Intracellular recordings were made from rabbit nodose neurones in vitro. Two temporally distinct spike after‐hyperpolarizations (a.h.p.s) were identified in a subpopulation of C‐type neurones. The fast a.h.p. after a single spike lasted no longer than 500 ms, while the slow a.h.p. persisted for seconds. Both a.h.p.s. were increased in amplitude in low K+ (0.56 mM) solutions and decreased in amplitude in high K+ (11.2 mM) solutions, and both were reversed at hyperpolarized membrane potentials. The slow a.h.p. was reduced in low Ca2+ (0.22 mM), in the presence of Ca2+ antagonists (Ni2+, 1 mM; Cd2+, 100 microM; or Co2+, 1 mM) and was enhanced in tetraethylammonium (5 mM). In approximately half of the cells tested, the fast a.h.p. was reduced in low Ca2+ and in the presence of the Ca2+ antagonists. In the remaining cells the fast a.h.p. was insensitive to these procedures. Prostaglandin (PGE1, 1‐10 micrograms/ml) reduced the slow a.h.p. in all cells tested. Neither the Ca2+‐sensitive nor the Ca2+‐insensitive fast a.h.p. was affected by the prostaglandin. It is concluded that there is a subpopulation of C‐type nodose neurones possessing a slow a.h.p. which is due to a Ca2+‐dependent K+ current. This subpopulation of neurones can further be divided on the basis of the presence of a Ca2+‐sensitive fast a.h.p. Furthermore, PGE1 pharmacologically separates the fast and slow a.h.p.s by selectively blocking the slow one. The blockage by the PGE1 is most probably not due to a reduction in Ca2+ influx.

SUMMARY Synaptic transmission and membrane properties of sympathetic neurons in superior cervical ganglia of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (VVKY), and Sprague-Dawley rats (SD) were investigated in vitro by extracellular and intracellular recording. The sympathetic neurons of SHR showed an atypical loss of spike accommodation. The spike discharge was insensitive to the sodium channel blocker tetrodotoxin, but it was reversibly blocked by a variety of calcium antagonists. The loss of accommodation in the neurons of SHR was not due to a loss of M-current, a potassium current involved in controlling spike frequency adaptation in sympathetic neurons. Superfusion of ganglia of SHR with muscarine (10 ^M), which suppresses M-current and leads to a loss of accommodation, potentiated the repetitive discharge. In the presence of muscarine the current-voltage curves in neurons of SHR and SD were shifted to similar extents. Resting membrane potentials of neurons of SHR and WKY were consistently depolarized as compared with neurons of SD. Synaptic efficacy through the ganglia of SHR, assessed by extracellular recordings of presynaptic and postsynaptic compound action potentials at 0.25 Hz stimulation, was elevated when compared with the ganglia of WKY, but was similar to that of the ganglia of SD. These results indicate that strain differences should be considered when attempting to attribute changes in sympathetic neuron membrane properties to hypertension. The sympathetic neurons of SHR appear to have lost their accommodative properties and might possess an exaggerated calcium conductance. This calcium conductance may explain the augmented calcium-dependent release of norepinephrine during sympathetic nerve stimulation in the SHR. (Hypertension 7: 268-276, 1985) KEY WORDS • membrane properties normotensive strains repetitive firing * calcium conductance E XAGGERATED activity in the sympathetic nervous system in the Okamoto-Aoki strain of spontaneously hypertensive rats (SHR) has been implicated in both the development and the maintenance of hypertension in this model. "2 Numerous studies with the SHR have shown that both central and peripheral neurogenic mechanisms are contributory factors, although they may not account for all the elevation in peripheral vascular resistance.2 There is an increased basal sympathetic tone in visceral and nonvisceral sympathetic nerves, and an elevated sympa-

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