Premium
Mechanisms of Sensory Feedback and Interactions with Neuromodulators in a Rhythmic Pattern Generator
Author(s) -
Dickinson P,
Dickinson E,
Harmon K,
Qu X,
Johnson A,
Ellers O
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.841.4
Subject(s) - central pattern generator , neuroscience , sensory system , mechanosensitive channels , heartbeat , homarus , contraction (grammar) , rhythm , fmrfamide , biology , chemistry , anatomy , neuropeptide , ion channel , medicine , receptor , endocrinology , computer science , ecology , computer security , crustacean
Although the effects of sensory feedback and of neuromodulators on the rhythmic outputs of central pattern generators (CPGs) have been characterized in a number of systems, there are few studies on the interactions of these two factors. Here we examined the mechanisms underlying stretch feedback in the cardiac neuromuscular system of the American lobster, Homarus americanus, and the interactions of stretch and a neuropeptide, SGRNFLRFamide (SGRN), in modulating CPG output. The neurogenic heartbeat is controlled by a 9‐neuron CPG, the cardiac ganglion; dendritic processes of these neurons have been postulated to serve as stretch receptors that provide direct feedback to the CPG. To examine the mechanisms underlying stretch sensitivity, we isolated the cardiac ganglion together with the muscle fibers surrounding the 4 small pacemaker cells of the CPG. We then stretched these muscle fibers, thereby stretching the mechanosensitive dendrites of these neurons, while recording intracellularly from one of the motor neurons, which are both electrically and chemically coupled to the pacemaker cells. During stretch, driver potential frequency increased and duration decreased; driver potential duration increased during release from stretch. To examine the interactions of peptides and stretch, we stretched the intact heart while perfusing it with SGRN, which enhanced cardiac activity, increasing both frequency and amplitude of cardiac contractions. When the intact heart was stretched, contraction frequency and amplitude usually increased; in the presence of SGRN, the increases in both frequency and amplitude elicited by stretch were enhanced, suggesting that feedback is itself modulated. Funding: NSF IOS‐1121973, NIH (INBRE) 5P20RR016463‐12 (NCRR) & 8P20GM103423‐12 (NIGMS)