Abstract
Many neuronal processes are temperature-sensitive. Cooling by 10 \({}^\circ\) C typically slows ion channel dynamics by more than a factor of two (Q \(_\textrm{10}\) \(> 2\) ). Nevertheless, behaviors can remain robust despite variations in brain temperature. For instance, cooling the premotor nucleus HVC in zebra finches by 10 \({}^\circ\) C slows song production by only a factor of Q \(_\textrm{10}\) \(\sim 1.3\) . Here we examine the temperature robustness of the synaptic chain network within HVC. Burst spike propagation along such a chain network is postulated to control the tempo of the song. We show that the dynamics of this network are resilient to cooling and that the slowing of burst propagation exhibits a Q \(_\textrm{10}\) similar to that observed for the song. We identify two key factors underlying this robustness: the reliance on axonal delays, which are more resistant to temperature changes than ion channels, and enhanced synaptic efficacy at lower temperatures. We propose that these mechanisms represent general principles by which neural circuits maintain functional stability despite temperature fluctuations in the brain.
Significance statement
Many animal behaviors remain robust despite temperature fluctuations in the brain. By studying timing circuits in songbirds, we identify key circuit elements that contribute to this resilience, including axonal delays and synaptic integration. Our work highlights how these mechanisms interact to maintain stable neuronal dynamics in response to temperature changes.
