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Ibias Martín, Javier

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0000-0002-4605-2450
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Ibias Martín
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Javier
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2018 - 201912020 - 20212
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Autor: Nazarian, Arbi × search.filters.applied.f.itemFacultad: Facultad de Psicología ×

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Mostrando 1 - 3 de 3
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    Pain-induced impulsivity is sexually dimorphic and mu-opioid receptor sensitive in rats
    (Springer Nature, 2021-08-24) Espinoza Serrano, Nidia; Saputra, Samuel G.; Company, Matthew; Nazarian, Arbi; Ibias Martín, Javier
    Rationale and objectives Pain sensation can negatively impact cognitive function, including impulsivity. Pain-induced changes in impulsivity can contribute to development of psychiatric comorbidities found in those with chronic pain conditions. The goal of this study was to determine whether complete Freund’s adjuvant (CFA)-induced pain manipulation enhances impulsivity in rats. Whether the pain-induced impulsivity is sexually dimorphic, and if mu-opioid receptors play a role in these processes. Methods Male and female rats were screened for trait impulsivity and designated as high or low impulsive using a delay discounting task. Rats then received a hind paw injection of CFA, and their impulsivity was assessed for 16 days. The effects of morphine on impulsivity were also examined. In a separate experiment, rats were pretreated with beta-funaltrexamine (β-FNA) to determine the role of mu-opioid receptors on impulsivity. Results CFA treatment increased impulsivity in males and females. The onset of CFA-induced impulsivity was faster in high impulsive females than males. Morphine blocked CFA-induced impulsivity in both sexes in a dose- and time-dependent manner. β-FNA prevented the actions of morphine on CFA-induced impulsivity in high impulsive males, but not high impulsive females. Moreover, β-FNA increased CFA-induced impulsivity in morphine naïve males, but not females. Conclusion These findings demonstrate unique sex differences in CFA-induced impulsivity, response to morphine, and the impact of mu-opioid receptors. A better understanding of cognitive deficits and their mechanisms can provide insight into the development of substance abuse and psychiatric comorbidities that occur in people with chronic pain.
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    Sex differences in nicotine-induced impulsivity and its reversal with bupropion in rats
    (SAGE, 2020-12) Nazarian, Arbi; Ibias Martín, Javier
    Abstract References Supplementary Material Get access Cite article Share options Information, rights and permissions Metrics and citations Abstract Background: Enhancement in cognitive impulsivity and the resulting alterations in decision making serve as a contributing factor for the development and maintenance of substance-use disorders. Nicotine-induced increases in impulsivity has been previously reported in male humans and rodents. Although the potential for sex differences in nicotine-induced impulsivity has not been examined. Aims and methods: In the present study, male and female Sprague Dawley rats were submitted to a delay discounting task, in which several consecutive measures of self-control were taken. Firstly, rats were tested with vehicle, and next with nicotine doses of 0.4 and 0.8 mg/kg. Thereafter, chronic treatment with bupropion started, and the animals were tested again. Half the animals continued to receive 0.8 mg/kg of nicotine, while the rest received nicotine and also a daily dose of 30 mg/kg of bupropion. Results: When the animals were first tested with nicotine, female rats showed a significant nicotine dose dependent increase of impulsive behaviour, whereas male rats only showed a decrease on their elections of the larger but delayed reward under the highest dose of 0.8 mg/kg of nicotine. Treatment with bupropion blocked the effect of nicotine on decision making in female rats, as they showed results close to their baseline levels. On the other hand, bupropion did not affect the nicotine-induced delay discounting in male rats. Conclusion: These findings demonstrate sexually dimorphic effects of nicotine on cognitive impulsivity which may help to shed light on nicotine use vulnerabilities observed in women.
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    Insulin dependent and independent normalization of blood glucose levels reduces the enhanced rewarding effects of nicotine in a rodent model of diabetes
    (Elsevier, 2018-10-01) O’Dell, Laura E.; Nazarian, Arbi; Ibias Martín, Javier
    The rewarding effects of nicotine have been previously shown to be enhanced in rodent models of diabetes. It is presently unclear whether the enhanced nicotine reward observed in the diabetes models are mediated via an insulin or glucose mechanism. This study examined whether the enhanced rewarding effects of nicotine observed in streptozotocin (STZ)-treated rats are insulin-mediated. Male and female rats were treated with STZ and the rewarding effects of nicotine (0.2 mg/kg) were measured using the conditioned place preference (CPP) procedure. Some STZ-treated animals received insulin supplementation via subcutaneous pellets immediately after STZ administration, while other rats received daily injections of dapagliflozin (10 mg/kg), a sodium-glucose cotransporter-2 inhibitor. Both male and female STZ-treated rats displayed hyperglycemia, and their blood glucose levels (BGLs) were normalized to control levels following insulin supplementation or dapagliflozin administration. STZ-treated male rats displayed higher nicotine CPP relative to vehicle-treated controls. This effect was abolished in rats that received insulin supplementation or dapagliflozin administration. STZ-treated female rats displayed reduced levels of nicotine CPP as compared to male rats, regardless of treatment condition. These results suggest that glucose plays a major role in modulating the rewarding effects of nicotine in male rats treated with STZ.