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This literature review seeks to understand how motherhood and profession affect women's sleep. After the birth of a child, there is an increase in dissatisfaction with the quantity and quality of sleep. Awakenings and sleep disturbances are more frequent and can lead to increased fatigue and stress to reconcile household activities and work demands. These changes in sleep can lead to physical and/or psychological health problems. Sleep hygiene and social support become fundamental for the performance of the maternal tasks, reducing risks and increasing prevention of future problems, both for women and children., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Research about the effects of hormonal contraceptives on sleep has been performed but is subjected to important levels of methodological heterogeneity. Hormonal contraceptives impact sleep, but the direction of this association is not clear. Most studies describe a negative sleep profile among contraceptive users, including increased sleepiness, insomnia symptoms, decreased sleep efficiency, and a reduced overall sleep quality. Hormonal intrauterine contraceptives are associated with less negative effects. More research on the field, especially randomized controlled trials, is needed to increase the level and certainty of evidence about the effects of hormonal contraceptives on sleep., (Copyright © 2023 Elsevier Inc. All rights reserved.)

This review encompasses the clinical features and relevance to investigate sleep in women with dysmenorrhea. Dysmenorrhea is a prevalent gynecologic dysfunction that affects the social and professional lives of women. It can occur at every menstrual cycle, depending on the cause and psychologic factors. Studies have reported poor sleep and insomnia symptoms in dysmenorrhea condition, which may intensify the dysmenorrhea manifestation and interfere negatively to its treatment. There is an urgent need to identify the main cause of this dysfunction and provide efficient treatments to minimize the detrimental effects of dysmenorrhea in quality of life of these women., (Copyright © 2023 Elsevier Inc. All rights reserved.)

There is an increased risk of becoming pregnant through fertility treatments using assisted reproductive technology (ART) during the COVID-19 pandemic. The aim of this review is to gather comprehensive data from the existing literature on the potential risks of fertility management during the pandemic period, and outline strategies to mitigate them, with a focus on the hormonal and surgical procedures of ART. A comprehensive search of the scientific literature on COVID-19 in relation to fertility was conducted in the PubMed database using the keywords "coronavirus," "COVID-19," "SARS-CoV-2" and "pregnancy," "fertility," "urogenital system," "vertical transmission," "assisted human reproduction," "controlled ovarian stimulation," "oocyte retrieval," "in vitro fertilization," "hormones," "surgical procedures," "embryos," "oocytes," "sperm," "semen," "ovary," "testis," "ACE-2 receptor," "immunology," "cytokine storm," and "coagulation," from January 2020-July 2022. Published data on pregnancy and COVID-19, and the interaction of the urogenital system and SARS-CoV-2 is reported. The immunologic and prothrombotic profiles of patients with COVID-19, and their increased risks from controlled ovarian stimulation (COS) and ART surgeries, and how these procedures could facilitate COVID-19 and/or contribute to the severity of the disease by enhancing the cytokine storm are summarized. Strategies to prevent complications during COS that could increase the risks of the disease in pre-symptomatic patients are considered. The impact of SARS-CoV-2 on pre-symptomatic infertile patients presents a challenge to find ways to avoid the increased hormonal, immunologic, and prothrombotic risks presented by the use of COS in ART protocols during the COVID-19 outbreak. Safe ART procedures and recommendations are highlighted., (Copyright © 2023 Elsevier Inc. All rights reserved.)

In this manuscript, we call attention to the importance of investigating affordable strategies to improve the management of diabetes. Studies indicate that imbalances in the gut microbiota may lead to the development and progression of this disease. At the same time, poor sleep and sleep disorders, which are very prevalent in individuals with diabetes, can be related to a worse prognosis for the disease and can be impacted by changes in the intestinal microbiome. A suggested treatment that may be effective in controlling diabetes and improving sleep quality through increased metabolic regulation is probiotic supplementation. Scientific evidence has shown a relationship between the use of probiotics and improvements in sleep, in glucose concentrations, and in the levels of high density lipoprotein cholesterol. We suggest that probiotic supplementation can play an important role in the management of diabetes and sleep disorders in diabetic patients. Further randomized clinical studies should be undertaken to better understand the impact and effectiveness of the use of probiotics in improving sleep and controlling diabetes., Competing Interests: Declaration of interest The authors declare that there is no conflict of interest., (Copyright © 2023 Primary Care Diabetes Europe. Published by Elsevier Ltd. All rights reserved.)

