PYLORIC MOTOR PATTERN MODIFICATION BY A NEWLY IDENTIFIED PROJECTION NEURON IN THE CRAB STOMATOGASTRIC NERVOUS-SYSTEM

1. We have used multiple, simultaneous intra- and extracellular record ings as well as Lucifer yellow dye-fills to identify modulatory commis sural neuron 5 (MCN5) and characterize its effects in the stomatogastr ic nervous system (STNS) of the crab, Cancer borealis. MCN5 has a soma and neuropilar arborization in the commissural ganglion (CoG; Figs. 1 and 2), and it projects through the inferior esophageal nerve (ion) a nd stomatogastric nerve (stn) to the stomatogastric ganglion (STG; Fig s. 1-3). 2. Within the CoGs, MCN5 receives esophageal rhythm-timed exc itation and pyloric rhythm-timed inhibition (Fig. 4). Additionally, du ring the lateral teeth protractor phase of the gastric mill rhythm, th e pyloric-timed inhibition of MCN5 is reduced or eliminated. 3. Intrac ellular stimulation of MCN5 excites the pyloric pace maker ensemble, i ncluding the anterior burster (AB), pyloric dilator (PD), and lateral posterior gastric (LPG) neurons. This produces a faster pyloric rhythm . MCN5 stimulation also inhibits all nonpacemaker pyloric neurons, red ucing or eliminating their activity (Figs. 5 and 6A; Tables 1 and 2). After MCN5 stimulation, bursting is enhanced for several cycles in som e pyloric neurons when compared with their prestimulus activity (Figs. 5 and 6A; Tables 1 and 2). 4. MCN5 evokes distinct responses from eac h pyloric pacemaker neuron (Figs. 6-8). The AB and LPG neurons respond with increased activity. The AB response includes the presence of lar ge amplitude excitatory postsynaptic potentials (EPSPs) that contribut e to a depolarization of the trough of its rhythmic oscillations (Fig. 6). LPG responds by exhibiting increased activity that prolongs the d uration of its burst beyond that of AB and PD (Fig. 7). In contrast, M CN5 stimulation initially produces decreased PD neuron activity, follo wed by a slight enhancement of each PD burst (Figs. 7 and 8). PD activ ity is further enhanced after MCN5 stimulation (Figs. 7 and 8). 5. MCN 5-elicited action potentials evoke discrete, constant latency inhibito ry postsynaptic potentials (IPSPs) in all nonpacemaker pyloric neurons , including the inferior cardiac (IC), lateral pyloric (LP), pyloric ( PY), and ventricular dilator (VD) neurons (Fig. 9). MCN5 activity also inhibits these neurons indirectly, via its excitation of the pacemake r neurons. The pyloric pacemaker neurons synaptically inhibit all four nonpacemaker neurons. 6. The increased activity in the VD neuron, aft er MCN5 stimulation, is not mimicked by either direct hyperpolarizatio n or by synaptically inhibiting VD via another pathway (Fig. 10). The poststimulation increase in IC neuron activity is stronger than that a fter hyperpolarizing current injection but is comparable with that res ulting from stimulation of another inhibitory pathway (Fig. 10). The e nhanced PY neuron activity is comparable with that resulting from eith er direct current injection or synaptic inhibition from another pathwa y (Fig. 10). 7. MCN5 activity increases the pyloric cycle frequency of both slow (<1 Hz) and fast (1-2 Hz) rhythms (Fig. 11), and it signifi cantly alters the phase relationships that define this motor pattern ( Fig. 12). These phase relationships change again after MCN5 stimulatio n (Fig. 12). 8. MCN5 acts in concert with the pyloric pacemaker ensemb le to elicit a pyloric rhythm that exhibits enhanced pacemaker neuron activity and reduced activity in all nonpacemaker neurons. Additionall y, despite their electrical coupling, the three types of pace maker ne urons exhibit distinct responses to MCN5 stimulation. This partially u ncouples their normally coactive bursts. The resulting motor pattern i s distinct from all previously characterized pyloric rhythms.