Long-term potentiation of nicotinic transmission by a heterosynaptic mechanism in the stellate ganglion of the cat

Abstract

1. In the anesthetized, scopolamine-treated cat, the compound action potential (CAP) evoked by a single supramaximal shock to the third thoracic white ramus (T3WR) was recorded in the inferior cardiac nerve (ICN). The CAP was depressed in a dose-dependent manner by the intravenous administration of the nicotinic antagonist hexamethonium (C6). 2. During steady intravenous infusion of C6, which reduced the amplitude of the CAP by 80-90%, a short train of stimuli (few seconds, 10-40 Hz) to the sympathetic trunk just below T4WR potentiated the CAP for periods of tens of minutes to 1-2 h (heterosynaptic long-term potentiation, LTP). An LTP of similar time course was obtained when both train and single shock were applied to T3WR (homosynaptic LTP). Magnitude and duration of the heterosynaptic LTP were dependent on number, frequency, and intensity of the stimuli. No LTP was produced by a train to the ICN. Heterosynaptic LTP was also observed in the absence of C6. Because of the limited subliminal fringe of the test input under this condition, the LTP was of small magnitude. Heterosynaptic LTP also of the heart rate (HR) response to a test stimulus was observed after a conditioning train. 3. The conditioning train produced a displacement to the right of the dose-response curve for C6. The intravenous dose of C6 required for 50% attenuation of the test CAP increased from 0.84 +/- 0.15 (SE) mg/kg pretrain to 2.56 +/- 0.46 mg/kg posttrain (n = 5, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Expression of gLTP in Sympathetic Ganglia from Stress-hypertensive Rats: Molecular Evidence

“…Evidence for involvement of the postsynaptic region is indicated by the role of carbon monoxide as retrograde transmitter in the induction of gLTP (Alkadhi et al 2001a, b; see review Alkadhi et al 2005a, b). Although earlier experiments in rat SCG suggest no involvement of the postsynaptic membrane (Briggs et al 1985), later it is shown in a variety of sympathetic ganglia from various species that the postsynaptic is, indeed, involved (Bachoo and Polosa 1991;Morales et al 1994).…”

A Neglected ‘Accessory’ Vasomotor Pathway: Implications for Blood Pressure Control

“…As noted above, all that is normally necessary to achieve ganglion blockade is to reduce the amplitude of strong EPSPs to below ganglion cell threshold. Indeed, Bachoo and Polosa 9 showed that potentiated ganglionic transmission of this type in the cat stellate ganglion could partly restore the potency of nicotinic inputs that had been reduced by hexamethonium treatment. To what extent the new enhanced state allowed summation of subthreshold EPSPs, or merely lowered ganglion cell threshold sufficiently for attenuated nicotinic (or other) EPSPs to trigger action potentials, we cannot say.…”

Role of Long-Term Potentiation of Sympathetic Ganglia (gLTP) in Hypertension

“…The induction of gLTP is not dependent on the activation of adrenergic, cholinergic, dopaminergic, or adenosine receptors (5,6,28,34,35). Recent evidence strongly suggests that gLTP in the rat SCG is strictly dependent on the activation of serotonin 5-HT 3 receptor (13).…”

“…Additionally, gLTP has been measured in ganglia in anesthetized animals in situ (10,11,28,136). The gLTP of the nicotinic pathway has been reported in various autonomic ganglia from various animal species, including rat SCG (4,8,13,29), cat SCG, lumbar and stellate ganglia (10,28,30), guinea pig SCG (12,31), chick parasympathetic ciliary ganglion (14), and bullfrog sympathetic ganglia (7,23,32,33).…”

“…Recent evidence strongly suggests that gLTP in the rat SCG is strictly dependent on the activation of serotonin 5-HT 3 receptor (13). The site of origin of gLTP may be presynaptic, postsynaptic, or through a combination of presynaptic and postsynaptic mechanisms, depending on the animal species and/ or experimental methods used (7,28,30,36,37).…”