There is a growing trend for women to delay having children, with a significant number of women postponing motherhood until the third or fourth decade of life. At the same time, these middle-aged women may be more concerned about skin aging and use dermatologic procedures to delay or repair the effects of aging, environmental factors, and oxidative stress on the skin. It has been suggested that the use of skin cosmetics and procedures may play a role in the reproductive system, although their possible effects have not yet been clearly elucidated. Another crucial factor that needs to be raised in this context is poor sleep, which seems to have an important relationship with both reduced fertility and accelerated skin aging, especially when it is associated with greater oxidative stress and hormonal imbalance. This review discusses the important triad of sleep, dermatology, and reproduction, a subject that has received relatively little attention; and, given its potentially wide-ranging implications, one that deserves more frequent and detailed consideration in future studies. Understanding this complex web of interactions could help to provide outcomes that include healthier skin, safety, improved self-esteem, and successful fertility treatments, all of which can directly affect quality of life., Competing Interests: Declaration of Competing Interest All authors declare no conflicts of interest., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Cannabidiol (CBD) is a natural cannabinoid present in the Cannabis sativa plant, widely prescribed as an anticonvulsant drug, especially for pediatric use. However, its effects on male reproduction are still little investigated. Therefore, the present study assessed the effects of CBD on the spermatogenesis and sperm quality. For this, twenty-one-day-old Swiss mice received CBD for 34 consecutive days by gavage at doses of either 15 or 30 mg/kg. Chronic exposure to CBD decreased the frequency of stages VII-VIII and XII of spermatogenesis and an increase in the frequency of stage IX were noted. Furthermore, the seminiferous epithelium height reduced at stage IX and increased at stage XII in both CBD-treated groups. There was a significant rise of sperm DNA damage, while no genotoxic effects were observed in leukocytes. The activities of superoxide dismutase and catalase decreased, while malondialdehyde levels increased in the sperm of mice treated with a higher dose of CBD. Mice exposed to 30 mg/kg of CBD showed a reduction in the mobile spermatozoa percentage and in curvilinear velocity, while straight line and average path velocity decreased in both treated groups. The number of acrosome-intact spermatozoa declined in the CBD 30 group, and the number of abnormal acrosomes raised in both CBD groups. On the other hand, the weight of reproductive organs, sperm count, and hormone levels were not affected by CBD treatment. These findings show that dysregulation of the endocannabinoid system by CBD can reduce sperm quality. The mechanisms responsible may be associated with disorders during spermatogenesis, especially during the final stages of nuclear remodelling and assembly of acrosome. However, changes in mitochondrial function, as well as the reduction on the antioxidant enzyme activities during epididymal transit, at least partly, may also be involved., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Multiple elements modulate drug use, including sleep, which is increasingly being considered as an important contributor to substance use and abuse. The present study aimed to evaluate the association between sleep, psychiatric and socioeconomic/demographic factors and substance use in a large-scale representative sample from the city of São Paulo, Brazil. Data from the 2007 São Paulo Epidemiological Sleep Study (EPISONO) database were used. In the EPISONO study, volunteers underwent a polysomnographic exam and completed a series of questionnaires to assess objective and subjective sleep quality and associated comorbidities. Drug use was assessed using the Alcohol, Smoking and Substance Involvement Screening Test (ASSIST). Linear (univariate and multivariate) and logistic regressions were performed to identify factors associated with the use of the 4 most commonly used substances in the sample (tobacco, alcohol, cannabis and cocaine/crack). Structural equation models were used to establish theoretical networks to explain the relationship between sleep, psychiatric and socioeconomic factors and use of these substances. The logistic regression results showed that psychiatric symptoms, lower income, and poorer subjective sleep were the main factors associated with tobacco consumption; gender and occupational status with alcohol intake; age and occupation with cannabis use; and education with cocaine/crack use. The structural equation models partially supported these findings and identified significant effects of psychiatric symptoms on tobacco consumption, both directly and mediated by sleep. Our results reinforce previous findings concerning factors associated with generally misused substances and suggest that sleep should be considered as an important element in future substance use disorder studies., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Although several studies demonstrate that stressful situations, such as sleep disturbances, negatively impact the innate and adaptive arms of the immune system, their influence on invariant Natural Killer T (iNKT) cells remains unclear. iNKT cells are CD1d-restricted innate T cells that recognize glycolipid antigens and rapidly produce polarizing cytokines being key players in several immune responses, and a potential target for immunotherapy. iNKT cells differ in several aspects from conventional T lymphocytes, including a unique dependence on CD1d-expressing double-positive (DP) thymocytes for intrathymic maturation. As a consequence of stress, DP thymocytes undergo glucocorticoid-induced apoptosis, which might compromise iNKT developmental pathway. Therefore, we used a paradoxical sleep deprivation (SD) model to determine the impact of sleep disturbance on iNKT cell biology. After 72 h of SD, C57Bl/6 mice exhibited a significant increase in systemic glucocorticoid levels and thymus atrophy. Despite marked decrease in the number of DP thymocytes, the ratio CD1d + /CD1d - was higher in SD mice, and the number of thymic iNKT cells remained unaltered, suggesting that SD did not compromise the iNKT developmental pathway. In contrast, SD reduced hepatic IFN-γ, but not, IL-4-producing iNKT cells, without further effect in the spleen. Despite this fact, SD did not affect stimulation of IFN-γ production by iNKT cells, or cytokine release, in response to α-galactosylceramide, a specific antigen. Furthermore, although SD impaired splenic NK cells activity against tumor cells, it did not affect iNKT cell-specific cytotoxicity. Thus, our study shows that SD-induced stress did not impair the iNKT cells' responses to a cognate antigen., (Copyright © 2020 Elsevier Inc. All rights reserved.)

