Abstract Background Comorbidity of major depression with substance abuse increases the risk of committing suicide. The objective of this work was to determine the psychological and socio-demographic ...factors associated with depression and suicide attempts in patients rehabilitating for drug consumption. Method 57 Patients attending a center for drug abuse treatment answered the following instruments: the Mini-international neuropsychiatric interview, a questionnaire of general information and background data on consumption of substances, depression and suicide attempts, and the Spanish adaptation of the Holmes and Rahe scale for the assessment of life events. Chi-square and logistic regression tests were used to establish associations between variables. Results 68.4% of the Patients had current major depression, of these, 75.4% experienced it before the onset of substance abuse. Patients attempting suicide before drug use corresponded to 26%, whilst 28.1% attempted suicide within the last year. Current depression-related variables were receiving a diagnosis of depression prior to the consumption of drugs and the first used drugs, which were alcohol or marijuana. The adverse life event “Familial drug abuse history”, was also significantly related to depression ( p =0.02). Variables associated with current suicide attempts were: receiving a diagnosis of depression prior to the consumption of drugs ( p =0.02), and suicide attempts previous to drug use ( p <0.003). Limitation A limitation of this study was the small size of the sample. Conclusion Patients with depression who attempted suicide prior to the use of drugs also experienced these conditions during the rehabilitation process. Substance use in the family was a risk factor for both, underscoring the need of actions aimed at preventing addictions in the household environment.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Abstract Chronic caffeine consumption has been inversely associated with the risk of developing dementia and Alzheimer's disease. Here we assessed whether chronic caffeine treatment prevents the ...behavioral and cognitive decline that male Wistar rats experience from young (≈3 months) to middle age (≈10 months). When animals were young they were evaluated at weekly intervals in three tests: motor activity habituation in the open field (30-min sessions at the same time on consecutive days), continuous spontaneous alternation in the Y-maze (8 min), and elevated plus-maze (5 min). Afterward, rats from the same litter were randomly assigned either to a caffeine-treated group ( n =13) or a control group ( n =11), which received only tap water. Caffeine treatment (5 mg/kg/day) began when animals were ≈4 months old, and lasted for 6 months. Behavioral tests were repeated from day 14 to day 28 after caffeine withdrawal, a time period that is far in excess for the full excretion of a caffeine dose in this species. Thirty days after caffeine discontinuation brains were processed for Golgi-Cox staining. Compared with controls, we found that middle-aged rats that had chronically consumed low doses of caffeine (1) maintained their locomotor habituation during the second consecutive day exposure to the open field (an index of non-associative learning), (2) maintained their exploratory drive to complete the conventional minimum of nine arm visits required to calculate the alternation performance in the Y-maze in a greater proportion, (3) maintained their alternation percentage above chance level (an index of working memory), and (4) did not increase the anxiety indexes assessed by measuring the time spent in the open arms of the elevated plus maze. In addition, morphometric analysis of hippocampal neurons revealed that dendritic branching (90–140 μm from the soma), length of 4th and 5th order branches, total dendritic length, and spine density in distal dendritic branches were greater in the basal but not the apical dendrites of CA1 pyramidal neurons from rats chronically treated with caffeine, in comparison with their age- and littermate-matched controls. Altogether, the present findings strengthen the epidemiological observations suggesting that prolonged caffeine intake prevents the cognitive decline associated with aging, and open the possibility that this process could be mediated by promoting the growth of dendrites and spines in neurons of the adult mammalian brain.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Increasing evidence suggests that sleep alterations could favor subsequent depression development. In order to identify the simultaneous occurrence of these parameters in young people, in this work ...we evaluated the prevalence of depressive symptoms, sleep habits, and possible sleep disturbances in college students.
Beck Depression Inventory (BDI), Epworth Sleepiness Scale (ESS), and a Sleep Habits Questionnaire were applied to students registered at the Autonomous University of Yucatan, Merida (mean age 20.2 ± 2.6 years). The final sample was composed of 340 (53%) women and 298 (47%) men. Reliability of the BDI and ESS was assessed by Cronbach's alpha method.
