Neuronal morphology and neuropil structure in the stomatogastric ganglion of the lobster, Homarus americanus.

The stomatogastric nervous system (STNS) has long been used as a model system for the study of central pattern generation, neuromodulation, and network dynamics. Anatomical studies of the crustacean stomatogastric ganglion (STG) in different species have mostly been restricted to subsets of neurons and/or general structural features. For the first time, we describe the morphology of all STG neurons belonging to the two circuits that produce the well-described pyloric and gastric rhythms in the lobster, Homarus americanus. Somata sit on the dorsal and lateral surface of the STG and send a single primary neurite into the core of the neuropil, which is mostly made up of larger lower order branches. The perimeter of the neuropil consists mostly of finer higher order branches. Immunohistochemical labeling for synaptic proteins is associated with the small diameter branches. Somata positions are not constant but show preferred locations across individuals. The number of copies is constant for all neuron types except the PY and GM neurons (PY neuron number ranges from 3 to 7, and GM neuron number ranges from 6 to 9). Branch structure is largely nondichotomous, and branches can deviate substantially from cylindrical shape. Diameter changes at branch points can be as large as 20-fold. Clearly, the morphology of a specific neuron type can be quite variable from animal to animal.

Red pigment concentrating hormone strongly enhances the strength of the feedback to the pyloric rhythm oscillator but has little effect on pyloric rhythm period.

The neuropeptide, red pigment concentrating hormone (RPCH), strengthened the inhibitory synapse from the lateral pyloric (LP) neuron to the pyloric dilator (PD) neurons in the pyloric network of the stomatogastric ganglion (STG) of the lobster, Homarus americanus. RPCH produced several-fold increases in the amplitude of both action potential-mediated and non-impulse-mediated transmission that persisted for as long as the peptide remained present. Because the LP to PD synapse is the only feedback to the pacemaker kernel of the pyloric network, which consists of the electrically coupled two PD neurons and the anterior burster (AB) neuron, it might have been expected that strengthening the LP to PD synapse would increase the period of the pyloric rhythm. However, the period of the pyloric rhythm increased only transiently in RPCH, and a transient increase in cycle period was observed even when the LP neuron was hyperpolarized. Phase response curves were measured using the dynamic clamp to create artificial inhibitory inputs of variable strength and duration to the PD neurons. Synaptic conductance values seen in normal saline were ineffective at changing the pyloric period throughout the pyloric cycle. Conductances similar to those seen in 10(-6) M RPCH also did not evoke phase resets at phases when the LP neuron is typically active. Thus the dramatic effects of RPCH on synaptic strength have little role in modulation of the period of the pyloric rhythm under normal operating conditions but may help to stabilize the rhythm when the cycle period is too slow or too fast.