The present study evaluated the effects of the coadministration of lithium (Li) and Cel on inflammatory parameters in an animal model of mania induced by dextroamphetamine (D-amph). It was used Wistar rats 60 days old (250-350 g). The animals (n = 10 per group) received D-amph (2 mg/kg) or saline solution of NaCl 0.9% (Sal) intraperitoneally once a day for 14 days. From day eight until 14, the animals from the D-amph and Sal groups received Li (24 mg/kg), Cel (20 mg/kg), Li + Cel or water via gavage. Behavioral analyses were performed using the open-field test. The levels of IL-1β, IL-4, IL-10, and TNF-α were evaluated. The administration of D-amph induced hyperactivity in the rats, as well increased the IL-4, IL-10, and TNF-α levels in the serum, frontal cortex, and striatum of rats compared to those of the controls, and treatment with Li plus Cel reversed these alterations. In general, the administration of Li or Cel per se did not have effects on the behavioral and biochemical parameters. However, the treatment with Cel per se decreased only the IL-10 levels in the serum of animals. Besides, the treatment with Li or Cel decreased the IL-4 levels in the serum and reversed the effects of D-amph on this parameter in the frontal cortex. The treatment with Li reversed the effects of D-amph on the TNF-α levels in all tissues evaluated, and the administration of Cel reversed this alteration only in the striatum. It can be observed that treatment with Li plus Cel was more effective against damages caused by D-amph when compared to the administration of both treatments per se, suggesting that the coadministration can be more effective to treat BD rather than Li or Cel itself. The treatment with Li plus Cel was effective against the inflammation induced by D-amph., (Copyright © 2019. Published by Elsevier Inc.)

