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Biomedical subjects

D McGinty

Publications and source records attributed to D McGinty.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effects of basal forebrain stimulation on the waking discharge of neurons in the midbrain reticular formation of cats.

Neurons in the lateral basal forebrain which discharge selectively during slow-wave sleep have been identified as projecting to the midbrain reticular formation. Such cells have been hypothesized to participate in sleep-related changes in reticular formation excitability. The effects of stimulation at these sites on reticular formation single unit discharge in behaving cats was quantified in the present study. Effects were compared to those evoked from medial basal forebrain sites, including the preoptic area/anterior hypothalamus. Stimulation at all of these basal forebrain sites typically produced biphasic responses, consisting of a brief, short-latency excitation, followed by discharge suppression. Stimulation at lateral sites resulted in significantly longer periods of discharge suppression compared to stimulation at medial sites. These results support the hypothesis that laterally situated basal forebrain neurons participate in the regulation of behavioral state, in part, via descending modulation of midbrain reticular formation arousal mechanisms.

Animals↗
PubMed1989

Sleep research.

Explore the source record for details and available documents.

Animals↗
PubMed1989

Sleep-waking discharge of basal forebrain projection neurons in cats.

We have previously described a population of neurons in the magnocellular basal forebrain which have selectively elevated discharge rates during slow-wave sleep compared to waking; we postulate that these sleep-active neurons are a component of a basal forebrain sleep-promoting system. The purpose of the present experiment was to determine if sleep-active neurons contribute axons to recently described basal forebrain projection pathways. In cats prepared for chronic single unit and EEG-sleep recordings, stimulating electrodes were placed in the mesencephalic reticular formation, and the external capsule and anterior cingulate bundle, fiber bundles known to contain axons of basal forebrain projection neurons. Fifty-nine neurons were antidromically driven; differences in antidromic response latencies were related to sleep-waking discharge profiles. Of the cells with short antidromic latencies (less than 5 msec), the majority (9 of 12) had high discharge rates during waking and low rates during slow-wave sleep. Cells with long antidromic latencies had either very low discharge rates (less than 1 spike/sec) across all states, or had elevated discharge rates in slow-wave sleep. Sleep-active neurons were antidromically driven from external capsule (n = 9), anterior cingulate bundle (n = 9), or mesencephalic reticular formation (n = 5). Projection sleep-active neurons were recorded in the substantia innominata, ventral to the globus pallidus and medial to the central nucleus of the amygdala. Our study found that identified basal forebrain projection neurons in cats exhibit a variety of sleep-waking discharge patterns and conduction velocities. Sleep-active neurons were found to have slowly conducting axons, and to be a source of both ascending and descending projections.

Animals↗
PubMed1988

Nocturnal hypotension in older men with sleep-related breathing disorders.

Sleeping and awake blood pressures were related to sleep oxygenation and awake control of breathing in hypertensive and normotensive older men. During sleep, episodes of both hypertension and hypotension were observed, but hypotension was prominent. Five of 26 subjects exhibited episodes with a minimum mean arterial pressure of 60 mm Hg or less. These hypotensive episodes were associated with hemoglobin desaturation below 80 percent, secondary to sleep-related breathing disorders, and elevated supine nasopharyngeal airway resistance. Hypotensive subjects were habitual snorers. Waking hypertension was not associated with sleep-related breathing disorders in this older sample. In some older persons with sleep-related breathing disorders, sympathetic reflexes may be impaired, permitting hypotension and risk of circulatory failure. Epidemiologic evidence supports the hypothesis that this mechanism can explain the elevated incidence of cerebral infarction during sleep.

Aged↗
PubMed1987

Sleep disorders in the elderly: rationale for clinical awareness.

Complaints about sleep are extremely common in the elderly, leading to an impression that aging-related sleep problems are virtually normal and benign. However, studies have shown that such complaints as habitual snoring, frequent awakening, nocturnal sweating, and awakening with anxiety, may be signs of genuine sleep disorders. The most prevalent and most serious aging-related sleep disorder is sleep apnea. There is recent evidence of an association between sleep apnea and circulatory disorders, including hypertension, stroke, and angina pectoris, and with reduced life expectancy. The older sleep apnea victim may not complain of daytime sleepiness, the usual symptom in younger patients. Sleep apnea, and several other sleep disorders of the elderly are treatable, once an accurate diagnosis is made. Physicians are urged to make questions about sleep as routine as the taking of blood pressure.

Aged↗
PubMed1986

Sleep-related neuronal discharge in the basal forebrain of cats.

Although evidence suggests that the basal forebrain contains a hypnogenic mechanism, putative sleep-promoting neural elements within this area have not been identified. We examined basal forebrain neuronal activity during waking, non-rapid-eye-movement (NREM) sleep, REM sleep and various transition states. Based on state-related discharge rates. 3 cell types were defined. Thirty-nine of 83 cells were classified as waking-active, i.e. waking discharge rates were greater than 2 times NREM sleep rates. Twenty-three of 82 cells were classified as state-indifferent (waking and NREM rates differed by a factor of less than 2). NREM sleep discharge rates of the remaining 20 cells were greater than 2 times waking rates. These were labeled sleep-active cells. Discharge rates of these cells during epochs of alert waking were low, averaging less than 1 spike/s. Maximal discharge rates occurred during NREM sleep, averaging 9.44 spikes/s. Increased discharge of sleep-active cells anticipated sleep onset; cells had an average discharge rate of 6.60 spikes/s during transitions between waking and NREM sleep. Sleep-active cells were confined to the ventral basal forebrain, in the horizontal limb of the diagonal bands of Broca, substantia innominata, entopeduncular nucleus and ventral globus pallidus. These areas overlap, in part, with those where chemical, thermal and electrical stimulations evoke sleep, and where lesions suppress sleep. Based on location and discharge pattern we consider sleep-active cells candidates for mediating some of the sleep-promoting functions of the basal forebrain.

