Role of ganglionic cotransmission in sympathetic control of the isolated bullfrog aorta.

Abstract

1. The relation between preganglionic activity and arterial tone was studied in preparations of bullfrog lumbar sympathetic ganglia 7-10 and the dorsal aorta. 2. Two or more stimuli evoked contractions when applied to the preganglionic C, but not the B pathway. Contractions were blocked when transmission in ganglia 9 and 10 was disrupted by cutting the sympathetic chain or adding (+)-tubocurarine. Contractions were antagonized by postganglionic action of guanethidine, but not by phentolamine or suramin. 3. Aortic responses to short trains (10-100 stimuli) were half-maximal at 0.3-0.5 Hz, saturated near 1 Hz and had a minimum latency of 8.9 s. By contrast, responses to 300 stimuli were half-maximal at 1 Hz and became 2.5-fold larger at 10 Hz. 4. Exogenous luteinizing hormone releasing hormone (LHRH) potentiated preganglionically evoked contractions. Endogenous LHRH mediated contractions evoked by 10 Hz stimulation in (+)-tubocurarine. These responses had a longer latency than in normal Ringer solution and were blocked by [D-pGlu1, D-Phe2, D-Trp3.6]-LHRH. The LHRH antagonist did not alter contractions evoked by continuous stimulation in normal Ringer solution or by bursts of stimuli in hexamethonium. 5. Exogenous neuropeptide Y (NPY) potentiated neurogenic contractions and responses to adrenaline. Benextramine blocked contractions produced by nerve stimulation, adrenaline and NPY, but not ATP. 6. The results show that contractions of the isolated aorta are tuned to physiological frequencies of activity in sympathetic C neurones. Peptidergic cotransmission in the ganglia can increase arterial tension, but not during synchronous activation of primary nicotinic synapses. It is suggested that the physiological role of LHRH arises from interactions with subthreshold nicotinic EPSPs and that postganglionic release of NPY shifts frequency tuning of the circuit during prolonged activity.

Interaction of vasomotor and exocrine neurons in bullfrog paravertebral sympathetic ganglia

“…There is considerable interest, therefore, in determining whether the pattern and frequency of preganglionic action potentials (AP) that occur in vivo would invoke peptidergic or muscarinic inhibitory or stimulatory effects and whether these have relevance to the overall physiology of the autonomic nervous system. These questions have been addressed by experiments done in vivo Smith 1995, 1997) and in vitro (Peng and Horn 1991;Jobling and Horn 1996; Thorne and Horn 1997). The frequency-dependence of ganglionic transmission in vitro is consistent with a physiological role for LHRH within the vasomotor C-fibre system, i.e., it may be involved in the transfer of information between pre-and postganglionic C-fibres in the intact animal (Thorne and Horn 1997).…”

“…These questions have been addressed by experiments done in vivo Smith 1995, 1997) and in vitro (Peng and Horn 1991;Jobling and Horn 1996; Thorne and Horn 1997). The frequency-dependence of ganglionic transmission in vitro is consistent with a physiological role for LHRH within the vasomotor C-fibre system, i.e., it may be involved in the transfer of information between pre-and postganglionic C-fibres in the intact animal (Thorne and Horn 1997). To explore the possible functional interrelationships between the C-fibre and B-fibre systems within the ganglia, Jobling and Horn (1996) recorded the response of the target tissue (cutaneous glands) to preganglionic B-fibre stimulation in vitro.…”

“…The late-slow EPSP results from the release of luteinizing hormone releasing hormone (probably chicken II LHRH) (Jones 1987b;Troskie et al 1997) from preganglionic C-fibres. Because the peptide diffuses a considerable distance within the ganglion, the postsynaptic response occurs in C-cells and in B-cells (Jan et al 1979(Jan et al , 1980Jobling and Horn 1996;Thorne and Horn 1997).…”

“…The larger, exocrine B-cells project primarily to mucous glands in the skin and most of the smaller C-cells project to blood vessels (Horn et al 1988;Ivanoff and Smith 1995;Jobling and Horn 1996;Thorne and Horn 1997). The anatomical separation of preganglionic B-fibre input to B-cells and C-fibre input to C-cells has established this preparation as a model system in which to study ganglionic transmission in vitro (Nishi and Koketsu 1968;Adams et al 1986;Smith and Weight 1986;Smith 1994;Jobling and Horn 1996;Thorne and Horn 1997;Karila and Horn 2000). In addition to the classical, fast, nicotinic excitatory postsynaptic potential (EPSP), stimulation of preganglionic fibres evokes three types of slow synaptic potential; the slow inhibitory postsynaptic potential (IPSP), the slow EPSP, and the late-slow EPSP.…”

Activation of nicotinic receptor-induced postsynaptic responses to luteinizing hormone-releasing hormone in bullfrog sympathetic ganglia via a Na + -dependent mechanism

“…Moreover, neuropeptide Y greatly potentiates the tension produced by epinephrine (29). Thus, in bullfrogs, nicotine at nanomolar concentrations could increase blood pressure via enhanced release of either epinephrine and͞or neuropeptide Y. Nicotine-induced LHRH release depolarized both ganglionic B and C cells and thus rendered them more excitable.…”