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The reinforcement-enhancing effect (REE) of nicotine refers to the drug’s ability to enhance the strength of other primary and conditioned reinforcers. The main aim was to investigate neuropharmacological mechanisms underlying nicotine’s strengthening of a primary visual reinforcer (i.e., a light cue), using a subcutaneous (SC) dose previously shown to provide plasma nicotine levels associated with habitual smoking. Adult male rats pressed an “active” lever to illuminate a brief cue light during daily 60-min sessions. Rats that showed a clear REE were tested with systemically administered pretreatment drugs followed by nicotine (0.1 mg/kg SC) or saline challenge, in within-subject counterbalanced designs. Pretreatments were mecamylamine (nicotinic, 0.1-1 mg/kg SC), SCH 39166 (D1-like dopaminergic, 0.003-0.2 mg/kg SC), naloxone (opioid, 1 and 5 mg/kg SC), prazosin (alpha1-adrenergic antagonist, 1 and 2 mg/kg IP), rimonabant (CB1 cannabinoid inverse agonist, 3 mg/kg IP), sulpiride (D2-like dopaminergic antagonist, 40 mg/kg SC), or propranolol (beta-adrenergic antagonist, 10 mg/kg IP). The nicotine REE was abolished by three antagonists at doses that did not impact motor output, i.e., mecamylamine (1 mg/kg), SCH 39166 (0.01 and 0.03 mg/kg), and naloxone (5 mg/kg). Prazosin and rimonabant both attenuated the nicotine REE, but rimonabant also suppressed responding more generally. The nicotine REE was not significantly altered by sulpiride or propranolol. In adult male rats, the reinforcement-enhancing effect of low-dose nicotine depends on nicotinic receptor stimulation and on neurotransmission via D1/D5 dopaminergic, opioid, alpha1-adrenergic, and CB1 cannabinoid receptors.

Background: A novel virus breakout in December 2019, with diverse clinical manifestations, initially identified as infecting the respiratory system, has spread rapidly around the world, with adverse effects which have caused acute myocardial injury and chronic damage to the cardiovascular system in some individuals. Aim: To present a clinical case with the manifestation of COVID-19 suspected to be either a mild case of either myocarditis or pericarditis. This case highlights a relatively atypical presentation of COVID-19 and the value of a coordinated approach to the unexpected sequences of patient recovery patterns that may require further specialist referral and intervention. Findings: A ribonucleic acid (RNA) viral infection was confirmed by a polymerase chain reaction with reverse transcription (RT-PCR) and the patient was diagnosed with coronavirus disease 2019 (COVID-19). The presenting symptoms failed to resolve and the patient was admitted to the accident and emergency (A&E) department. Upon the second visit to the A&E department at 27 days postinfection, an electrocardiograph (ECG) was conducted revealing T wave inversion. Implications: A coordinated approach is needed to combat the infection, develop cardiac-protective strategies and direct supportive measures.

Public health interventions such as occupational social distancing and remote working, while critical to slow the spread of the coronavirus, are severely disrupting labour markets. We examine the impact of educational attainment on a worker’s potential to engage in both occupational social distancing in the workplace and working from home requirements for the Irish case. We identify that remote working has a more significant economic effect on labour market inequalities than occupational social distancing. In fact, the results indicate the relationship between occupational social distancing and differences in worker demographics are small. Remote working inequalities are primarily related to differences in individual education levels and a worker’s gender.