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Lawrence Lumeng - One of the best experts on this subject based on the ideXlab platform.
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The expression of an alcohol Deprivation effect in the high-alcohol-drinking replicate rat lines is dependent on repeated Deprivations.
Alcoholism clinical and experimental research, 2000Co-Authors: Zachary A. Rodd-henricks, William J. Mcbride, David L. Mckinzie, James M. Murphy, Lawrence LumengAbstract:Background: The alcohol Deprivation effect (ADE) is a temporary increase in the ratio of alcohol/total fluid intake and voluntary intake of ethanol (EtOH) solutions over baseline drinking conditions when EtOH access is reinstated after a period of alcohol Deprivation. The ADE has been posited to be an animal model for alcohol craving. In the current study, we examined the effects of initial Deprivation length and number of Deprivation exposures on the ADE in the replicate lines of the high-alcohol-drinking (HAD) rats. Methods: Adult male HAD-1 and HAD-2 rats received 24 hr free-choice access to 10% (v/v) EtOH and water for 6 weeks. Rats were then assigned to groups deprived of EtOH for 0 (control), or 2 to 8 weeks. All deprived groups were then given 24 hr access to EtOH for 2 weeks before being deprived of EtOH for another 2 weeks. This cycle of 2 weeks of access and 2 weeks of Deprivation was carried out for a total of four Deprivations. Results: After the initial EtOH Deprivation period, EtOH consumption in HAD-1 and HAD-2 rats returned to baseline levels but failed to exhibit either an early onset ADE (initial 2 hr) or prolonged ADE (24 hr). An ADE was observed in two of the four deprived groups for the HAD-1 rats (2 week and 6 week groups) and in all deprived groups for the HAD-2 rats after a second Deprivation, and in all deprived groups of both lines after a third Deprivation. In the HAD-2 line, but not in the HAD-1 line, the duration of the ADE was prolonged into the second reinstatement day after the fourth Deprivation. Conclusions: The expression of an ADE was observed only after repeated Deprivation periods in the HAD lines. The duration of the ADE was prolonged in the HAD-2 line, but not in the HAD-1 line, with repeated Deprivations, which suggests a dissociation between selection for alcohol preference and the effects of repeated Deprivations on the duration of the ADE.
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Alcohol Deprivation effect is prolonged in the alcohol preferring (P) rat after repeated Deprivations
Alcoholism clinical and experimental research, 2000Co-Authors: Zachary A. Rodd-henricks, William J. Mcbride, David L. Mckinzie, James M. Murphy, Saame Raza Shaikh, Lawrence LumengAbstract:Background: The alcohol Deprivation effect (ADE) is a temporary increase in the ratio of ethanol/total fluid intake and the voluntary intake of ethanol solutions over baseline drinking conditions when ethanol access is reinstated after a period of alcohol Deprivation. The ADE has been posited to be an animal model for alcohol craving. The current study examined the effects of initial Deprivation length and number of Deprivation exposures on the ADE in alcohol-preferring (P) rats. Methods: Adult female P rats received 24-hr free-choice access to 10% (v/v) ethanol and water for 6 weeks. Rats were then randomly assigned to five groups deprived of ethanol for O (control), 2, 4, 6, or 8 weeks (W). All deprived groups were then given 24-hr access to ethanol for 2 weeks before bbeing deprived of ethanol for another 2 weeks. Results: After the initial ethanol Deprivation period, the deprived groups displayed a similar 2-fold ADE (e.g., 4-W group; 4.6 ± 0.5 for baseline vs. 10.5 ± 0.3 g/kg/day for the 1st reinstatement day) during the initial 24-hr period. Ethanol consumption began to return to control levels 48 (7.1 ± 0.4 g/kg/day) and 72 (6.4 ± 0.4 g/kg/day) hrs later. In addition, each deprived group showed increases in the ratio of ethanol/total fluid intake upon reinstatement, and there was a tendency for sustained higher ethanol intake ratlos during the first 3 postexposure days for the 4-, 6-, and 8-W grups, but only during the first 2 reinstatement days for the 2-W group. The second Deprivation did not increase the magnitude of the ADE over that observed in the first Deprivation during the initial 24-hr period of re-exposure, but it did prolong the duration of the ADE into the 2nd and 3rd reinstatement day for the 2-, 4-, and 6-W groups and into the 5th reinstatement day for the 8-W group. Conclusions: Equivalent robust ADEs can be seen in P rats with Deprivation periods of 2–8 W, which suggests that the ADE has a rapid onset and is not affected by the durations of Deprivation that were tested. The duration of the ADE was prolonged in P rats exposed to a second Deprivation period, suggesting that factors associated with the ADE phenomenon could be strengthened by repated Deprivations.
R. Tölle - One of the best experts on this subject based on the ideXlab platform.
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Sleep Deprivation therapy.
