The effect of burst patterning of preganglionic input on the efficacy of transmission at the cat stellate ganglion

Abstract

SUMMARY1. The effect of burst patterned preganglionic stimulation on the efficacy of transmission at the cat stellate ganglion in vivo was studied to determine whether the increase in acetylcholine (ACh) release that occurs at preganglionic terminals with similar stimulation is synaptically active.2. Stimulation of the whole or a portion of the thoracic sympathetic trunk between rami T4 and T5 with recording of evoked compound action potentials in the inferior cardiac nerve yielded a preparation with a subliminal fringe with a mean value 2-5 times the size of the discharge zone.3. Preganglionic stimulation with 05 s bursts at 10, 20 and 40 Hz with 10 s interburst intervals caused an increase with time in the area of the compound action potential evoked by a single interburst test stimulus. The increase reached 70}75 o of the final value after the first burst, 75-90 % after 5 bursts and was virtually complete after 5 min. It was then maintained without attenuation as stimulation was continued.4. On cessation of burst patterned stimulation test compound action potentials returned to control levels with a half-time of 5 min.5. The increase in area of test compound action potentials with 40 Hz intraburst frequency was always as great as the increase following tetanization of the pathway. The increases with 20 and 10 Hz bursts were less.6. There was no increase in area of compound action potentials when equally spaced pulses at 2 Hz or less were applied preganglionically, nor was there any increase when 40 Hz burst patterns were delivered directly to the inferior cardiac nerve.7. It is concluded that burst patterned preganglionic activity at frequencies similar to those observed in vivo can recruit rapidly into the discharge zone all of the ganglionic neurones that were originally in the subliminal fringe. It is proposed that this effect is related directly to the increase in ACh release at ganglionic synapses that such activity has been shown to induce.

Fifty years of microneurography: learning the language of the peripheral sympathetic nervous system in humans

“…First, despite the above limitations and options for complex recruitment patterns, Birks and colleagues (Birks 1978;Birks and Isacoff 1988;Birks et al 1981) reported a predictable change in amplitude of the postganglionic compound AP following graded stimulation of the preganglionic neurons. Furthermore, delicate studies by John Horn's group in the bullfrog provided evidence that the aorta vasoconstrictor response scaled to the preganglionic sympathetic stimulation, and this vasoconstriction was minimized by both inhibition of postganglionic neurotransmitter release (guanethidine) and reduction in ganglionic transmission through postjunctional antagonism with tubocurarine (Thorne and Horn 1997).…”

Respiratory modulated sympathetic activity: a putative mechanism for developing vascular resistance?

“…Gain at the pre‐to‐postganglionic node in the vasoconstrictor pathway is known to occur, especially during bursts of activity (Birks et al . ; Birks & Isacoff, ). Sympathetic preganglionic neurones in the un‐anaesthetised ( in situ ) Wistar‐Kyoto rat fire at 2.5 Hz with an SD of 1.6 Hz (Briant et al .…”

Functional selectivity of cardiac preganglionic sympathetic neurones in the rabbit heart

“…The interpretation of the data from the method employed, by which additional preganglionic axons joining the sympathetic chain at each segment were stimulated, seems justified by studies of the electrophysiological properties of sympathetic ganglia. Larrabee and Bronk [ 10 ] and Birks et al [ 23 ] examined the electrophysiological properties of postganglionic neurones in the cat stellate ganglion and clearly showed that maximal stimulation of different populations of preganglionic axons in the sympathetic chain, evoked compound action potentials in different groups of postganglionic neurones in the inferior cardiac nerve. Therefore, in the present study it seems reasonable to conclude that the magnitude of the functional cardiac response reflected the number of preganglionic axons activated at each electrode position.…”