Taking 10 as ESS cut-off point, it was found that 31.6% of the students had a high level of sleepiness. Students with depressive symptoms had a greater number of days with somnolence during class (
p <0.05) and perceived that this affected their academic performance at a higher level (
p <0.001) than the students without symptoms. In comparison to subjects without depressive symptoms, students with those symptoms rated their sleep quality as poor (
p <0.001), perceived a greater latency to initiate sleep after going to bed (
p <0.03), and experienced a greater number of awakenings (
p <0.04).
We found diverse sleep alterations in a large proportion of the studied subjects, which were more severe in those who showed depressive symptoms. Educating students for appropriate sleep hygiene and encouraging them to seek professional advice to treat sleep disturbances may be useful to prevent depression.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
The possible synergism between caffeine and muscarinic antagonists to inhibit haloperidol-induced catalepsy was investigated with the bar test in rats. Pretreatment with low doses of caffeine (1–3 ...mg/kg), a non-selective adenosine antagonist, dose dependently reduced the intensity and increased the onset latency of catalepsy induced by haloperidol (0.5–2 mg/kg). Similar effects were produced by the muscarinic antagonists atropine (4.1 mg/kg), and trihexyphenidyl (THP, 0.01–3 mg/kg). THP inhibited catalepsy intensity with an ED
50 of 0.38 mg/kg, and increased its onset latency with an ED
50 of 0.52 mg/kg. The anticataleptic effect of anticholinergics was potentiated when a low dose of caffeine (1 mg/kg) was applied simultaneously. In the presence of caffeine, THP inhibited catalepsy intensity with an ED
50 of 0.19 mg/kg, and prolonged the latency with an ED
50 of 0.30 mg/kg. The synergism was more evident when THP was administered at subthreshold doses that were unable to modify haloperidol-induced catalepsy when applied alone, but produced a clear inhibition of catalepsy when injected with caffeine. To assess whether repeated administration of caffeine could induce tolerance to the synergism with THP, a group of rats was pretreated with three daily doses of caffeine (1 mg/kg) for seven days, and the catalepsy test was performed on the eighth day. In these animals, caffeine was still able to enhance the anticataleptic actions of THP, suggesting that repeated administration of 1 mg/kg caffeine does not induce tolerance to the synergism with anticholinergics. These results indicate that low doses of caffeine enhance the anticataleptic actions of muscarinic antagonists, and leave open the possibility of using caffeine as adjunctive therapy to reduce the doses and the adverse effects of anticholinergics in Parkinson’s disease.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, SAZU, SBCE, UL, UM, UPCLJ, UPUK
Trihexyphenidyl (THP) is a drug commonly used to reduce parkinsonian symptoms. An important side effect of this agent is memory impairment. Since caffeine enhances the potency of THP to inhibit ...haloperidol-induced catalepsy, caffeine may be used as an adjuvant of lower doses of THP, in order to improve its antiparkinsonian effects without causing memory disruption. To further assess the synergism between caffeine and THP, both drugs were tested in reserpinized rats, another preclinical model of Parkinson’s disease. Four groups of rats (
n = 7) were treated with reserpine (5
mg/kg, i.p.). A control group (
n = 7) was treated only with the vehicle for reserpine (dimethylsulphoxide). The spontaneous locomotor behavior was tested 24
h later in a box with infrared sensors, 30
min after receiving one of the following treatments: distilled water (1
ml/kg), caffeine (1
mg/kg), THP (0.1
mg/kg) or caffeine plus THP. The levels of horizontal locomotion (14 ± 5%) and vertical exploration (15 ± 10%) were significantly lower in reserpinized rats treated with distilled water, compared with the mean activity values (100%) recorded in animals pretreated only with the vehicle for reserpine. The reserpine-induced hypokinesia was neither reversed by caffeine alone nor by THP alone. However, the combination of caffeine plus THP restored locomotion (141 ± 19%) and vertical exploration (82 ± 17%) to levels not significantly different to those of non-reserpinized rats. Moreover, the time-course of locomotion and exploration displayed the characteristic habituation over time, in which short-term memory processes are involved. Also, the thigmotaxis index indicated that the combined treatment did not induce anxiety-like behavior. Hence, these results support the proposal that low, subthreshold doses of caffeine plus THP have the potential to alleviate the motor disabilities in parkinsonian patients, with a low risk of causing anxiety or memory impairment.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
•HU-580 dose-dependently increased wakefulness.•Slow wave sleep was decreased by HU-580 injections.•HU-580 enhanced extracellular levels of dopamine.