Biological psychiatry, 1991Co-Authors: H. Kuhs, R. TölleAbstract:Abstract This review reports, with as much detail as possible, on the literature relating to therapeutic sleep Deprivation (or induced-wakefulness therapy) since it was first described in 1971. The antidepressive effect of sleep Deprivation has been substantiated by numerous studies. A series of clinical predictors of response to sleep Deprivation are also described. Partial sleep Deprivation late in the night is equivalent to total sleep Deprivation in terms of therapeutic value and —because of its simpler application—can be regarded today as the sleep Deprivation method of choice. The status of sleep Deprivation in the overall treatment schedule for depressive disorders is discussed in detail. Numerous findings, some of them contradictory, have been published on the effect of sleep Deprivation on biological variables. To date, no unequivocal explanation has been found for the mechanism of action of sleep Deprivation.
Robert E Strecker - One of the best experts on this subject based on the ideXlab platform.
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sleep Deprivation in rats produces attentional impairments on a 5 choice serial reaction time task
Sleep, 2006Co-Authors: Christopher A Cordova, Bishoy Said, Robert W Mccarley, Mark G Baxter, Andrea A Chiba, Robert E StreckerAbstract:Study Objectives: To develop a rodent model of the attentional dysfunction caused by sleep loss. Design: The attentional performance of rats was assessed after 4, 7, and 10 hours of total sleep Deprivation on a 5-choice serial reaction time task, in which rats detect and respond to brief visual stimuli. Setting: The rats were housed, sleep deprived, and behaviorally tested in a controlled laboratory setting. Participants: Ten male Long-Evans rats were used in the study. Interventions: Rats were trained to criteria and subsequently tested in daily sessions of 100 trials at approximately 4:00 PM (lights on 8:00 AM-8:00 PM). Attentional performance was measured after 4, 7, 10 hours of total sleep Deprivation induced by gentle handling. Results: Sleep Deprivation produced a monotonic increase in response latencies across the 4-hour, 7-hour, and 10-hour Deprivations. Sleep Deprivation also led to increased omission errors, but the overall number of perseverative and premature responses was unchanged. Subgroups of rats were differentially affected in the number of omission errors and perseverative responses. Conclusions: The effects of sleep Deprivation on rats are compatible with a range of human findings on the effects of sleepiness on selective attention, psychomotor vigilance, and behavioral control. Rats also exhibited differential susceptibility to the effects of sleep Deprivation, consistent with ‘trait-like’ susceptibility that has been found in humans. These findings indicate the feasibility of using the 5-choice serial reaction time task as an animal model for investigating the direct links between homeostatic sleep mechanisms and resulting attentional impairments within a single animal subject.
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76 sleep Deprivation in rats produces attentional impairments on a five choice serial reaction time task
Journal of Investigative Medicine, 2006Co-Authors: Christopher A Cordova, Bishoy Said, Robert W Mccarley, Mark G Baxter, Andrea A Chiba, Robert E StreckerAbstract:The effects of sleep Deprivation on behavior and cognition have generally been understood in terms of a homeostatic process that increases the drive for sleep with extended wakefulness, a process whose neurochemical origins have recently begun to be elucidated. As decrements in vigilance and attention are among the first signs of sleep loss and sleepiness, it has been hypothesized that common neural systems are involved in the processes of the sleep drive and sustained attention. For example, the activity of the basal forebrain cholinergic system has been proposed to promote cortical arousal and wakefulness as well as attention. Furthermore, we and others have hypothesized that an inhibition of this cortically projecting cholinergic system mediates the sleepiness associated with prolonged wakefulness. We only know of one study that has used an attentional measure in a behavioral assessment of sleep-deprived animals. Hence, the goal of the present study was to develop a rodent model of the attentional dysfunction caused by sleep loss that could be used to elucidate the effects of sleep drive on neurobiological processes of attention. The attentional performance of rats was assessed after 4, 7, and 10 h of total sleep Deprivation (SD) on a 5CSRTT, where rats detect and respond to brief visual stimuli. SD produced a monotonic increase in response latencies across the three Deprivations. SD also led to increased omission errors, but the overall number of perseverative and premature responses was unchanged. The effects of sleep Deprivation on rats are compatible with a range of human findings on the effects of sleepiness on selective attention, psychomotor vigilance, and behavioral control. Rats also exhibited differential susceptibility to the effects of sleep Deprivation, consistent with ‘trait-like’ susceptibility that has been found in humans. These findings indicate the feasibility of using the 5CSRTT as an animal model for investigating the direct links between homeostatic sleep mechanisms and resulting attentional impairments within a single animal subject.
Zachary A. Rodd-henricks - One of the best experts on this subject based on the ideXlab platform.
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The expression of an alcohol Deprivation effect in the high-alcohol-drinking replicate rat lines is dependent on repeated Deprivations.
