Limits...
Photoperiodic and circadian bifurcation theories of depression and mania.

Kripke DF, Elliott JA, Welsh DK, Youngstedt SD - F1000Res (2015)

Bottom Line: Seasonal effects on mood have been observed throughout much of human history.  Seasonal changes in animals and plants are largely mediated through the changing photoperiod (i.e., the photophase or duration of daylight).  We review that in mammals, daylight specifically regulates SCN (suprachiasmatic nucleus) circadian organization and its control of melatonin secretion.  The timing of melatonin secretion interacts with gene transcription in the pituitary pars tuberalis to modulate production of TSH (thyrotropin), hypothalamic T3 (triiodothyronine), and tuberalin peptides which modulate pituitary production of regulatory gonadotropins and other hormones.  Pituitary hormones largely mediate seasonal physiologic and behavioral variations.  As a result of long winter nights or inadequate illumination, we propose that delayed morning offset of nocturnal melatonin secretion, suppressing pars tuberalis function, could be the main cause for winter depression and even cause depressions at other times of year.  Irregularities of circadian sleep timing and thyroid homeostasis contribute to depression.  Bright light and sleep restriction are antidepressant and conversely, sometimes trigger mania.  We propose that internal desynchronization or bifurcation of SCN circadian rhythms may underlie rapid-cycling manic-depressive disorders and perhaps most mania.  Much further research will be needed to add substance to these theories.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Center for Circadian Biology, University of California, San Diego, CA, 92093-0603, USA.

ABSTRACT
Seasonal effects on mood have been observed throughout much of human history.  Seasonal changes in animals and plants are largely mediated through the changing photoperiod (i.e., the photophase or duration of daylight).  We review that in mammals, daylight specifically regulates SCN (suprachiasmatic nucleus) circadian organization and its control of melatonin secretion.  The timing of melatonin secretion interacts with gene transcription in the pituitary pars tuberalis to modulate production of TSH (thyrotropin), hypothalamic T3 (triiodothyronine), and tuberalin peptides which modulate pituitary production of regulatory gonadotropins and other hormones.  Pituitary hormones largely mediate seasonal physiologic and behavioral variations.  As a result of long winter nights or inadequate illumination, we propose that delayed morning offset of nocturnal melatonin secretion, suppressing pars tuberalis function, could be the main cause for winter depression and even cause depressions at other times of year.  Irregularities of circadian sleep timing and thyroid homeostasis contribute to depression.  Bright light and sleep restriction are antidepressant and conversely, sometimes trigger mania.  We propose that internal desynchronization or bifurcation of SCN circadian rhythms may underlie rapid-cycling manic-depressive disorders and perhaps most mania.  Much further research will be needed to add substance to these theories.

No MeSH data available.


Related in: MedlinePlus

Theoretical schematic of circadian bifurcation in humans.In this diagram, each line of the ordinate represents a 24-hour day and the abscissa represents the 24 hours within that day. The grey shading depicts very dim light or darkness, whereas the white background represents daylight and artificial light. The light-dark cycle is modelled as commencing with LD16:8 and transitioning in the middle days to LDLD8:4:8:4, with return to LD16:8 in the final days. The orange shading represents SCN multiunit neuronal firing that gradually splits apart and bifurcates into two antiphase patterns of firing during LDLD8:4:8:4, representing two distinct populations of coupled SCN neurons. During LD16:8, firing might be spread out over a longer interval in the light than is shown, but there may be insufficient data to model the pattern of neuronal timing more exactly. After return to LD16:8 or to continuous darkness (DD), the two components of neuronal firing gradually fuse together again. The blue regions represent melatonin secretion during the dark intervals. Suppressed by neuronal firing and light suppression, it is plausible that melatonin secretion would be partly or completely inhibited during the transitions from LD16:8 to LDLD8:4:8:4 and back again, during which melatonin secretion would bifurcate and then fuse again. These patterns are theoretical, because the transitions of neuronal firing and melatonin secretion from an LD pattern to a bifurcating LDLD pattern and back again have never been observed simultaneously in detail, certainly not in a diurnal mammal.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4490783&req=5

f2: Theoretical schematic of circadian bifurcation in humans.In this diagram, each line of the ordinate represents a 24-hour day and the abscissa represents the 24 hours within that day. The grey shading depicts very dim light or darkness, whereas the white background represents daylight and artificial light. The light-dark cycle is modelled as commencing with LD16:8 and transitioning in the middle days to LDLD8:4:8:4, with return to LD16:8 in the final days. The orange shading represents SCN multiunit neuronal firing that gradually splits apart and bifurcates into two antiphase patterns of firing during LDLD8:4:8:4, representing two distinct populations of coupled SCN neurons. During LD16:8, firing might be spread out over a longer interval in the light than is shown, but there may be insufficient data to model the pattern of neuronal timing more exactly. After return to LD16:8 or to continuous darkness (DD), the two components of neuronal firing gradually fuse together again. The blue regions represent melatonin secretion during the dark intervals. Suppressed by neuronal firing and light suppression, it is plausible that melatonin secretion would be partly or completely inhibited during the transitions from LD16:8 to LDLD8:4:8:4 and back again, during which melatonin secretion would bifurcate and then fuse again. These patterns are theoretical, because the transitions of neuronal firing and melatonin secretion from an LD pattern to a bifurcating LDLD pattern and back again have never been observed simultaneously in detail, certainly not in a diurnal mammal.

