Abstract
The crustacean stomatogastric nervous system (STNS) has long been a model system for the study of small circuits and central pattern generation, and in particular, the study of the effects of neuromodulators on small circuits. The B-type allatostatin (AST-B), a peptide originally discovered as a hormone in crick- ets and later shown to be physiologically active in the crustacean STNS, acts to control the pyloric rhythm in vitro. In this study we used immunohistochemical methods to locate the endogenous peptide. We demonstrated that the peptide exists in cells with somata in the comisseral ganglia (CoG) and oesophogeal gan- glion (OG), both which have descending modulatory inputs to the central pattern generating ganglion in the STNS, the stomatogastric ganglion. We also used a variety of intracellular and extracellular methods to further characterize the effect of the AST-Bs on the STNS. Intracellular recordings show that the AST-Bs hyper- polarize the lateral pyloric neuron (LP) and the pyloric dilator neuron (PD). We also further characterized the frequency dependent effect of the AST-B. Previous studies showed that the AST-B had minimal effect on the pyloric rhythm at nor- mal network frequencies, but evidenced a strong decrease in frequency when the network had already been slowed down by removal of modulatory input. In this study, I used alternative methods to influence frequency independently from mod- ulation. Injecting the pacemaker neuron PD with hyperpolarizing current slowed the pyloric rhythm and produced similar results to other slow preparations with regards to AST-B effect. These results further elucidate the action of the AST-B peptides and give suggestions as to its physiological purpose.