Dual effects of proctolin on the rhythmic burst activity of the cardiac ganglion

Abstract

The neuropeptide proctolin has distinguishable excitatory effects upon premotor cells and motorneurons of Homarus cardiac ganglion. Proctolin's excitation of the small, premotor, posterior cells is rapid in onset (5-10 s) and readily reversible (less than 3 min). Prolonged bursts in small cells often produce a "doublet" ganglionic burst mode via interactions with large motorneuron burst-generating driver potentials. In contrast to small cell response, proctolin's direct excitatory effects upon motorneuron are slow in onset (60-90 s to peak) and long-lasting (10-20 min). The latter include: a concentration-dependent (10(-9)-10(-7)M) depolarization of the somatic membrane potential; increases in burst frequency and enhancement of the rate of depolarization of the interburst pacemaker potential. Experiments on isolated large cells indicate: the slow depolarization is produced by a decrease in the resting GK and proctolin can produce or enhance motorneuron autorhythmicity . A two- tiered non-hierarchical network model is proposed. The differential pharmacodynamics exhibited by the two cell types accounts for the sequential modes of ganglionic burst activity produced by proctolin.

Nitric Oxide Inhibits the Rate and Strength of Cardiac Contractions in the LobsterHomarus americanusby Acting on the Cardiac Ganglion

“…In crustaceans, short-term control over cardiac performance is provided by excitatory and inhibitory nerves that modulate heart rate and contractility for periods of up to several seconds (Florey, 1960;Field and Larimer, 1975). Longer-term excitation is provided by a variety of circulating hormones that increase the rate and strength of the heartbeat for periods lasting from minutes to hours (Cooke and Hartline, 1975;Benson, 1984;Miller et al, 1984;Sullivan and Miller, 1984;Worden et al, 1995;Berlind, 1998). This raises the question of whether crustaceans might also employ long-term inhibitory mechanisms to counteract these long-lasting excitatory mechanisms.…”

Identification of a calcitonin-like diuretic hormone that functions as an intrinsic modulator of the American lobster,Homarus americanus, cardiac neuromuscular system

“…Cruz-Bermúdez and Marder, 2007;Kuramoto and Ebara, 1984;Wilkens et al, 1996). In H. americanus this includes proctolin (Miller and Sullivan, 1981;Sullivan and Miller, 1984;Wilkens et al, 2005;Worden et al, 1995), crustacean cardioactive peptide (CCAP) (Wilkens et al, 1996), a number of FMRFamide-like peptides (Wilkens et al, 2005;Dickinson et al, 2007), two tachykinin-related peptides and the allatostatin C-like peptide SYWKQCAFNAVSCFamide . However, to the best of our knowledge, no peptide has previously been localized to the CG itself.…”

Sites and modes of action of proctolin and the FLP F2 on lobster cardiac muscle

“…The potentiated tetani following PR exposure could arise directly from increased Ca 2+ entry or indirectly by enhancing Ca 2+ entry as a consequence of decreasing K + currents. We did not attempt to measure or modify potassium currents, but PR can reduce K + currents in neurons of the cardiac ganglion (Sullivan and Miller, 1984) and in other muscles (locust, Walther et al, 1998;isopod, Erxleben et al, 1995).…”

“…PR should increase presynaptic transmitter release since it increases Na + and decreases K + conductances (Sullivan and Miller, 1984;Walther et al, 1998;Freschi, 1989;Golowasch and Marder, 1992;Erxleben et al, 1995) and FLPs increase transmitter release from lobster and crayfish motoneuron terminals (Worden et al, 1995;Mercier et al, 2003). The cardiac ganglion motoneurons appear to be glutamatergic in lobsters (Anderson, 1973) and a variety of other crustaceans (see Sakurai and Yamagishi, 1996;Yazawa et al, 1998).…”

“…Enhanced tetani following a contracture may be due to enhanced voltage-gated Ca 2+ current and sarcoplasmic reticular (SR) Ca 2+ loading. The SR Ca 2+ loading appears to be specific for PR and F 2 , since glutamic-acid-induced contractures are not followed (Erxleben et al, 1995;Sullivan and Miller, 1984). In locust skeletal muscle PR decreases K + conductance via a G protein mediated pathway; (Walther et al, 1998).…”