Post‐tetanic depolarization in sympathetic neurones of the guinea‐pig

Abstract

SUMMARY1. Repetitive intracellular stimulation at a frequency of 5-30 Hz for 1-10 s evoked in neurones of the isolated inferior mesenteric and superior cervical ganglia of the guinea-pig three types of post-spike membrane potential changes: (i) hyperpolarization, (ii) hyperpolarization followed by a slow depolarization, and (iii) a second hyperpolarization following the initial two responses.2. The initial post-spike hyperpolarization had a mean duration of 2-0 s and was often associated with a fall in membrane resistance; it could be elicited in every sympathetic neurone studied. This response was termed the post-tetanic hyperpolarization (PTH).3. The slow depolarization which could be induced only in a portion of neurones had a mean amplitude and duration of 2-2 mV and 27-5 s, respectively; it was termed the post-tetanic depolarization (PTD).4. PTD was associated with a fall in membrane resistance, augmented by membrane hyperpolarization, and reduced by depolarization; its mean extrapolated equilibrium potential was -38 mV.5. PTD was not blocked by nicotinic and muscarinic antagonists, or a-and /1-adrenergic receptor antagonists, whereas it was suppressed by adrenaline, noradrenaline, Co2+ and a low Ca2+ solution. 6. The amplitude of the single spike after-hyperpolarization in normal Krebs solution as well as in high K+ solution was increased during PTD; furthermore, conditioning hyperpolarization to the level of EK increased the amplitude of PTD in normal Krebs as well as in high K+ solution.7. PTD with similar amplitude, time course and membrane characteristics could be evoked in a portion of neurones of the rabbit superior cervical ganglia; however, PTD was not detected in neurones of the rat superior cervical ganglia.8. Decentralization of the guinea-pig and rabbit superior cervical ganglia for 14 d did not alter the number of neurones in which PTD could be elicited, its amplitude, or its time course. 9. Our results suggest that a chemical substances) is responsible for the generation of PTD; it may be released from the soma and/or dendrites and acts in an auto-receptive manner on the cells in question. The nature and origin of the second hyperpolarization remain to be clarified.

Synaptic and Extrasynaptic Secretion of Serotonin

“…For example, in peptidergic neurons of the superior cervical and mesenteric ganglion of rabbit and guinea pig, intracellular stimulation produces a post-tetanic depolarization that persists after preganglionar denervation. This effect was explained by the somatic release of a substance released from the soma of these neurons (Dun and Minota, 1982), and was latter confirmed by electron microscopy using tannic acid to stabilize the nucleus of dense core vesicles after exocytosis (Zaidi and Matthews, 1997;. The neurohormones vasopressin and oxytocin also undergo calcium-dependent somatodendritic release within the supraoptic and paraventricular hypothalamic nuclei upon stimulation with trains of action potentials at frequencies higher than 13 Hz (Soldo et al, 2004).…”

Extrasynaptic exocytosis and its mechanisms: a source of molecules mediating volume transmission in the nervous system

“…The discovery of extrasynaptic receptors by Miledi ( 1960 ), was followed by observations by Dun and Minota ( 1982 ) of peripheral neuronal responses that could be attributed to somatic exocytosis of signaling molecules upon electrical stimulation. In addition, the discovery of extracellular concentrations of monoamines at a distance from synaptic endings, and the mismatch between peptide exocytosis sites and receptors, led Fuxe and colleagues to propose volume transmission as a way of communication in the nervous system, parallel to that of hard-wired circuits (Agnati et al, 1986a , b ; Fuxe et al, 2012 ; see also Fuxe et al, in this issue).…”

Extrasynaptic Neurotransmission Mediated by Exocytosis and Diffusive Release of Transmitter Substances

“…The evidence was soon expanded to other transmitters and peptides, thus leading to the mechanistic concept of volume transmission, defined by Fuxe et al ( 2007 ) as a form of communication mediated by extracellular diffusion of transmitter substances through the extracellular space (for review see Borroto-Escuela et al, 2015 ). Indirect evidence for the somatic release of transmitters came from experiments by Dun and Minota ( 1982 ) showing that electrical stimulation of the soma of peripheral neurons changed the membrane potential in a non-synaptic manner. Direct demonstrations of the extrasynaptic release of all sorts of low molecular transmitters and peptides came later, from experiments in central and peripheral neurons of vertebrates and invertebrates (for review see Trueta and De-Miguel, 2012 ).…”