Obstructive sleep apnea (OSA) has been associated with increased risk of cardiovascular morbidity and mortality. Although inflammatory markers may mediate this association, it is unknown the influence of gender in this mechanism. Thus, we aimed to evaluate the interaction effects between OSA and gender on metabolic and inflammatory profile in a population sample. This study is part of EPISONO cohort, in which 1042 participants underwent polysomnography, answered questionnaires, and had their blood collected for analysis of fasting glucose, total cholesterol and fractions, leptin, ghrelin, liver transaminases, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and C-reactive protein. The results showed that men with OSA had higher leptin levels, shorter sleep latency and lower N3 sleep stage compared to men control (CTRL). They also presented higher apnea index and number of central apneas compared to both CTRL men and OSA women. In women, OSA was related to longer REM sleep latency, higher apnea-hypopnea index (AHI) during REM sleep and increased TNF-α levels compared to CTRL women. A multivariate model showed that male gender, ghrelin and total cholesterol were negatively associated with TNF-α, while IL-6, triglycerides and hypopnea index were positively associated (R 2 =0.21). Additionally, gender (men), body mass index, ghrelin, apnea index and smoking were positive predictors of leptin levels (R 2 =0.55). Of note, postmenopause was associated with changes observed in both TNF-α and AHI during REM sleep in women with OSA. Taken together, our study suggests that OSA consequences may differ between genders and this could indicate a need for different OSA management in women according to their reproductive life's stage., (Copyright © 2016 Elsevier Inc. All rights reserved.)

It has been demonstrated that a prolonged period (48 h) of paradoxical sleep deprivation (PSD) potentiates amphetamine (AMP)-induced behavioral sensitization, an animal model of addiction-related neuroadaptations. In the present study, we examined the effects of an acute short-term deprivation of total sleep (TSD) (6h) on AMP-induced behavioral sensitization in mice and compared them to the effects of short-term PSD (6 h). Three-month-old male C57BL/6J mice underwent TSD (experiment 1-gentle handling method) or PSD (experiment 2-multiple platforms method) for 6 h. Immediately after the sleep deprivation period, mice were tested in the open field for 10 min under the effects of saline or 2.0 mg/kg AMP. Seven days later, to assess behavioral sensitization, all of the mice received a challenge injection of 2.0 mg/kg AMP and were tested in the open field for 10 min. Total, peripheral, and central locomotion, and grooming duration were measured. TSD, but not PSD, potentiated the hyperlocomotion induced by an acute injection of AMP and this effect was due to an increased locomotion in the central squares of the apparatus. Similarly, TSD facilitated the development of AMP-induced sensitization, but only in the central locomotion parameter. The data indicate that an acute period of TSD may exacerbate the behavioral effects of AMP in mice. Because sleep architecture is composed of paradoxical and slow wave sleep, and 6-h PSD had no effects on AMP-induced hyperlocomotion or sensitization, our data suggest that the deprivation of slow wave sleep plays a critical role in the mechanisms that underlie the potentiating effects of TSD on both the acute and sensitized addiction-related responses to AMP., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Objective: The aim of this study was to evaluate overall genetic damage induced by total sleep deprivation in obese, female Zucker rats of differing ages., Method: Lean and obese Zucker rats at 3, 6, and 15 months old were randomly distributed into two groups for each age group: home-cage control and sleep-deprived (N = 5/group). The sleep-deprived groups were deprived sleep by gentle handling for 6 hours, whereas the home-cage control group was allowed to remain undisturbed in their home-cage. At the end of the sleep deprivation period, or after an equivalent amount of time for the home-cage control groups, the rats were brought to an adjacent room and decapitated. The blood, brain, and liver tissue were collected and stored individually to evaluate DNA damage., Results: Significant genetic damage was observed only in 15-month-old rats. Genetic damage was present in the liver cells from sleep-deprived obese rats compared with lean rats in the same condition. Sleep deprivation was associated with genetic damage in brain cells regardless of obesity status. DNA damage was observed in the peripheral blood cells regardless of sleep condition or obesity status., Conclusion: Taken together, these results suggest that obesity was associated with genetic damage in liver cells, whereas sleep deprivation was associated with DNA damage in brain cells. These results also indicate that there is no synergistic effect of these noxious conditions on the overall level of genetic damage. In addition, the level of DNA damage was significantly higher in 15-month-old rats compared to younger rats.

