Menthol blunts the interoceptive discriminative stimulus effects of nicotine in female but not male rats

Huynh, Y. Wendy; Raimondi, Anthony J.; Finkner, Andrew; Kuck, Jordan D.; Selleck, Carly; Bevins, Rick A.

doi:10.1007/s00213-020-05542-8

Cited by 8 publications

(4 citation statements)

References 44 publications

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“…One possible explanation for this difference is that the dose of nicotine (0.4 mg/kg) used in the current study produced a ceiling effect, masking possible sex differences. In support of this interpretation, we recently found sex differences in a nicotine drug discrimination task utilizing 0.1 mg/kg as the training dose (Huynh et al ., 2020). In that study by Huynh et al .…”

Section: Discussionmentioning

confidence: 68%

“…d-Amphetamine doses are reported in salt form whereas nicotine doses are in base form – per field standards. All doses, IPIs and routes of administration were based on published research (Palmatier et al ., 2005; Slezak et al ., 2018; Huynh et al ., 2020).…”

Section: Methodsmentioning

confidence: 99%

“…A large body of research suggests that nicotine dependency is largely maintained by processes other than primary reinforcement (Caggiula et al, 2009). These include learning processes, such as conditioning involving the interoceptive stimulus effects of nicotine (Huynh et al, 2020), conditioned reinforcement of nicotine associated stimuli (Charntikov et al, 2020;Palmatier et al, 2007a) and enhancement of the rewarding effects of other environmental stimuli by nicotine (Barrett and Bevins, 2012). This reward-enhancing effect has been characterized in a growing body of research as increased responding for and consumption of non-nicotine reinforcers when nicotine is administered [cf.…”

Section: Introductionmentioning

confidence: 99%

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Reward-enhancing effects of d-amphetamine and its interactions with nicotine were greater in female rats and persisted across schedules of reinforcement

McNealy

Ramsay

Barrett

et al. 2021

Behavioural Pharmacology

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Nicotine enhances the value of environmental stimuli and rewards, and reward enhancement can maintain nicotine consumption. Stimulants such as d-amphetamine are misused more by women and are commonly co-used with nicotine. d-Amphetamine potentiates nicotine’s effects in human and animal research. To date, there are no published studies examining this interaction in a reward-enhancement task. The current study sought to investigate the reward-enhancing effects of nicotine alongside and coadministered with d-amphetamine. Further, we evaluated the persistence of reward enhancement across ratio and temporal schedules of reinforcement. We used 10 male and 10 female Sprague–Dawley rats. Enhancement was assessed within subjects by examining active lever pressing for a visual stimulus reinforcer on variable ratio 3, variable interval 30 s and variable time 30 s – variable ratio 3 schedules. Before 1-h sessions, rats received one injection of saline, 0.1 or 0.3 mg/kg d-amphetamine and one of saline or 0.4 mg/kg nicotine, making six possible drug combinations (saline + saline, saline + nicotine, 0.1 d-amphetamine + aline, 0.1 d-amphetamine + nicotine, 0.3 d-amphetamine + saline and 0.3 d-amphetamine + nicotine) experienced in a randomized order by each rat. When d-amphetamine was coadministered with nicotine, we found an interaction effect on reward enhancement that persisted across schedules of reinforcement. Males and females exhibited reward enhancement by 0.3 d-amphetamine, while only females showed reward enhancement by 0.1 d-amphetamine. Further, females responded more for the visual stimulus than males in all d-amphetamine conditions. Future studies should assess how reward enhancement is involved in high nicotine-amphetamine comorbidity rates and enhanced amphetamine misuse in women.

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Section: Discussionmentioning

confidence: 68%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Reward-enhancing effects of d-amphetamine and its interactions with nicotine were greater in female rats and persisted across schedules of reinforcement

McNealy

Ramsay

Barrett

et al. 2021

Behavioural Pharmacology

Self Cite

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“…To be specific, the activity of the cold- and menthol-activated TRPM8 diminishes over time in the presence of extracellular Ca 2+ ( Yudin et al, 2011 ; Diver et al, 2019 ), which is manifested by a decrease in the cooling effect over time when exposed to menthol, along with a decrease in TRPM8 activity ( Cliff and Green, 1994 ; Reid and Flonta, 2001 ; Matsu-ura et al, 2006 ; Daniels et al, 2009 ). In addition, menthol can cause a short-lasting cross-desensitization of other irritant chemicals-induced stimulus including capsaicin ( Cliff and Green, 1996 ; Green and McAuliffe, 2000 ; Naganawa et al, 2015 ), citric acid ( Morice et al, 1994 ; Plevkova et al, 2013 ), cinnamaldehyde ( Zanotto et al, 2008 ; Klein et al, 2011 ), and nicotine ( Dessirier et al, 2001 ; Fan et al, 2016 ; Huynh et al, 2020 , etc. ), that is, a reduction in irritation evoked by compounds other than itself ( Dessirier et al, 2001 ).…”

Section: Analgesic Mechanism Of Mentholmentioning

confidence: 99%

The distinctive role of menthol in pain and analgesia: Mechanisms, practices, and advances

Zhang

Wang

et al. 2022

Front. Mol. Neurosci.

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Menthol is an important flavoring additive that triggers a cooling sensation. Under physiological condition, low to moderate concentrations of menthol activate transient receptor potential cation channel subfamily M member 8 (TRPM8) in the primary nociceptors, such as dorsal root ganglion (DRG) and trigeminal ganglion, generating a cooling sensation, whereas menthol at higher concentration could induce cold allodynia, and cold hyperalgesia mediated by TRPM8 sensitization. In addition, the paradoxical irritating properties of high concentrations of menthol is associated with its activation of transient receptor potential cation channel subfamily A member 1 (TRPA1). Under pathological situation, menthol activates TRPM8 to attenuate mechanical allodynia and thermal hyperalgesia following nerve injury or chemical stimuli. Recent reports have recapitulated the requirement of central group II/III metabotropic glutamate receptors (mGluR) with endogenous κ-opioid signaling pathways for menthol analgesia. Additionally, blockage of sodium channels and calcium influx is a determinant step after menthol exposure, suggesting the possibility of menthol for pain management. In this review, we will also discuss and summarize the advances in menthol-related drugs for pathological pain treatment in clinical trials, especially in neuropathic pain, musculoskeletal pain, cancer pain and postoperative pain, with the aim to find the promising therapeutic candidates for the resolution of pain to better manage patients with pain in clinics.

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Understanding the stimulus effects of nicotine and bupropion in a drug-drug discriminated goal-tracking task

et al. 2022

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Menthol blunts the interoceptive discriminative stimulus effects of nicotine in female but not male rats

Cited by 8 publications

References 44 publications

Reward-enhancing effects of d-amphetamine and its interactions with nicotine were greater in female rats and persisted across schedules of reinforcement

Reward-enhancing effects of d-amphetamine and its interactions with nicotine were greater in female rats and persisted across schedules of reinforcement

The distinctive role of menthol in pain and analgesia: Mechanisms, practices, and advances

Understanding the stimulus effects of nicotine and bupropion in a drug-drug discriminated goal-tracking task

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