Mentions: Perhaps we may gain further insight into mechanisms that could trigger mania by considering circadian rhythm bifurcation, which is the division of the circadian rhythm into two components, with the two peaks being separately entrainable. Circadian research has developed certain laboratory models that “bifurcate” nocturnal rodent activity into two circadian components (bouts of activity) about 12 hours apart from each other. These two activity bouts can be entrained in a stable manner by a special light-dark cycle consisting of two photophases (light intervals) and two scotophases (dark phases) within each 24 hours (for example, light-dark-light-dark hours abbreviated as LDLD7:5:7:5)144. A large set of studies utilizing Syrian hamsters, Siberian hamsters, and mice have demonstrated stable entrainment of bifurcated scotophase activity bouts, body temperature peaks, and melatonin peaks145. Taken together, these studies lead to the hypothesis that LDLD entrainment bifurcates the neural oscillators in the SCN into two or more components, each driving activity, body temperature, and melatonin secretion. Bifurcated-rhythm hamsters develop and maintain summer gonadal size and presumed reproductive fertility146, perhaps because the duration of each bout of melatonin secretion is brief (as in the short nights of summer). The bifurcated activity components and bifurcated melatonin secretion in the scotophases represent the control of two independently-entrainable circadian pacemakers which are yet mutually coupled, and which will fuse into a single component if the bifurcated photophase is withdrawn71,147. In this model, the circadian bifurcation seems to result from two different populations of neurons in the SCN that assume almost opposite phases, though the two bifurcated SCN populations appear to be bilaterally symmetrical148,149. It should be emphasized that the two scotophases and two photophases per 24 hr day do not need to be absolutely symmetrical, especially once the bifurcation has occurred. When the bifurcated photoperiod is replaced by constant dark and the bifurcated activity bouts rejoin each other, the melatonin secretion components presumably also fuse. The two activity bouts can be recoupled either by the day-scotophase activity component delaying or by the day component advancing in reference to the night-scotophase activity component (Figure 2)71.


Photoperiodic and circadian bifurcation theories of depression and mania.

Kripke DF, Elliott JA, Welsh DK, Youngstedt SD - F1000Res (2015)

Theoretical schematic of circadian bifurcation in humans.In this diagram, each line of the ordinate represents a 24-hour day and the abscissa represents the 24 hours within that day. The grey shading depicts very dim light or darkness, whereas the white background represents daylight and artificial light. The light-dark cycle is modelled as commencing with LD16:8 and transitioning in the middle days to LDLD8:4:8:4, with return to LD16:8 in the final days. The orange shading represents SCN multiunit neuronal firing that gradually splits apart and bifurcates into two antiphase patterns of firing during LDLD8:4:8:4, representing two distinct populations of coupled SCN neurons. During LD16:8, firing might be spread out over a longer interval in the light than is shown, but there may be insufficient data to model the pattern of neuronal timing more exactly. After return to LD16:8 or to continuous darkness (DD), the two components of neuronal firing gradually fuse together again. The blue regions represent melatonin secretion during the dark intervals. Suppressed by neuronal firing and light suppression, it is plausible that melatonin secretion would be partly or completely inhibited during the transitions from LD16:8 to LDLD8:4:8:4 and back again, during which melatonin secretion would bifurcate and then fuse again. These patterns are theoretical, because the transitions of neuronal firing and melatonin secretion from an LD pattern to a bifurcating LDLD pattern and back again have never been observed simultaneously in detail, certainly not in a diurnal mammal.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4490783&req=5

