Peptide Neuromodulation Supports Temperature-Robust Neuronal Activity by Increasing Dendritic Electrical Spread


Media is loading



Download Presentation (7.8 MB)

Publication Date


Document Type


Presentation Type


Degree Type



Biological Sciences


Wolfgang Stein

Mentor Department

Biological Sciences


Acute temperature changes can disrupt neuronal activity, leading to loss of motor control and failure of vital behaviors. Acute warming of the isolated crab stomatogastric nervous system from 10°C to 13°C disrupts the rhythmic neuronal activity underlying mastication by silencing an important motor neuron, the Lateral Gastric neuron (LG). The disruption of activity in response to a 3°C temperature increase contrasts with observations that in vivo the same neuron is active after the temperature has increased b even more than 10°C. It was recently discovered that peptide neuromodulation present in vivo but not in vitro restores LG’s rhythmic activity and thereby allows the animal to sustain its ability to chew over a large temperature range. This effect could be replicated in vitro if the peptide neuromodulator was augmented experimentally. Neuronal activity depends on adequate signal spread throughout the dendrites - a process sensitive to shunting when ion channel conductances increase. We hypothesize that warming leads to an overall increase in membrane shunt, which disrupts rhythmic activity in LG by reducing signal spread in the dendrites. However, peptide neuromodulation restores LG’s rhythmic activity by counterbalancing the membrane shunt and reinstating the signal spread necessary for neuronal activity. To test these hypotheses, we quantified signal spread in LG’s dendrites while increasing the temperature from 10°C to 13°C, and applying the neuropeptide, Cancer borealis tachykinin-related peptide Ia (CabTRP Ia). We used two approaches to quantify signal spread; fluorescent Calcium imaging and two-electrode current- and voltage-clamp. We found that membrane shunt increased and signal spread decreased as the system warmed, but was reversed in the presence of CabTRP Ia. Our results indicate that peptide neuromodulation restores neuronal activity at warmer temperatures by increasing signal spread and opposing membrane shunt in the dendrites. CabTRP Ia activates an NMDA-like current called the modulator-induced current (IMI). To assess whether IMI increased LG’s temperature robustness, we introduced IMI into LG using a computer-brain interface. We found that introducing IMI at 13°C was sufficient to increase signal spread in the dendrites and restore LG’s rhythmic activity. Altogether, our results indicate that peptide activation of an NMDA-like current increases signal spread in the dendrites to sustain neuronal activity during temperature changes.


Authors: Margaret L. DeMaegd and Wolfgang Stein

Peptide Neuromodulation Supports Temperature-Robust Neuronal Activity by Increasing Dendritic Electrical Spread