Cannabidiolic acid methyl ester (HU-580) is a ...more stable compound than cannabidiolic acid (CBDA) which has been shown to be effective in reducing nausea, anxiety, depression behaviors in animal models. Here we extend the investigation of this compound to determine its effect on the sleep-wake cycle in male Wistar rats. HU-580 dose-dependently (0.1, 1.0 or 100 μg/Kg, i.p.) prolonged wakefulness (W) and decreased slow wave sleep (SWS) duration whereas rapid eye movement sleep (REMS) showed no statistical change. In addition, the brain microdialysis probes either placed at nucleus accumbens (NAc) or into the basal forebrain in freely moving animals were used to evaluate the effects of HU-580 treatment on neurotransmitters related to the sleep-wake cycle modulation. HU-580 enhanced extracellular levels of dopamine, serotonin collected from NAc while adenosine and acetylcholine were increased in basal forebrain. In summary, HU-580 seems to possess wake-promoting pharmacological properties and enhances the levels of wake-related neurochemicals. This is the first report of effects of HU-580 on sleep modulation expanding the very limited existent data on the neurobiological effects of HU-580 on rats.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
We investigated whether the infection with
Trypanosoma cruzi in rats could produce functional alterations of the central nervous system. The experimental group received an injection of 150,000 ...trypomastigotes / rat, whereas the control group received a saline injection. Spontaneous alternation behavior (SAB) tests and sleep-wake cycle recordings were obtained at the end of the parasitaemia. Results showed that the infected animals had significant sleep impairments, as denoted by an increase in the number of wake periods and a reduction of rapid eye movement sleep amount. SAB performance was also found to be impaired in these animals, as compared to the control group. Our results suggest that the rat is a suitable model for brain dysfunction studies in Chagas’ disease.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Previous studies show that prenatal exposure to alcohol results in sleep deficits in rats, including reductions in paradoxical sleep. Little is known, however, about the extent or duration of sleep ...impairments beyond the neonatal period. The present experiment examined effects of prenatal exposure on sleep in young adulthood. Three-hour, daytime sleep EEGs were obtained in 6-month-old female rats prenatally exposed to alcohol. Compared to isocaloric pair-fed and ad libitum control groups, the alcohol-exposed group showed reduced paradoxical sleep. Non-paradoxical sleep did not differ between groups. Concurrent deficits were obtained in radial arm maze, but not inhibitory (passive) avoidance, performance. One year later, at the age of 18 months, alcohol-exposed rats showed deficits in spontaneous alternation behavior which were reversed by administration of glucose (100 mg/kg). Deficits in paradoxical sleep at 6 months of age were highly correlated with deficits in spontaneous alternation behavior at 18 months of age, in individual, alcohol-exposed animals. These results provide the first evidence that prenatal exposure to alcohol results in selective and persistent deficits in sleep. They also show that measures of paradoxical sleep can predict impaired memory over a large portion of the life span, and suggest that glucose can attenuate memory deficits in this population.
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IJS, IMTLJ, KILJ, KISLJ, NUK, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Administration of d-glucose enhances learning and memory in several tasks and also attenuates memory impairments and other behavioral effects of several drugs, including morphine. The present ...experiment compared the effects of peripherally administered d-glucose with those of l-glucose, a stereoisomer of d-glucose that is not metabolized and does not readily cross the blood-brain barrier. Like d-glucose, though at somewhat different doses, peripherally administered l-glucose attenuated morphine-induced deficits in spontaneous alternation performance in rats and mice and attenuated morphine-induced hyperactivity in mice. l-Glucose did not raise circulating levels of plasma d-glucose, suggesting that the effects of l-glucose are not secondary to increased availability of d-glucose. Using direct injections of d- and l-glucose and morphine into the medial septum of rats, the findings indicate that d-glucose but not l-glucose attenuated morphine-induced deficits in spontaneous alternation performance; indeed, intraseptal injections of l-glucose alone impaired spontaneous alternation performance. These findings suggest that peripheral l-glucose antagonizes morphine-induced behavioral effects by a peripheral signaling mechanism, one distinct from the mechanisms that mediate at least some of the effects of d-glucose on brain function.
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IJS, IMTLJ, KILJ, KISLJ, NUK, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
