Retinohypothalamic Tract


Author(s):  
Miriam E. Reyes‐Méndez ◽  
J. Manuel Herrera‐Zamora ◽  
Fernando Osuna‐López ◽  
Ricardo A. Navarro‐Polanco ◽  
Néstor Mendoza‐Munoz ◽  
...  


2021 ◽  
Vol 11 (5) ◽  
pp. 559
Author(s):  
Mikhail Kanarskii ◽  
Julia Nekrasova ◽  
Svetlana Vitkovskaya ◽  
Pranil Pradhan ◽  
Sergey Peshkov ◽  
...  

Objective: The aim of this study is to compare the secretion level of nocturnal melatonin and the characteristics of the peripheral part of the visual analyzer in patients with chronic disorders of consciousness (DOC). Materials and Methods: We studied the level of melatonin in 22 patients with chronic DOC and in 11 healthy volunteers. The fundus condition was assessed using the ophthalmoscopic method. Results: The average level of nocturnal melatonin in patients with DOC differed by 80% from the level of indole in healthy volunteers. This reveals a direct relationship between etiology, the level of consciousness, gaze fixation, coma recovery scale-revised score and the level of melatonin secretion. Examination by an ophthalmologist revealed a decrease in the macular reflex in a significant number of DOC patients, which in turn correlates negatively with the time from brain injury and positively with low values of nocturnal melatonin.



2020 ◽  
Author(s):  
Manuel Spitschan ◽  
Corrado Garbazza ◽  
Susanne Kohl ◽  
Christian Cajochen

AbstractLight is strong zeitgeber to the human circadian system, entraining internal rhythms in physiology and behaviour to the external world. This is mediated by the melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), which sense light in addition to the classical photoreceptors, the cones and rods. Circadian responses depend on light intensity, with exposure to brighter light leading to bigger circadian phase shifts and melatonin suppression. In congenital achromatopsia (prevalence 1 in 30,000 to 50,000 people), the cone system is non-functional, resulting in light avoidance and photophobia at light levels which are tolerable and habitual to individuals with a normal, trichromatic retina. Here, we examined chronotype and self-reported sleep, actigraphy-derived rest-activity cycles and increases melatonin in the evening in a group of genetically confirmed congenital achromats. We found normal rest-activity patterns in all participants, and normal melatonin phase angles of entrainment in 2/3 of our participants. Our results suggest that a functional cone system and exposure to daytime light intensities are not necessary for regular behavioural and hormonal entrainment. This may point to a compensation mechanism in circadian photoreception, which in conjunction with non-photic zeitgebers, ensures synchronisation of activity to the external world.Significance statementRhythms in physiology and behaviour are synchronised to the external cycle of light exposure. This is mediated by the retinohypothalamic tract, which connects the photoreceptors in the eye with the “circadian pacemaker” in our brain, the suprachiasmatic nucleus. What happens to our circadian rhythm when we lack the cone photoreceptors in the eye that enable us to see in daylight? We examined this question in a group of rare congenital achromats. Our work reveals that normal rhythms in rest and activity, and production of hormones, does not require a functional cone system.



1990 ◽  
Vol 259 (3) ◽  
pp. E384
Author(s):  
S A Rivkees ◽  
S M Reppert

In a marsupial species, the gray short-tailed opossum (Monodelphis domestica), the suprachiasmatic nuclei (SCN), the site of a circadian clock, are formed postnatally and begin oscillating as a circadian clock on day 20. In this study, we examined how the timing (phase) of the SCN clock in the developing opossum is coordinated to the environmental light-dark cycle. When pups were reared from birth in darkness by intact dams, the circadian phases in SCN metabolic activity (monitored by 2-deoxy-D-[14C]glucose autoradiography) in 27-day-old pups were desynchronized. When pups were reared in a light-dark cycle that was 12 h out of phase with the circadian time of blinded dams, the pattern of SCN metabolic activity on day 20 was rhythmic and in phase with the light-dark cycle but out of phase with the circadian time of the dam. On day 20, retina-mediated light activation of SCN metabolic activity was also demonstrated, and anterograde tract-tracing studies revealed the presence of the retinohypothalamic tract within the SCN. These results show there is no influence of the opossum dam on the timing of the pup's biological clock. Instead, from the inception of the daily rhythm in SCN metabolic activity, its timing is regulated by retina-mediated light-dark entrainment.





2006 ◽  
Vol 95 (6) ◽  
pp. 3727-3741 ◽  
Author(s):  
Mykhaylo G. Moldavan ◽  
Robert P. Irwin ◽  
Charles N. Allen

Presynaptic GABAB receptor activation inhibits glutamate release from retinohypothalamic tract (RHT) terminals in the suprachiasmatic nucleus (SCN). Voltage-clamp whole cell recordings from rat SCN neurons and optical recordings of Ca2+-sensitive fluorescent probes within RHT terminals were used to examine GABAB-receptor modulation of RHT transmission. Baclofen inhibited evoked excitatory postsynaptic currents (EPSCs) in a concentration-dependent manner equally during the day and night. Blockers of N-, P/Q-, T-, and R-type voltage-dependent Ca2+ channels, but not L-type, reduced the EPSC amplitude by 66, 36, 32, and 18% of control, respectively. Joint application of multiple Ca2+ channel blockers inhibited the EPSCs less than that predicted, consistent with a model in which multiple Ca2+ channels overlap in the regulation of transmitter release. Presynaptic inhibition of EPSCs by baclofen was occluded by ω-conotoxin GVIA (≤72%), mibefradil (≤52%), and ω-agatoxin TK (≤15%), but not by SNX-482 or nimodipine. Baclofen reduced both evoked presynaptic Ca2+ influx and resting Ca2+ concentration in RHT terminals. Tertiapin did not alter the evoked EPSC and baclofen-induced inhibition, indicating that baclofen does not inhibit glutamate release by activation of Kir3 channels. Neither Ba2+ nor high extracellular K+ modified the baclofen-induced inhibition. 4-Aminopyridine (4-AP) significantly increased the EPSC amplitude and the charge transfer, and dramatically reduced the baclofen effect. These data indicate that baclofen inhibits glutamate release from RHT terminals by blocking N-, T-, and P/Q-type Ca2+ channels, and possibly by activation of 4-AP–sensitive K+ channels, but not by inhibition of R- and L-type Ca2+ channels or by Kir3 channel activation.



1990 ◽  
Vol 87 (20) ◽  
pp. 8065-8069 ◽  
Author(s):  
J. R. Moffett ◽  
L. Williamson ◽  
M. Palkovits ◽  
M. A. Namboodiri


Author(s):  
Jens Hannibal ◽  
Morten Moller ◽  
Ole Petter Ottersen ◽  
Jan Fahrenkrug


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