Circadian Rhythms and Depression: Clinical and Experimental Models

Rosenwasser, Alan M.; Wirz‐Justice, Anna

doi:10.1007/978-3-662-09355-9_17

Cited by 42 publications

(25 citation statements)

References 101 publications

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“…For example, alterations in free-running circadian period have been described during chronic administration of several different classes of antidepressants (Wollnik, 1992;Klemfuss and Kripke, 1994;Rosenwasser and Wirz-Justice, 1997;Duncan et al, 1998), the anxiolytic benzodiazepine, diazepam (Subramanian and Subbaraj, 1996), the putative depressogenic agent, clonidine (Rosenwasser, 1996), and ethanol (Dwyer and Rosenwasser, 1998;Rosenwasser et al, 2005). Surprisingly, both lengthening and shortening of free-running period have been observed, even for a given agent, and these effects appear to be modulated by a variety of factors, including both lighting conditions and individual differences in baseline period (Rosenwasser, 1996;Rosenwasser et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, emerging evidence from animal experiments suggests that both adult (Mistlberger and Nadeau, 1992;Dwyer and Rosenwasser, 1998;Rosenwasser et al, 2005) and perinatal (Earnest et al, 2001) ethanol treatment can modify the free-running circadian period, a fundamental parameter of the circadian pacemaker. Indeed, chronic ethanol treatment can evoke both lengthening and shortening of free-running circadian period (Rosenwasser et al, 2005), similar to the period-altering effects of chronic treatment with other mood-altering drugs (Rosenwasser, 1996;Subramanian and Subbaraj, 1996;Rosenwasser and Wirz-Justice, 1997).…”

Section: Introductionmentioning

confidence: 91%

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Chronic Ethanol Intake Alters Circadian Period‐Responses to Brief Light Pulses in Rats

Rosenwasser

Logan

Fecteau

2005

Chronobiology International

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Although chronic alcohol intake is associated with widespread disruptions of sleep-wake cycles and other daily biological rhythms in both human alcoholics and experimental animals, the extent to which the chronobiological effects of alcohol are mediated by effects on the underlying circadian pacemaker remains unknown. Nevertheless, recent studies indicate that both adult and perinatal ethanol treatments may alter the free-running period and photic responsiveness of the circadian pacemaker. The present experiment was designed to further characterize the effects of chronic ethanol intake on the response of the rat circadian pacemaker to brief light pulses. Ethanol-treated and control animals were exposed to 15-min light pulses during either early or late subjective night on the first day of constant darkness following entrainment to a 12:12 light-dark cycle. Relative to pulses delivered during early subjective night and to "no-pulse" conditions, light pulses delivered during late subjective night resulted in period-shortening after-effects under constant darkness, but only in control animals, not in ethanol-treated animals. These results indicate that chronic ethanol intake reduces the responsiveness of the circadian pacemaker to acute photic stimulation, and suggest that the chronobiological disruptions seen in human alcoholics are due in part to alterations in circadian pacemaker function.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

Chronic Ethanol Intake Alters Circadian Period‐Responses to Brief Light Pulses in Rats

Rosenwasser

Logan

Fecteau

2005

Chronobiology International

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“…Indeed, major depression in humans, as well as modeled depression in animals, often show altered amplitudes of different circadian rhythms [4,5].…”

Section: Discussionmentioning

confidence: 99%

“…Alterations in circadian rhythmicity are a common feature of human depression [3][4][5]. Among the little information available on the circadian organization in rodents neonatally treated with monoamine reuptake inhibitors, Rosenwasser and Hayes [24] described period lengthening, increased circadian amplitude and altered effects of both photic and pharmacological treatments on free-running period after neonatal desipramine treatment in rats.…”

Section: Effects Of Neonatal Clomipramine Treatment In Syrian Hamstersmentioning

confidence: 99%

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Effects of Neonatal Clomipramine Treatment on Locomotor Activity, Anxiety-Related Behavior and Serotonin Turnover in Syrian Hamsters

Yannielli¹,

Kargieman²,

Gregoretti³

et al. 1999

Neuropsychobiology

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Day-night differences in locomotor and anxiety-related behavior and brain serotonin metabolism were examined in adult Syrian hamsters that received clomipramine (15 mg/kg) or vehicle from day 8 to day 21 of life. Locomotor activity was significantly greater at the beginning of scotophase (20.00 h) than at noon (12.00 h) and it was highest in hamsters treated with clomipramine at both examined times. Significant day-night differences in anxiety-related behavior, as measured in a plus-maze paradigm, were found in saline-treated hamsters only, with higher values at night. Clomipramine-treated hamsters exhibited augmented 5-hydroxyindoleacetic acid/serotonin ratio in hypothalamus and midbrain raphe, while serotonin content decreased in frontal cortex and hypothalamic areas. The results indicate that neonatal clomipramine treatment produces a long-lasting change in locomotion and anxiety-related behavior, as well as reduces brain serotonin content in hamsters.

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Genetic polymorphism at theCLOCK gene locus and major depression

et al. 2000

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Genetic analysis in both mouse and Drosophila has indicated that the product of the CLOCK gene is an essential component of a circadian rhythm timing system. A single nucleotide polymorphism (SNP), T3111C, in the 3' flanking region of the human CLOCK gene has been identified. Homozygotes or heterozygotes for the 3111C allele have been reported to have higher mean scores on a measure of evening preference for activity (vs. morning preference) than subjects homozygous for the 3111T allele. Since major depression is hypothesized to be closely linked to circadian rhythms, we explored whether this polymorphism might be related to susceptibility to major depression. We also ascertained allele frequency in an African-American control population, to begin to evaluate population variation at this locus. CLOCK T3111C allele frequencies were determined in 280 European American (EA) subjects, 143 with a history of major depression and 137 screened controls, and in 58 African American (AA) screened control subjects, using a polymerase chain reaction (PCR) - restriction fragment length polymorphism (RFLP) method. There was no significant difference between EA depressed and control subjects in allele frequency. There was a significant difference in allele frequency between EA and AA subjects, demonstrating a potential for population stratification. In none of these groups were significant deviations from Hardy-Weinberg equilibrium found. The present data do not support an association between CLOCK gene alleles at the T3111C locus and major depression.

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Circadian Rhythms and Depression: Clinical and Experimental Models

Cited by 42 publications

References 101 publications

Chronic Ethanol Intake Alters Circadian Period‐Responses to Brief Light Pulses in Rats

Chronic Ethanol Intake Alters Circadian Period‐Responses to Brief Light Pulses in Rats

Effects of Neonatal Clomipramine Treatment on Locomotor Activity, Anxiety-Related Behavior and Serotonin Turnover in Syrian Hamsters

Genetic polymorphism at theCLOCK gene locus and major depression

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