1. To study the basic mechanisms of neuronal thermosensitivity, rat hypothalamic tissue slices were used to record and compare intracellular activity of temperature-sensitive and -insensitive neurones. This study tested the hypothesis that different neuronal types have thermally dependent differences in the transient potentials that determine the interspike interval. 2. Most spontaneously firing neurones displayed depolarizing prepotentials that preceded each action potential. In warm-sensitive neurones, warming increased the rate of rise of the depolarizing prepotential which, in turn, decreased the interspike interval and increased the firing rate. In contrast, temperature had little or no effect on the rate of rise in prepotentials of temperature-insensitive neurones. 3. Prepotential depolarization can be due to increasing depolarizing conductances or decreasing hyperpolarizing conductances. There are differences in the ionic conductances responsible for prepotentials in temperature-sensitive and -insensitive neurones. In warmsensitive neurones, the net ionic conductance decreased as the prepotential depolarized towards threshold, suggesting that the prepotential is primarily determined by a decrease in outward potassium conductances. In contrast, in low-slope temperature-insensitive neurones, the net conductance remained constant during the interspike interval, suggesting a more balanced combination of both depolarizing and hyperpolarizing conductances. 4. Transient outward potassium currents, including A-currents, are important determinants of neuronal firing rates. These currents were identified in all warm-sensitive neurones tested, as well as in many temperature-insensitive and silent neurones. Since warming increased the rates of inactivation of these currents, transient K+ currents may contribute to the temperature-dependent prepotentials of some hypothalamic neurones.

Rat brain slices were used to investigate regional interactions between thermosensitive neurons in different diencephalic regions. Horizontal tissue slices rested over three thermodes. This permitted independent thermal stimulation of rostral, middle, and caudal regions. Thermocouples measured tissue temperatures in these three locations, and extracellular recordings measured neuronal responses to temperature changes both locally (at the site of the recorded neuron) and in remote regions of the slice. Many of the neurons that were sensitive to remote temperatures were located near the lateral border of the diencephalic nuclei, especially in the perifornical area. All neurons displaying remote thermosensitivity also displayed local thermosensitivity. These neurons usually showed opposite responses to remote and local temperatures; i.e., most of these neurons were locally warm sensitive but showed cold sensitivity to remote temperatures. These findings indicate that thermosensitive synaptic networks extend throughout the diencephalon and may explain the effect of temperature on a variety of homeostatic systems.

The thermoregulatory preoptic‐anterior hypothalamus (POAH) contains both temperature sensitive and insensitive neurons. While controversial, recent studies suggest that POAH neuronal thermosensitivity is due to vanilloid‐sensitive transient receptor potential (TRPV) channels. This hypothesis was tested by determining the responses of POAH neurons to ruthenium red, a ryanodine receptor antagonist that blocks TRPV‐mediated responses. Whole‐cell patch microelectrodes recorded the intracellular activity of POAH neurons in rat hypothalamic tissue slices perfused with control ACSF and experimental media containing 1–100 μM ruthenium red. Each neuron was characterized by its spontaneous firing rate at 36°C and its firing rate thermosensitivity (impulses/sec/°C) during changes in tissue temperature. Ruthenium red did not reduce the firing rate thermosensitivity nor the membrane potential thermosensitivity of POAH warm sensitive neurons. This supports our previous studies indicating that hypothalamic neuronal thermosensitivity is not determined by TRP channels nor by thermally‐induced changes in the resting membrane potential. [Supported by NIH grants NS‐14644 and NS‐045758]

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