Modulatory role of hippocampal dopamine receptors in antinociceptive responses induced by chemical stimulation of the lateral hypothalamus in an animal model of persistent inflammatory pain

• Published in: Brain research bulletin 2020-09, Vol.162, p.253-260
• Main Authors: Zakeri, Masoud, Soltanizadeh, Saeed, Karimi-Haghighi, Saeideh, Haghparast, Abbas
• Format: Article
• Language: English
• Subjects: CA1 region of hippocampus; D1-like dopamine receptor; D2-like dopamine receptor; Formalin test; Lateral hypothalamus; Pain
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/j.brainresbull.2020.06.017

•Dopaminergic system in CA1 modulate pain behaviors in both phases of formalin test.•Intra-CA1 SCH23390 dose-dependently reduced the LH-induced antinociception.•Blockade of D2-like receptor in CA1 reduced LH-induced antinociceptive responses.•Both antagonists had nearly a same effect on pain-related responses in both phases. The lateral hypothalamus (LH) plays a complicated role in the modulation of inflammatory pain. There are a number of connections between the LH and the hippocampus. This study evaluated the pain modulatory role of intra-CA1 dopamine receptors in LH chemical stimulation-induced antinociception in the formalin test (persistent inflammatory pain model). Vehicle control groups received saline or DMSO into the CA1 and saline into the LH. Carbachol control groups received carbachol (250 nM) into the LH 5 min after saline or DMSO injections into the CA1. In the treatment groups, intra-CA1 administration of SCH-23,390 or Sulpiride (D1- or D2-like dopamine receptor antagonists, respectively) was performed 5 min before carbachol injection. Formalin tests were done in all rats 5 min after the second injection. LH chemical stimulation-induced antinociception during both phases of the formalin test was alleviated by the intra-CA1 administration of dopamine receptor antagonists. The inhibitory effects of the D1 or D2-like dopamine receptor antagonist on LH chemical stimulation-induced analgesia was nearly the same in the both phases of formalin‐induced pain-related behaviors. The findings show that the LH-CA1 pathway contributes to the modulation of formalin-induced pain. Moreover, the results indicate that D1- and D2-like dopamine receptors in the CA1 participate in the LH chemical stimulation-induced antinociception.