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Biomedical subjects

M Terman

Publications and source records attributed to M Terman.

At least 19 recordsLinked to original sources
PubMed1991

The visual input stage of the mammalian circadian pacemaking system: I. Is there a clock in the mammalian eye?

Threads of evidence from recent experimentation in retinal morphology, neurochemistry, electrophysiology, and visual perception point toward rhythmic ocular processes that may be integral components of circadian entrainment in mammals. Components of retinal cell biology (rod outer-segment disk shedding, inner-segment degradation, melatonin and dopamine synthesis, electrophysiological responses) show self-sustaining circadian oscillations whose phase can be controlled by light-dark cycles. A complete phase response curve in visual sensitivity can be generated from light-pulse-induced phase shifting. Following lesions of the suprachiasmatic nuclei, circadian rhythms of visual detectability and rod outer-segment disk shedding persist, even though behavioral activity becomes arrhythmic. We discuss the converging evidence for an ocular circadian timing system in terms of interactions between rhythmic retinal processes and the central suprachiasmatic pacemaker, and propose that retinal phase shifts to light provide a critical input signal.

Animals↗
PubMed1991

The visual input stage of the mammalian circadian pacemaking system: II. The effect of light and drugs on retinal function.

Acute light pulses as well as long-term light exposure may not only modulate photoreceptive properties, but also induce reversible or irreversible damage to the retina, depending on exposure conditions. Illuminance levels in laboratory animal colonies and manipulations of lighting regimens in circadian rhythm research can threaten retinal structure and physiology, and may therefore modify zeitgeber input to the central circadian system. Given the opportunity to escape light at any time, the nocturnal rat self-selects a seasonally varying "naturalistic skeleton photoperiod" that protects the eyes from potential damage by nonphysiological light exposures. Both rod rod-segment disk shedding and behavioral circadian phase shifts are elicited by low levels of twilight stimulation. From this vantage point, we hypothesize that certain basic properties of circadian rhythms (e.g., Aschoff's rule and splitting) may reflect modulation of retinal physiology by light. Pharmacological manipulations with or without the addition of lighting strategies have been used to analyze the neurochemistry of circadian timekeeping. Drug modulation of light input at the level of the retina may add to or interact with direct drug modulation of the central circadian pacemaking system.

Animals↗
PubMed1990

Is seasonal affective disorder a variant of atypical depression? Differential response to light therapy.

Similar symptomatology has been described for both seasonal affective disorder (SAD) and atypical depression. For example, hyperphagia, hypersomnia, and intense lethargy are common to both, suggesting that they might be subtypes of the same disorder. If SAD and atypical depression are different manifestations of the same underlying pathophysiology, treatment effective for one might also benefit the other. Bright artificial lights (2500 lux, 6-8 a.m. and p.m.) were significantly less effective in treating eight patients diagnosed as having atypical depression without a seasonal pattern than 25 SAD patients. Differential treatment outcome suggests that SAD and atypical depression are separate disorders.

Adult↗
PubMed1990

Prevalence of seasonal affective disorder at four latitudes.

The Seasonal Pattern Assessment Questionnaire (SPAQ) was mailed to a sample population balanced for sex and randomly selected from local telephone directories in four areas: Nashua, NH, New York, NY, Montgomery County, MD, and Sarasota, FL. On the basis of responses to this questionnaire, prevalence rates of winter seasonal affective disorder (winter SAD), summer seasonal affective disorder (summer SAD), and subsyndromal winter SAD were estimated for the four areas. Rates of winter SAD and subsyndromal SAD were found to be significantly higher at the more northern latitudes, while no correlation was found between latitude and summer SAD. The positive correlation between latitude and prevalence of winter SAD applied predominantly to the age groups over 35.

Adult↗
PubMed1990

Efficacy of brief, intense light exposure for treatment of winter depression.

A high-intensity fluorescent lighting system, tilted downward toward the head, and emitting negligible levels of ultraviolet radiation, was tested under two random crossover protocols in winter-depressed patients: 30-minute sessions at (a) 3,000 lux vs. 10,000 lux in early morning, and (b) morning vs. evening sessions at 10,000 lux. Judgment of clinical remission was based jointly on relative and absolute score improvements on a Structured Interview Guide for the Hamilton Depression Scale--Seasonal Affective Disorder Version (SIGH-SAD) and a set of supplementary atypical-vegetative items. Data are presented for 24 subjects who showed relapse upon withdrawal. An overall remission rate of 75 percent was found for morning light at 10,000 lux. The rates for evening light (25%) and 3,000 lux morning light (19%) were significantly lower. The remission rate for morning light treatment of 10,000 lux for 30 minutes approximately equalled 2,500 lux treatment for 2 hours (data from our earlier studies), suggesting a reciprocity between dosing dimensions of intensity and duration. No pathological changes were revealed by ophthalmological examinations given after 2 to 6 weeks of daily treatment.

Affect↗
PubMed1989

Light therapy for seasonal affective disorder. A review of efficacy.

