Role of pituitary adenylate-cyclase activating polypeptide in mouse models of nocifensive behaviours and hyperalgesia
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1
University of Pecs, Department of Pharmacology and Pharmacotherapy, Hungary
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2
University of Pécs and Gedeon-Richter Ltd.; , Hungary
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3
Medical School of Osaka University, Japan
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4
University of Pécs, Department of Anatomy, Hungary
Pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) and its receptors (PAC1 and VPAC) are present in the spinal dorsal horn, dorsal root ganglia, and both central and peripheral terminals of capsaicin-sensitive sensory neurones. Data concerning the role of PACAP in central pain transmission are contraversial and we have recently published its divergent peripheral effects on nociceptive processes. Our aim was to investigate acute somatic and visceral nocifensive behaviors, partial sciatic nerve ligation-evoked neuropathic as well as resiniferatoxin-induced inflammatory mechanical and thermal hyperalgesia in PACAP deficient (PACAP-/-) mice to elucidate its overall function in pain transmission. The number of paw lickings in the early and late phases of the formalin test reflecting acute somatic chemonocifensive behavior and acute inflammatory nociception, respectively, was markedly diminished in PACAP-/- mice. Acetic acid-evoked abdominal contractions referring to acute visceral chemonociception was also significantly attenuated in the PACAP-/- group. Neuropathic mechanical hyperalgesia was absent in PACAP-deficient animals. Resiniferatoxin-evoked mechanical hyperalgesia which involves both peripheral and central mechanisms was decreased, but thermal hyperalgesia mediated by only peripheral mechanisms was increased in PACAP-/- mice. These data demonstrate that the overall role of PACAP in pain transmission originating from both exteroceptive and interoceptive areas is excitatory, it is involved in central sensitization. The signal transduction mechanisms of its identified receptors leading to neuronal excitation, explain these findings. In contrast, it has an inhibitory action on the peripheral sensory nerve endings and decreases their sensitization to heat. This suggests the existence of a potential, presently unknown, inhibitory mechanism in peripheral nerve terminals. Hungarian Grants K72592, K73044, RET-008/2005, ETT-06-348/2006, ETT-06-284/2006 and Janos Bolyai Postdoctoral Research Fellowship. PACAP+/- mice were kindly provided by Dr. Nobuhisa Iwata, RIKEN Brain Science Institute, Saitama, Japan.
Conference:
12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009.
Presentation Type:
Poster Presentation
Topic:
Pathophysiology and neurology - non-degenerative disorders
Citation:
Helyes
Z,
Sándor
K,
Kormos
V,
Botz
B,
Imreh
A,
Bolcskei
K,
Szolcsanyi
J,
Norihito
S,
Hashimoto
H,
Baba
A and
Reglődi
D
(2009). Role of pituitary adenylate-cyclase activating polypeptide in mouse models of nocifensive behaviours and hyperalgesia.
Front. Syst. Neurosci.
Conference Abstract:
12th Meeting of the Hungarian Neuroscience Society.
doi: 10.3389/conf.neuro.01.2009.04.031
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Received:
26 Feb 2009;
Published Online:
26 Feb 2009.
*
Correspondence:
Zsuzsanna Helyes, University of Pecs, Department of Pharmacology and Pharmacotherapy, Pecs, Hungary, helyes.zsuzsanna@pte.hu