TITLE:
Activation of the corticotropin-releasing factor receptor from the basolateral or central amygdala modulates nociception in guinea pigs
AUTHORS:
Alberto Ferreira Donatti, Christie Ramos Andrade Leite-Panissi
KEYWORDS:
Amygdala; α-Helical CRF9-41; Nociception; Acute Pain; Hot Plate Test
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.4 No.6A,
June
20,
2013
ABSTRACT: Corticotropin-releasing
factor (CRF) is a peptide that is released from the hypothalamus into widespread
areas of the brain. Evidence has suggested that CRF is involved as a
neuromodulator outside of the hypothalamic-pituitary-adrenal axis, playing an
important role in fear, anxiety, depression and pain modulation. Our previous
report demonstrated that CRF receptor activation in basolateral (BLA) or
central nuclei of the amygdala (CeA) produces innate fear in guinea pigs.
Inhibition of these receptors via administration of α-helical CRF9-41 (a nonspecific antagonist) into the
CeA or BLA decreased innate fear behavior [1]. Additionally, there is strong
evidence that emotional behavior and nociception can be modulated simultaneously.
The present study was conducted to investigate the involvement of the CRF
receptors of the BLA or CeA in nociception in guinea pigs. Guinea pigs were
treated with CRF and α-helical CRF>9-41> in three different doses or injected with α-helical
CRF9-41 preceded by CRF into the BLA or CeA, and they were evaluated
using the hot plate test. Our findings indicated that activation of CRF
receptors in the BLA and in the CeA promoted antinociception, and this effect
was reversed by preadministration of α-helical
CRF9-41 in the same area. The treatment with α-helical CRF>9-41> per se
into the BLA and CeA did not alter nociception. Thus, nociception modulation
occurs in a phasic manner, whereas defensive behavior can occur tonically
because the α-helical CRF9-41 did not cause any modification on the index of analgesia in the hot plate test
but did reduce innate fear behavior [1].