f2: Theoretical schematic of circadian bifurcation in humans.In this diagram, each line of the ordinate represents a 24-hour day and the abscissa represents the 24 hours within that day. The grey shading depicts very dim light or darkness, whereas the white background represents daylight and artificial light. The light-dark cycle is modelled as commencing with LD16:8 and transitioning in the middle days to LDLD8:4:8:4, with return to LD16:8 in the final days. The orange shading represents SCN multiunit neuronal firing that gradually splits apart and bifurcates into two antiphase patterns of firing during LDLD8:4:8:4, representing two distinct populations of coupled SCN neurons. During LD16:8, firing might be spread out over a longer interval in the light than is shown, but there may be insufficient data to model the pattern of neuronal timing more exactly. After return to LD16:8 or to continuous darkness (DD), the two components of neuronal firing gradually fuse together again. The blue regions represent melatonin secretion during the dark intervals. Suppressed by neuronal firing and light suppression, it is plausible that melatonin secretion would be partly or completely inhibited during the transitions from LD16:8 to LDLD8:4:8:4 and back again, during which melatonin secretion would bifurcate and then fuse again. These patterns are theoretical, because the transitions of neuronal firing and melatonin secretion from an LD pattern to a bifurcating LDLD pattern and back again have never been observed simultaneously in detail, certainly not in a diurnal mammal.
Mentions: Perhaps we may gain further insight into mechanisms that could trigger mania by considering circadian rhythm bifurcation, which is the division of the circadian rhythm into two components, with the two peaks being separately entrainable. Circadian research has developed certain laboratory models that “bifurcate” nocturnal rodent activity into two circadian components (bouts of activity) about 12 hours apart from each other. These two activity bouts can be entrained in a stable manner by a special light-dark cycle consisting of two photophases (light intervals) and two scotophases (dark phases) within each 24 hours (for example, light-dark-light-dark hours abbreviated as LDLD7:5:7:5)144. A large set of studies utilizing Syrian hamsters, Siberian hamsters, and mice have demonstrated stable entrainment of bifurcated scotophase activity bouts, body temperature peaks, and melatonin peaks145. Taken together, these studies lead to the hypothesis that LDLD entrainment bifurcates the neural oscillators in the SCN into two or more components, each driving activity, body temperature, and melatonin secretion. Bifurcated-rhythm hamsters develop and maintain summer gonadal size and presumed reproductive fertility146, perhaps because the duration of each bout of melatonin secretion is brief (as in the short nights of summer). The bifurcated activity components and bifurcated melatonin secretion in the scotophases represent the control of two independently-entrainable circadian pacemakers which are yet mutually coupled, and which will fuse into a single component if the bifurcated photophase is withdrawn71,147. In this model, the circadian bifurcation seems to result from two different populations of neurons in the SCN that assume almost opposite phases, though the two bifurcated SCN populations appear to be bilaterally symmetrical148,149. It should be emphasized that the two scotophases and two photophases per 24 hr day do not need to be absolutely symmetrical, especially once the bifurcation has occurred. When the bifurcated photoperiod is replaced by constant dark and the bifurcated activity bouts rejoin each other, the melatonin secretion components presumably also fuse. The two activity bouts can be recoupled either by the day-scotophase activity component delaying or by the day component advancing in reference to the night-scotophase activity component (Figure 2)71.

Bottom Line: Seasonal effects on mood have been observed throughout much of human history.  Seasonal changes in animals and plants are largely mediated through the changing photoperiod (i.e., the photophase or duration of daylight).  We review that in mammals, daylight specifically regulates SCN (suprachiasmatic nucleus) circadian organization and its control of melatonin secretion.  The timing of melatonin secretion interacts with gene transcription in the pituitary pars tuberalis to modulate production of TSH (thyrotropin), hypothalamic T3 (triiodothyronine), and tuberalin peptides which modulate pituitary production of regulatory gonadotropins and other hormones.  Pituitary hormones largely mediate seasonal physiologic and behavioral variations.  As a result of long winter nights or inadequate illumination, we propose that delayed morning offset of nocturnal melatonin secretion, suppressing pars tuberalis function, could be the main cause for winter depression and even cause depressions at other times of year.  Irregularities of circadian sleep timing and thyroid homeostasis contribute to depression.  Bright light and sleep restriction are antidepressant and conversely, sometimes trigger mania.  We propose that internal desynchronization or bifurcation of SCN circadian rhythms may underlie rapid-cycling manic-depressive disorders and perhaps most mania.  Much further research will be needed to add substance to these theories.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Center for Circadian Biology, University of California, San Diego, CA, 92093-0603, USA.

ABSTRACT
Seasonal effects on mood have been observed throughout much of human history.  Seasonal changes in animals and plants are largely mediated through the changing photoperiod (i.e., the photophase or duration of daylight).  We review that in mammals, daylight specifically regulates SCN (suprachiasmatic nucleus) circadian organization and its control of melatonin secretion.  The timing of melatonin secretion interacts with gene transcription in the pituitary pars tuberalis to modulate production of TSH (thyrotropin), hypothalamic T3 (triiodothyronine), and tuberalin peptides which modulate pituitary production of regulatory gonadotropins and other hormones.  Pituitary hormones largely mediate seasonal physiologic and behavioral variations.  As a result of long winter nights or inadequate illumination, we propose that delayed morning offset of nocturnal melatonin secretion, suppressing pars tuberalis function, could be the main cause for winter depression and even cause depressions at other times of year.  Irregularities of circadian sleep timing and thyroid homeostasis contribute to depression.  Bright light and sleep restriction are antidepressant and conversely, sometimes trigger mania.  We propose that internal desynchronization or bifurcation of SCN circadian rhythms may underlie rapid-cycling manic-depressive disorders and perhaps most mania.  Much further research will be needed to add substance to these theories.

No MeSH data available.


Related in: MedlinePlus