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. 2015 Jun 2;2(2):277–296. doi: 10.1080/23328940.2015.1048928

Table 1.

Evidence for the thermoregulatory function of capsaicin-sensitive warm sensors in the POA

1) Microinjection of capsaicin induces dose-dependent immediate coordinated heat-loss response.
2) After repeated microinjections desensitization to the effects of capsaicin occurs.
3) POA-desensitized rats in subsequent days show impaired physiological and behavioral regulation against overheating in warm Ta and fall in body temperature to s.c. capsaicin is inhibited but not abolished.
4) Microiontophoretic application of capsaicin to warm-sensitive POA neurons enhanced their firing rate and inhibited the activity of the cold one.
5) Systemic injection of capsaicin to thermocontrolled POA induces pronounced activation of the warm-sensitive units and inhibition of the cold-sensitive ones.
6) After systemic capsaicin pretreatment a long-term reduction ofa) heat-loss response to POA heating or to capsaicin microinjection into the POA occursb) the proportion of warm or cold units in the POA is reduced by about 50%c) mitochondrial swelling milder than in the dorsat root ganglia in a group of POA neurons below the anterior commissure was observed in electronmicroscopic preparations.
7) After preoptic lesions heat-loss responses evoked by subcutaneous capsaicin injection was diminished, shortened but never abolished.
8) Presence of TRPV1 in the POA region has been demonstrated by mRNA138 or H3RTX-binding assays150 but by Cre-reporter TRPV1 positivity was described not in the POA but in the dorsal part of the hypothalamus.108,139