpolarization (greater than 0.5 s) was not observed in any of these cells. 6. An early transient outward rectification sensitive to 4‐aminopyridine and probably mediated by A‐current was apparent in low‐threshold burst and non‐burst neurones and affected both the low‐threshold burst and non‐burst firing patterns. 7. Alteration of resting membrane potential, such as occurs in vivo during the depolarization associated with desynchronized sleep, may inactivate the low‐threshold spike and the transient outward conductance responsible for the distinctive responses observed from more hyperpolarized membrane potentials and produce a more homogeneous non‐burst response pattern. Membrane potential effects on intrinsic conductances thus may furnish an important mechanism for changes in mPRF neuronal responsivene