Abstract
Numerous neuronal properties including the synaptic vesicle release process, neurotransmitter receptor complement, and postsynaptic ion channels are involved in transforming synaptic inputs into postsynaptic spiking. Temperature is a significant influencer of neuronal function and synaptic integration. Changing temperature can affect neuronal physiology in a diversity of ways depending on how it affects different members of the cell’s ion channel complement. Temperature’s effects on neuronal function are critical for pathological states such as fever, which can trigger seizure activity, but are also important in interpreting and comparing results of experiments conducted at room vs physiological temperature. The goal of this study was to examine the influence of temperature on synaptic properties and ion channel function in thalamocortical (TC) relay neurons in acute brain slices of the dorsal lateral geniculate nucleus, a key synaptic target of retinal ganglion cells in the thalamus. Warming the superfusate in patch clamp experiments with acutely-prepared brain slices led to an overall inhibition of synaptically-driven spiking behavior in TC neurons in response to a retinal ganglion cell spike train. Further study revealed that this was associated with an increase in presynaptic synaptic vesicle release probability and synaptic depression and altered passive and active membrane properties. Additionally, warming the superfusate triggered activation of an inwardly rectifying potassium current and altered the voltage-dependence of voltage-gated Na+ currents and T-type calcium currents. This study highlights the importance of careful temperature control in ex vivo physiological experiments and illustrates how numerous properties such as synaptic inputs, active conductances, and passive membrane properties converge to determine spike output.
Highlights
Temperature is understood to be an important factor regulating neuronal excitability and synaptic transmission, it is not known how temperature affects the multiple processes involved in turning strong sensory-driven synaptic inputs into spike outputs in thalamic relay neurons
In order to determine how temperature affects the integration of synaptic inputs and the spike generation mechanism(s) in TC neurons in the mouse dorsal lateral geniculate nucleus (dLGN), retinal ganglion cells (RGCs) axons in coronal slices from Chx10-Cre;Ai32 mice were stimulated with a 460 nm LED flash while synaptically-driven spiking behavior was recorded from TC neurons at room temperature (~23–24 ̊C) and in warmed conditions (~33 ̊C)
The results of this study show that warming leads to a decrease in spiking responses of thalamocortical relay neurons in the dLGN during optogenetic stimulation of retinal ganglion cell axon terminals
Summary
Temperature is understood to be an important factor regulating neuronal excitability and synaptic transmission, it is not known how temperature affects the multiple processes involved in turning strong sensory-driven synaptic inputs into spike outputs in thalamic relay neurons. Temperature effects in the dLGN output spiking in distinct neuron classes is important for translating findings from reduced ex vivo preparations to understanding neuronal function in vivo. Experiments in human subjects have shown that modest changes in body temperature appear able to alter visually-evoked potentials [11] and lowering body temperature has a neuroprotective effect on the survival and function of retinal neurons in a model of optic nerve injury [12]
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