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Temperature effects on neuronal membrane potentials and inward currents in rat hypothalamic tissue slices
1Department of Physiology and Cell Biology, 201 Hamilton Hall, Ohio State University, 1645 Neil Avenue, Columbus, OH 43210, USA.
The Journal of Physiology
|February 8, 2005
Summary
Neuronal thermosensitivity in the preoptic-anterior hypothalamus (PO/AH) is not due to resting ionic currents. Instead, it is regulated by currents that influence rapid membrane potential changes, challenging previous hypotheses about warm-induced depolarization.
Area of Science:
- Neuroscience
- Physiology
- Thermoregulation
Background:
- Preoptic-anterior hypothalamic (PO/AH) neurons regulate body temperature.
- Neuronal thermosensitivity is hypothesized to involve warm-induced depolarization.
- Tetrodotoxin (TTX)-sensitive sodium currents and TRP channels have been implicated in thermosensitivity.
Purpose of the Study:
- To investigate the ionic basis of thermosensitivity in PO/AH neurons.
- To determine if specific resting currents correlate with warm-sensitive neuronal activity.
- To test the role of TTX-sensitive currents in neuronal temperature responses.
Main Methods:
- Intracellular recordings in rat hypothalamic tissue slices.
- Comparison of thermal effects on membrane potentials and currents in different neuronal types.
- Voltage clamp recordings to analyze persistent inward cationic currents, with and without TTX.
Main Results:
- All neuronal types showed minor depolarization with warming and hyperpolarization with cooling.
- No significant differences in membrane potential thermosensitivity were found between neuronal types.
- TTX reduced current thermosensitivity but did not reveal differences between neuronal types; no unique resting current for warm-sensitive neurons was identified.
Conclusions:
- Neuronal thermosensitivity in the PO/AH is not mediated by a unique resting ionic current.
- Thermosensitivity appears to be controlled by currents that regulate rapid membrane potential changes, rather than resting currents.
- The findings challenge the hypothesis that warm-induced depolarization via specific resting currents is the primary mechanism of neuronal thermosensitivity.