Alcoholism clinical and experimental research, 2000Co-Authors: Zachary A. Rodd-henricks, William J. Mcbride, David L. Mckinzie, James M. Murphy, Lawrence LumengAbstract:Background: The alcohol Deprivation effect (ADE) is a temporary increase in the ratio of alcohol/total fluid intake and voluntary intake of ethanol (EtOH) solutions over baseline drinking conditions when EtOH access is reinstated after a period of alcohol Deprivation. The ADE has been posited to be an animal model for alcohol craving. In the current study, we examined the effects of initial Deprivation length and number of Deprivation exposures on the ADE in the replicate lines of the high-alcohol-drinking (HAD) rats. Methods: Adult male HAD-1 and HAD-2 rats received 24 hr free-choice access to 10% (v/v) EtOH and water for 6 weeks. Rats were then assigned to groups deprived of EtOH for 0 (control), or 2 to 8 weeks. All deprived groups were then given 24 hr access to EtOH for 2 weeks before being deprived of EtOH for another 2 weeks. This cycle of 2 weeks of access and 2 weeks of Deprivation was carried out for a total of four Deprivations. Results: After the initial EtOH Deprivation period, EtOH consumption in HAD-1 and HAD-2 rats returned to baseline levels but failed to exhibit either an early onset ADE (initial 2 hr) or prolonged ADE (24 hr). An ADE was observed in two of the four deprived groups for the HAD-1 rats (2 week and 6 week groups) and in all deprived groups for the HAD-2 rats after a second Deprivation, and in all deprived groups of both lines after a third Deprivation. In the HAD-2 line, but not in the HAD-1 line, the duration of the ADE was prolonged into the second reinstatement day after the fourth Deprivation. Conclusions: The expression of an ADE was observed only after repeated Deprivation periods in the HAD lines. The duration of the ADE was prolonged in the HAD-2 line, but not in the HAD-1 line, with repeated Deprivations, which suggests a dissociation between selection for alcohol preference and the effects of repeated Deprivations on the duration of the ADE.
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Alcohol Deprivation effect is prolonged in the alcohol preferring (P) rat after repeated Deprivations
Alcoholism clinical and experimental research, 2000Co-Authors: Zachary A. Rodd-henricks, William J. Mcbride, David L. Mckinzie, James M. Murphy, Saame Raza Shaikh, Lawrence LumengAbstract:Background: The alcohol Deprivation effect (ADE) is a temporary increase in the ratio of ethanol/total fluid intake and the voluntary intake of ethanol solutions over baseline drinking conditions when ethanol access is reinstated after a period of alcohol Deprivation. The ADE has been posited to be an animal model for alcohol craving. The current study examined the effects of initial Deprivation length and number of Deprivation exposures on the ADE in alcohol-preferring (P) rats. Methods: Adult female P rats received 24-hr free-choice access to 10% (v/v) ethanol and water for 6 weeks. Rats were then randomly assigned to five groups deprived of ethanol for O (control), 2, 4, 6, or 8 weeks (W). All deprived groups were then given 24-hr access to ethanol for 2 weeks before bbeing deprived of ethanol for another 2 weeks. Results: After the initial ethanol Deprivation period, the deprived groups displayed a similar 2-fold ADE (e.g., 4-W group; 4.6 ± 0.5 for baseline vs. 10.5 ± 0.3 g/kg/day for the 1st reinstatement day) during the initial 24-hr period. Ethanol consumption began to return to control levels 48 (7.1 ± 0.4 g/kg/day) and 72 (6.4 ± 0.4 g/kg/day) hrs later. In addition, each deprived group showed increases in the ratio of ethanol/total fluid intake upon reinstatement, and there was a tendency for sustained higher ethanol intake ratlos during the first 3 postexposure days for the 4-, 6-, and 8-W grups, but only during the first 2 reinstatement days for the 2-W group. The second Deprivation did not increase the magnitude of the ADE over that observed in the first Deprivation during the initial 24-hr period of re-exposure, but it did prolong the duration of the ADE into the 2nd and 3rd reinstatement day for the 2-, 4-, and 6-W groups and into the 5th reinstatement day for the 8-W group. Conclusions: Equivalent robust ADEs can be seen in P rats with Deprivation periods of 2–8 W, which suggests that the ADE has a rapid onset and is not affected by the durations of Deprivation that were tested. The duration of the ADE was prolonged in P rats exposed to a second Deprivation period, suggesting that factors associated with the ADE phenomenon could be strengthened by repated Deprivations.
H. Kuhs - One of the best experts on this subject based on the ideXlab platform.
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Sleep Deprivation therapy.
Biological psychiatry, 1991Co-Authors: H. Kuhs, R. TölleAbstract:Abstract This review reports, with as much detail as possible, on the literature relating to therapeutic sleep Deprivation (or induced-wakefulness therapy) since it was first described in 1971. The antidepressive effect of sleep Deprivation has been substantiated by numerous studies. A series of clinical predictors of response to sleep Deprivation are also described. Partial sleep Deprivation late in the night is equivalent to total sleep Deprivation in terms of therapeutic value and —because of its simpler application—can be regarded today as the sleep Deprivation method of choice. The status of sleep Deprivation in the overall treatment schedule for depressive disorders is discussed in detail. Numerous findings, some of them contradictory, have been published on the effect of sleep Deprivation on biological variables. To date, no unequivocal explanation has been found for the mechanism of action of sleep Deprivation.
