Progressive potentiation of peptide release during a neuronal discharge

Abstract

1. In response to electrical stimulation, the bag cell neurons of Aplysia generate an afterdischarge that lasts 20-40 min. During this afterdischarge several neuroactive peptides are released. We have now studied the time course of release of two of these peptides, egg-laying hormone (ELH) and acidic peptide (AP). For the collection of released peptides, the artery to the bag cell clusters was perfused. The medium surrounding the clusters (artificial seawater, ASW) was completely exchanged at 5-min intervals before, during, and after stimulation of an afterdischarge. Peptides released into the external medium were analyzed with the use of high-pressure liquid chromatography. 2. Before stimulation, no detectable ELH and AP were found in the external medium. After the onset of an afterdischarge, the amount of ELH and AP released increased progressively until 15-20 min of firing. Toward the conclusion of an afterdischarge, the release of ELH and AP returned to control levels. 3. In contrast to the pattern of release of the peptides, the firing rate of the bag cell neurons is maximal within the first minute of afterdischarge and thereafter declines. 4. Release of the peptides from axonal varicosities occurs within the vascularized connective-tissue sheath that covers the clusters of bag cell neurons. Experiments were therefore carried out to establish whether the observed time course of release is affected by diffusion of the peptides through the vasculature into the external medium and, in particular, to determine whether the maximal rate of release at 15-20 min into the afterdischarge could be accounted for by a delay in transport of peptides from the neurites.(ABSTRACT TRUNCATED AT 250 WORDS)

A Store-Operated Ca2+Influx Pathway in the Bag Cell Neurons ofAplysia

“…The bag cell neuron afterdischarge is an ~30-min barrage of action potentials that triggers neuropeptide secretion and egg-laying behavior (Conn and Kaczmarek 1989;Kupfermann 1967;Kupfermann and Kandel 1970;Pinsker and Dudek 1977;Rothman et al 1983). Along with voltage-gated Ca 2+ channels, store-operated Ca 2+ influx could promote neuropeptide secretion, particularly late in the afterdischarge when release is maintained despite lowered firing frequency (Loechner et al 1990;Michel and Wayne 2002). The afterdischarge is also associated with IP 3 -dependent release of Ca 2+ from intracellular stores (Fink et al 1988;Fisher et al 1994).…”

Long-term potentiation and long-term depression of primary afferent neurotransmission in the rat spinal cord

“…Although the results mentioned above suggest that the maintenance of positive amplitude modulation of EPSPs following high-frequency stimulation depends on properties of the presynaptic terminals, they do not rule out a contribution from other mechanisms. These include increase in sensitivity of DH neurons to locally applied AMPA receptor ligands (Davies et al, 1989;, activation of parallel neural networks affecting transmission at either preor postsynaptic levels, co-release of EAAs and peptides from terminals (Loechner et al, 1990) resulting in the modulation of the amount of released transmitter (Kangrga and Rand%, 1990) or sensitivity of postsynaptic EAA receptors (RandiC et al, 1990;Rusin and RandiC, 1991;Rusin et al, 1992Rusin et al, , 1993a, and activation of second messenger systems Ceme et al, , 1993. At present we have no evidence for or against the involvement of any of these mechanisms.…”

Voltage gated calcium channels in molluscs: classification, Ca2+ dependent inactivation, modulation and functional roles

“…The latter interpretation is suggested by the observation that with Ba 2+ replacing external Ca 2+, each individual spike induces an increase in [Ca 2+] (Fisher et al, 1991(Fisher et al, , 1994. A permissive role for action potentials is further suggested by observations that egg laying hormone secretion by bag cells progressively increases during the discharge (Loechner et al, 1990) and that inhibition of firing early on in the discharge by application of hyperosmotic saline also blocks hormone release (Loechner et al, 1992a). Similar data come from CDCs, where both internal calcium (Dreijer and Kits, 1994;K.…”