Abstract
Environmental temperature perturbations pose a constant threat to the stability of neuronal function. The cardiac ganglion (CG), a central pattern generator (CPG), is able to maintain healthy rhythmic activity over a 30°C temperature range, modifying its output with changes as slight as 0.5°C (Jury and Watson, 2000). Recent studies have confirmed the role of neuromodulators as agents of regulation of crustacean CPGs in response to both acute and mild temperature changes (Chen et al., 2014; Städele et al., 2015). The goal of the present study is to observe the effects of neuromodulatory substances on the isolated CG across a broad range of biologically-relevant temperatures. I recorded activity from the CG extracellularly from 7°C to 31°C in saline and in the presence of one of five neuromodulatory substances. Q10 temperature coefficients of the CG’s burst frequency in control conditions (n=31) were 1.76±.45, with some CGs nearly temperature invariant (Q10 = 1.1) while others increased 6-fold over the observed range (Q10 = 2.7). The efficacy of each substance in altering the CG’s burst frequency and number of spikes per burst was found to have its own signature temperature dependence. In the presence of excitatory modulators, the change in burst rate over temperature increased, causing previously temperature-invariant CGs to become more temperature dependent. CCAP, typically considered excitatory, elicited a wide range of temperature-dependent responses on an animal-to-animal basis. The inhibitory substances GABA and Allatostatin-3 (AST-3) completely silenced activity of the CG at low temperatures. Interestingly, most but not all preparations overcame silencing at high temperatures, ranging from reduced to elevated frequencies in comparison to temperature-paired controls. These data enrich our knowledge of neuromodulatory dynamics in a temperature-varying environment.