Studies have shown alterations in mitochondrial complexes of bipolar disorder (BD) patients. However, changes in the Krebs cycle enzymes have been little studied. The animal model of mania induced by amphetamine has been widely used for the study of bipolar mania. The aim of this study is to assess behavioral and energy metabolism changes in an animal model of mania induced by methamphetamine (m-AMPH). Wistar rats were first given m-AMPH or saline for 14 days, and then, between days 8 and 14, rats were treated with lithium (Li), valproate (VPA), or saline (Sal). Locomotor behavior was assessed using the open-field task and activities of Krebs cycle enzymes (citrate synthase and succinate dehydrogenase), mitochondrial respiratory chain complexes (I, II, III, and IV), and creatine kinase measured in the brain structures (prefrontal, amygdala, hippocampus, and striatum). Li and VPA reversed m-AMPH-induced hyperactivity. The administration of m-AMPH inhibited the activities of Krebs cycle enzymes and complexes of the mitochondrial respiratory chain in all analyzed structures. Li and VPA reversed m-AMPH-induced energetic metabolism dysfunction; however, the effects of Li and VPA were dependent on the brain region analyzed. From the results obtained in this study, we suggested that the decreased Krebs cycle enzymes activity induced by m-AMPH may be inhibiting mitochondrial respiratory chain complexes. Therefore, changes in the Krebs cycle enzymes may also be involved in BD., (Copyright © 2012. Published by Elsevier Inc.)

Many studies indicate that thimet oligopeptidase (EC3.4.24.15; TOP) can be implicated in the metabolism of bioactive peptides, including dynorphin 1-8, α-neoendorphin, β-neoendorphin and GnRH. Furthermore, the higher levels of this peptidase are found in neuroendocrine tissue and testis. In the present study, we have evaluated the effect of acute cocaine administration in male rats on TOP specific activity and mRNA levels in prosencephalic brain areas related with the reward circuitry; ventral striatum, hippocampus, and frontal cortex. No significant differences on TOP specific activity were detected in the hippocampus and frontal cortex of cocaine treated animals compared to control vehicle group. However, a significant increase in activity was observed in the ventral striatum of cocaine treated-rats. The increase occurred in both, TOP specific activity and TOP relative mRNA amount determined by real time RT-PCR. As TOP can be implicated in the processing of many neuropeptides, and previous studies have shown that cocaine also alters the gene expression of proenkephalin and prodynorphin in the striatum, the present findings suggest that TOP changes in the brain could play important role in the balance of neuropeptide level correlated with cocaine effects., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Behavioral sensitization in rodents is hypothesized to reflect neuronal adaptations that are related to drug addiction in humans. We evaluated the effects of group exposure on the acute hyperlocomotion and behavioral sensitization induced by four drugs of abuse in C57BL/6 mice: methylenedioxymethamphetamine (MDMA), d-amphetamine, morphine and ethanol., Methods: In the priming session, animals received an ip injection of one of the drugs of abuse and were exposed to an open field either individually or in groups of four. Seven days later, we assessed behavioral sensitization in the challenge session. All animals received an ip injection of the same drug and were exposed to the open field in the same social conditions described for the priming session. Locomotion and social interaction were quantified during each session., Results: Acute MDMA, morphine and ethanol, but not d-amphetamine, increased social interaction. However, group exposure only potentiated MDMA-induced hyperlocomotion. After a challenge injection of each drug, there was no sensitization to the facilitating effect of MDMA, morphine or ethanol on social interaction, but locomotion sensitization developed to all drugs of abuse except ethanol. This sensitization was potentiated by group exposure in MDMA-treated animals, attenuated in morphine-treated animals and not modified in d-amphetamine-treated animals. Acute MDMA enhanced body contact and peaceful following, while acute morphine and ethanol increased social sniffing., Conclusions: These results provide preclinical evidence showing that while different drugs of abuse affect different components of social interaction, the neuronal adaptations related to drug dependence can be critically and specifically influenced by group exposure., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Patients with chronic renal failure exhibit massive oxidative genome damage and an elevated risk of cancer. Previous studies have demonstrated the relationship between DNA damage and carcinogenesis. The current study aimed to investigate whether the progression of chronic kidney disease induces genomic damage in an animal model. Adult Wistar rats were assigned to either the control or chronic kidney disease groups. The chronic kidney disease group was subdistributed into five groups with progressively longer durations of disease (30, 60, 90, 120 and 150 days). The results showed that chronic kidney disease induced genomic damage in the blood, liver and kidney cells during all periods evaluated, as indicated by the mean tail moment measured in the comet assay. In brain cells, no genetic damage was induced at early/intermediate disease durations; however, positive genotoxicity was found at 120 and 150 days. Blood pressure and pro-inflammatory cytokine levels (IL-1α, IL-1β, IL-6 and TNFα) were increased after chronic kidney disease induction, while blood iron concentration was significantly reduced in these animals. The results suggest that chronic kidney disease progression contributes to DNA damage in blood, liver, kidney and brain and that such damage can be mediated by hypertension, an inflammatory status and iron deficiency. Additionally, the brain was sensitive to genotoxic insult after extended chronic kidney disease, suggesting a potentially important role of genetic damage in the neurological disorders of end-stage renal patients., (Copyright © 2010 Elsevier Inc. All rights reserved.)

