Effects of adolescent nicotine and SR 147778 (Surinabant) administration on food intake, somatic growth and metabolic parameters in rats

@article{Lamota2008EffectsOA,
  title={Effects of adolescent nicotine and SR 147778 (Surinabant) administration on food intake, somatic growth and metabolic parameters in rats},
  author={Laura Lamota and Francisco Javier Berm{\'u}dez-Silva and Eva M. Marco and Ricardo Llorente and Araceli Gallego and Fernando Rodrı́guez de Fonseca and Maria-Paz Viveros},
  journal={Neuropharmacology},
  year={2008},
  volume={54},
  pages={194-205}
}
Sex‐dependent effects of maternal deprivation and adolescent cannabinoid treatment on adult rat behaviour
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The present results indicate that early MD and adolescent cannabinoid exposure exerted distinct sex‐dependent long‐term behavioural and physiological modifications that could predispose to the development of certain neuropsychiatric disorders, though no synergistic effects were found.
Adolescent exposure to nicotine and/or the cannabinoid agonist CP 55,940 induces gender-dependent long-lasting memory impairments and changes in brain nicotinic and CB1 cannabinoid receptors
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Both, nicotine and cannabinoid treatments induced a long-lasting increase in CB1 receptor activity (CP-stimulated GTPγS binding) in male rats and the nicotine treatment also induced a decrease in nicotinic receptor density in the prefrontal cortex of females.
PROTECTIVE EFFECT OF CELECOXIB ON NICOTINE TOXICITY AND ALTERATIONS IN TRACE ELEMENT LEVELS
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Surinabant did not improve smoking cessation rates compared with placebo, but had a small effect on reducing post-cessation weight gain.
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The pattern of CB1 receptor downregulation was similar to that observed in adults treated with cannabinoids in previous studies; however, its magnitude was smaller in adolescents, which may contribute to some acute behavioral effects, the pharmacological cross‐tolerance and the long‐lasting, adverse psychological consequences of cannabinoid exposure during adolescence.
Effects of chronic nicotine on food intake and anxiety-like behaviour in CB1 knockout mice
Activation of the cholinergic antiinflammatory pathway ameliorates obesity-induced inflammation and insulin resistance.
TLDR
It is shown that adipose tissue possesses a functional cholinergic signaling pathway that is important in mediating the antiinflammatory effect of nicotine, and inactivating this pathway in α7KO mice results in significantly increased adipOSE tissue infiltration of classically activated M1 macrophages and inflammation in α 7KO mice than their WT littermates.
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