4.7 Article

Salmon Calcitonin Attenuates Some Behavioural Responses to Nicotine in Male Mice

Journal

FRONTIERS IN PHARMACOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2021.685631

Keywords

appetite-regulatory hormones; amylin receptors; calcitonin receptors; reward; pharmacological treatments

Funding

  1. Swedish Research Council [2015-03219, 2019-01676]
  2. LUA/ALF from the Sahlgrenska University Hospital [723941]
  3. Arvid Carlsson foundation
  4. Swedish Research Council [2019-01676] Funding Source: Swedish Research Council

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The study shows that the amylinergic pathway regulates certain nicotine-induced behaviors but does not affect nicotine-induced reward acquisition and expression. Additionally, the results demonstrate that sCT blocks nicotine's stimulatory effects and dopamine release, while preventing its impact on locomotor sensitization.
The behavioural responses to nicotine involve appetite-regulatory hormones; however, the effects of the anorexigenic hormone amylin on reward-related behaviours induced by nicotine remain to be established. Previous studies have shown that the amylinergic pathway regulates behavioural responses to alcohol, amphetamine and cocaine. Here, we evaluated the effects of salmon calcitonin (sCT), an amylin and calcitonin receptor (CTR) agonist, on nicotine-induced locomotor stimulation and sensitisation as well as dopamine release in the nucleus accumbens (NAc) shell. Moreover, we investigated the effects of sCT on the acquisition and expression of nicotine-induced reward in the conditioned place preference (CPP) paradigm. Finally, we performed Western Blot experiments in an attempt to identify the levels of the amylin receptor components CTRa, CTRb, and RAMP1 in reward-related areas of mice responding differently to repeated injections of sCT and nicotine in the locomotor sensitisation test. We found that sCT blocked nicotine's stimulatory and dopamine-releasing effects and prevented its ability to cause locomotor sensitisation. On the other hand, sCT did not alter nicotine-induced acquisition and expression of CPP. Lastly, sCT-nicotine treated mice from the locomotor sensitisation experiment displayed higher levels of total CTR, i.e. CTRa and CTRb together, in the reward-processing laterodorsal tegmental area (LDTg) of the brain compared to mice treated with vehicle-nicotine. Overall, the present data reveal that activation of CTR or/and amylin receptors attenuates certain nicotine-induced behaviours in male mice, further contributing to the understanding of appetite-regulatory peptides in reward regulation.

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