The present study attempted to evaluate the effects of chronic intermittent hypoxia (CIH) associated with sleep restriction in hemodynamic parameters and the plasma renin-angiotensin system. Wistar-Hannover rats were submitted to isolated CIH exposure (1000-1600 h), sleep restriction (1600-1000 h), defined as 18-h paradoxical sleep deprivation followed by 6-h sleep permission period and CIH associated to sleep restriction for 21 days. The CIH and sleep restriction group showed a preferential increase in renal sympathetic nervous system (rSNA) associated with a reduction in plasma angiotensin (1-7) concentrations. However, CIH-sleep restriction rats did not modify rSNA and showed a higher angiotensin (1-7) concentration when compared to isolated CIH and sleep restriction. These results suggest that CIH and sleep restriction impaired the cardiovascular system, and its association to sleep loss can modify these effects by partially restoring circulating angiotensin (1-7)., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Interactions between sleep and epilepsy have been widely documented. Sleep can modulate epileptic phenomena, and epilepsy and seizures disorganize the macro- and micro-architecture of sleep. In turn, sleep deprivation exerts a strong influence on the occurrence of seizures and interictal epileptiform discharges. Recently, sleep disturbances occurring in conjunction with epilepsy have been suggested to lead to a worsening of the quality of life for patients with epilepsy. In addition, data from animal models clarify many gaps in this relationship. In this brief review, we present an outline of the interactions between sleep and epilepsy based on a thorough review of the existing literature., (Copyright (c) 2010 Elsevier B.V. All rights reserved.)

Activation of the immune system elicits several behavioral changes that are collectively called sickness behavior and consists in a strategy to overcome infection. Sleep deprivation can increase susceptibility to pathogens and to behavioral alterations. Thus, the present study aimed to determine how paradoxical sleep deprivation (PSD) affects the behavioral and neurochemical responses to lipopolysaccharide (LPS, potent activator of the immune response). Adult inbred mice were paradoxical sleep deprived (72 h), whereas the control group was kept in their home cages. Both groups received either an injection of saline or LPS (5, 10 or 20 microg/animal ip) before behavioral tasks and tissue collection. During the recovery sleep period, LPS provoked a strong inhibition of sleep rebound due to a suppression of paradoxical sleep. PSD increased the susceptibility of mice to LPS-induced immobility in the open field, which was capable of affecting the anxiety-like behavior also. These altered behavioral responses to LPS were accompanied by reduction in dopamine turnover within the striatum and increased expression of cyclooxygenase-2 in the cortex. The study provides some insights into how the sleep-wake cycle affects the expression of sickness behavior induced by LPS.

The present study was designed to investigate the effects of a hyperlipidic diet (HD) on penile erection (PE) and ejaculation (EJ) induced by cocaine in paradoxical sleep deprived (PSD) rats. Secondly, we aimed to verify the influence of HD cafeteria diet on steroid hormone levels. Twenty-one day-old male Wistar rats were randomly assigned into two groups: rats fed with commercial chow diet and rats fed with a palatable HD containing chow mixed with peanuts, milk chocolate and sweet cookies in the proportion of 3:2:2:1. After nine weeks of treatment, the animals were submitted to PSD or maintained as home cage control group for 96 h and challenged with cocaine (7 mg/kg, i.p.). Results showed that the HD led to a reduction in the frequency of erection in the PSD+cocaine group when compared to the PSD+cocaine fed with standard diet. Regardless of the diet, testosterone concentrations were significantly lower and progesterone was higher in the PSD rats than in the respective home-cage control rats. Although there were no hormonal alterations, the findings showed that a long-term HD might modify the stimulating effects of cocaine in potentiating genital reflexes in PSD rats.