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Max Planck Institut für Physiologische und Klinische Forschung, W. G. Kerckhoff Institut, 61231 Bad Nauheim, Germany
In
addition to the well-documented ability of calcitonin to lower blood
calcium levels, blood-borne calcitonin may also affect neurons located
outside the blood-brain barrier, e.g., in the subfornical organ (SFO),
where numerous receptors for this peptide have been described. In an in
vitro preparation of the rat SFO, calcitonin activated 61% of 36 neurons, only 1 neuron was inhibited, and the remainder were
unresponsive. All but two of the neurons excited by
10
7 M calcitonin were also
stimulated by 10
7 M ANG II.
The threshold concentration for the excitatory effects of calcitonin
was 10
9 M and was thus
similar to ANG II. Like ANG II, subcutaneous injection of calcitonin
stimulated water intake, although to a lower extent. These results
suggest that blood-borne calcitonin could stimulate drinking by its
excitatory effect on neurons in the SFO. Calcitonin, which is released
during food intake, might be involved in prandial drinking, which is
presently considered an acquired behavior.
drinking; thirst; osmoregulation; electrophysiology; thyroid; angiotensin II
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