On the role of muscarinic and peptidergic receptors in ganglionic transmission in bullfrogs in vivo

Abstract

Synaptic activity of individual B and C cells in the paravertebral sympathetic ganglia of urethan-anesthetized bullfrogs was monitored with intracellular electrodes. Postganglionic activity from the B and C fiber populations was monitored with suction electrodes. Intravenous infusion of muscarine (0.1 ml of 8 microM) excited individual B cells and increased the amplitude and rate of spontaneous, postganglionic B fiber population discharges. Muscarine also increased the number of action potentials (APs) within each burst of synaptic activity in individual C cells. Because atropine (0.1 ml of 0.1 microM) had little or no effect on postganglionic population B or C fiber activity, the muscarinic slow inhibitory postsynaptic potentials and slow excitatory postsynaptic potentials (EPSPs) are unlikely to be involved in the transmission, modulation, or integration of postganglionic outflow in vivo. Atropine did, however, decrease the number of APs per burst in individual C cells, an effect that could be explained if excitatory presynaptic muscarinic receptors exist on C fiber terminals. Stimulation of preganglionic C fibers at "physiological" frequencies evoked a lasting afterdischarge in postganglionic B fibers that was blocked by a combination of atropine and [D-pyro-Glu1,D-Phe2,D-Trp3,6]-luteinizing hormone-releasing hormone (LHRH). Release of LHRH from C fiber terminals and activation of the peptidergic, late-slow EPSP mechanism in B cells may therefore play a role in ganglionic transmission in vivo.

Interaction of vasomotor and exocrine neurons in bullfrog paravertebral sympathetic ganglia

“…Another issue raised by the present results is their relationship to our finding that C-fibre-B-cell interaction in vivo can only be prevented by combining atropine with d-pyro-LHRH (Ivanoff and Smith 1997). It is possible that atropine antagonizes a postsynaptic effect of ACh that spills over from C-fibre terminals onto B-cells.…”

“…The average burst frequency seen in nerve trunks is 3.48 Hz (Ivanoff and Smith 1997). This is about 6 times greater than that seen in individual C-cells (0.56 Hz; Ivanoff and Smith 1995).…”

“…This lack of effect may be attributable to the actions of plasma peptidases and (or) poor access of the antagonist peptide from the blood to ganglionic neurons. Combination of D-pyro-LHRH with atropine did however successfully attenuate the in vivo C-fibre-B-cell interaction (Ivanoff and Smith 1997).…”

“…The ability of total C-fibre stimulation to invoke an increase in B-cell excitability was attenuated by atropine, but this decrease is not significant (P > 0.3). In view of our previous in vivo results with atropine plus D-pyro-LHRH (Ivanoff and Smith 1997), we also tested whether the combination of drugs had a larger effect than D-pyro-LHRH alone. As already mentioned, a 215 ± 43% increase in number of spikes was still seen in the presence of D-pyro-LHRH (n = 9; Fig.…”

“…Moreover, this initial level of in vivo B-fibre activity is restored following orthodromic stimulation of cut preganglionic C-fibres with bursts of stimuli that approximate in vivo C-fibre activity. Surprisingly however, this interaction is not impaired following intravenous injection of the antagonist [D-pyro-Glu 1 ,D-Phe 2 ,D-Trp 3,6 ]-LHRH (D-pyro-LHRH) (Ivanoff and Smith 1997). This lack of effect may be attributable to the actions of plasma peptidases and (or) poor access of the antagonist peptide from the blood to ganglionic neurons.…”