Bright artificial light has been found effective in reducing winter depressive symptoms of Seasonal Affective Disorder, although conclusions about the true magnitude of treatment effect and importance of time of day of light exposure have been limited by methodologic problems. Individual subjects' data from 14 research centers studying 332 patients over 5 years were analyzed with a pooled clustering technique. Overall, 2500-lux intensity light exposure for at least 2 hours daily for 1 week resulted in significantly more remissions--Hamilton Depression Rating Scale (HAM-D) score reduction of 50% or more to a level under 8--when administered in the early morning (53%) than in the evening (38%) or at midday (32%). All three times were significantly more effective than dim light controls (11%). Dual daily exposures (morning-plus-evening light) provided no benefit over morning light alone. In morning-evening crossovers, remission rates were 62% under morning light alone, compared with 28% under evening light alone, with a differential morning-evening response present in 59% of morning responders compared with 10% of evening responders (p less than 0.001). Remission rates with morning light were highest given low severity at baseline (HAM-D score of 10-16: 67% remission), as compared with moderate-to-severe cases (HAM-D score above 16: approximately 40% remission) where no morning-evening differences were found. Firmer conclusions await treatment studies with larger sample sizes and full assessment of atypical vegetative symptoms seen in winter depression but underrepresented in the Hamilton scale. Longer treatment course and greater light intensity may help clarify clinical response despite the impossibility of achieving a conventional blind placebo control.

Circadian Rhythm↗
PubMed1988

Response of the melatonin cycle to phototherapy for Seasonal Affective Disorder. Short note.

It is well-established that human nocturnal melatonin secretion is suppressed by presentation of artificial light greater than 2,000 lux, a level that is also therapeutically effective in alleviating winter depression symptoms of Seasonal Affective Disorder [SAD]. Furthermore, early-morning bright light induces phase advances of the melatonin cycle in SAD patients (Lewy et al., 1987a). The functional significance of melatonin in SAD remains unclear. With plasma melatonin sampled at 20-min intervals in a series of overnight studies, we found marked phase delays of the cycle, relative to that previously reported for normals, in 4/5 depressed SAD patients. 2,500 lux light exposure at 6-8 a.m. resulted in exponentially declining melatonin levels that approached low daytime baselines within two hours (t1/2 = 45.52 min). All five patients showed clinical remissions as well as phase advances of the melatonin cycle of 0.75 to 3.27 hours (mean, 1.94 +/- 0.84 hours) after one week of daily exposure from 6-8 a.m. and p.m. These results suggest that the combination of early morning and early evening light exposures induces circadian phase adjustments similar to those of morning light alone, by impacting a photosensitive interval when, in SAD, melatonin secretion overshoots its normal nocturnal phase.

Adult↗
PubMed1985

A circadian pacemaker for visual sensitivity?

Visual signal detectability oscillates as a circadian rhythm, capable of free-running in constant conditions, and entrainment by external lighting schedules. These functions persist after lesioning of the suprachiasmatic nucleus (SCN), implicating a separate pacemaker for visual sensitivity. Its locus, physiology, and mode of interaction with the SCN have yet to be established.

Animals↗
PubMed1984

Daily meal anticipation: interaction of circadian and interval timing.

Both short-interval and circadian timing systems support anticipatory response accelerations prior to food reinforcement. In the first case, the behavior pattern is determined by a scalar timing process with an arbitrary-reset property. In contrast, under daily cycles of food-availability, behavior reflects a self-sustaining oscillation. With rats as subjects, the concurrent operation of timing of both kinds was studied by addition of premeal auditory cues on the circadian baseline, in the absence of a day-night illumination cycle. Cues within both minute and hour ranges served to lower the level of premeal anticipatory responding, although exponential accelerations were similar to the uncued case. Cues within the minutes range yielded interval-timing functions that reflected approximate superposition. Cues within the hours range suppressed respondings at their outset, in proportion to cue duration. When one of the shorter cues was suddenly lengthened, short-interval accelerations appeared at inappropriate circadian phases. When a premeal cue was extended through mealtime, anticipation rates increased markedly, suggesting that cue termination at the start of mealtime is a potent anchor for premeal anticipation regardless of cue duration. By use of meal-omission probes without external cues, peak rates were located after the onset of expected mealtime, often near its termination. The results suggest interactions between the scalar interval timer and the circadian anticipation timer, as modulated by the circadian free-run timer.

Animals↗
PubMed1980

Food availability and daily biological rhythms.

Restricted daily feeding schedules result in the partial or complete synchronization of a wide range of rhythmic biological functions in rodents. In some cases, exemplified by drinking behavior and liver tyrosine transaminase activity, this represents primarily a direct, exogenous influence of food intake. In others, synchronization is achieved by entrainment of a circadian time-keeping mechanism distinct from that which underlies free-running rhythms in these functions. This food-entrained mechanism is responsible for the timing of anticipatory increases in locomotor and lever-pressing activity immediatley prior to food delivery, and may also underlie similar anticipatory increases in body temperature, corticosterone secretion, and in the activities of some intestinal enzymes. It is suggested that such a mechanism may enable an animal to recognize and take advantage of the periodic recurrence of significant events in its biotic environment.

Animals↗