Animals↗
PubMed1986

Sleep suppression following kainic acid-induced lesions of the basal forebrain.

We have described elsewhere neurons in the ventral basal forebrain of cats that have elevated discharge rates during sleep and during transitions from waking to sleep, yet have comparatively low discharge rates during waking. These sleep-active neurons may mediate the hypnogenic properties of the basal forebrain. To further evaluate their role in the control of sleep, we examined the effects of basal forebrain lesions produced by microinjections of the relatively cell-selective neurotoxin, kainic acid, on sleep. Lesions were made bilaterally in two regions that contain high densities of sleep-active neurons: the horizontal limb of the diagonal bands of Broca and the lateral preoptic area-substantia innominata. Twelve-hour polygraph recordings were made before and at various intervals after basal forebrain damage in a total of eight cats. The lesions resulted in reduced time spent in deep, nonrapid eye-movement sleep and REM sleep, and increased time spent awake. These abnormalities persisted through 6 to 7 weeks postlesion. Reductions in deep non-REM sleep were due to decreases in bout number, particularly in the number of extended deep non-REM episodes (i.e., those greater than 5 min in duration). The number of REM sleep episodes was also significantly reduced. The average duration of epochs of waking was elevated throughout the postlesion period. Thus, in the postlesion period, cats exhibited an impaired ability to initiate and maintain consolidated periods of sleep, particularly of deeper sleep stages. Lesions were also associated with reduced EEG spindling during sleep. These results are consistent with our hypothesis that sleep-active neurons are a component of a basal forebrain sleep- and EEG-regulating mechanism.

Animals↗
PubMed1986

Circadian rhythm of plasma renin activity in older normal and essential hypertensive men: relation with inactive renin, aldosterone, cortisol and REM sleep.

The 24-h pattern of plasma renin activity (PRA), inactive renin (IR), plasma aldosterone (PA) and cortisol was studied in 13 normal men and 12 male patients with essential hypertension, all of whom were older than 55 years. Following gradual habituation over 4 days to the sleep laboratory and intravenous lines, blood samples were obtained every 2 h between 0900-2100 h and every 30 min between 2100-0900 h, during which sleep was also monitored. Plasma renin activity showed a circadian rhythm in both groups, but mean levels were lower in the hypertensive subjects (0.92 +/- 0.03 versus 1.41 +/- 0.06 ng/ml per h). The circadian rhythm of PRA in older men appeared to follow the same pattern described in younger individuals. Rapid eye movement (REM) sleep was associated with a small decrease in PRA, but this link was only evident in the normotensive group. Mean 24-h IR levels were also lower in the hypertensive group (7.26 +/- 0.18 versus 15.10 +/- 0.47 ng/ml per h) but were not affected by clock-time and generally showed no association with the 24-h PRA cycle. Mean 24-h PA was closely related to cortisol but not to PRA in both groups. Mean PA levels of the two groups were similar. Thus, the PA:PRA ratio was higher in the hypertensive group. The higher basal PA:PRA ratio in older hypertensives that emerged over the 24-h study period may reflect increased sensitivity of the adrenal gland to angiotensin II (ANG II) in hypertension of the elderly.

Aging↗
PubMed1984

Awake abnormalities of control of breathing and of the upper airway. Occurrence in healthy older men with nocturnal disordered breathing.

We hypothesized that preexisting diminished chemical control of breathing and narrowing of the upper airway are associated with sleep-related disordered breathing (SRDB) in healthy older men. Twenty-six subjects, aged 55 to 70, were studied. An SRDB episode was a decrease in arterial oxygen saturation (SaO2) of at least 4 percent. Some of these episodes occurred while airflow continued (ie, nonapneic episodes), and the rest occurred with apnea. Sixteen subjects had greater than 12 SRDB episodes per hour of sleep (SRDB subjects) and ten subjects had less than 8 episodes per hour (controls). During waking, the mean hypercapnic ventilatory response was lower, and the mean supine nasal airway resistance (SNAR) was higher in SRDB subjects than in control subjects. During waking, 12 of 16 SRDB subjects had one or more respiratory abnormalities: four had an elevated SNAR; four had a reduced hypercapnic response; three had a reduced hypoxic ventilatory response, and two had an abnormal flow-volume curve. Only one of ten control subjects had a respiratory abnormality (an elevated SNAR). Also, the number of SRDB episodes per hour correlated with the SNAR, and the minimum SaO2 during sleep correlated with the magnitude of the hypercapnic response. We conclude that SRDB occurs commonly in otherwise healthy older men with preexisting abnormalities of control of breathing or of the upper airway.

Age Factors↗
PubMed1983

Dissociation of rapid eye movement (REM) sleep features: possible implications for REM triggering mechanisms.

Neurophysiological and biochemical mechanisms regulating REM sleep episodes were studied in behaving cats with chronic electrodes. Push-pull perfusion of the midbrain or pontine reticular formation (RF) by a protein synthesis inhibitor, chloramphenicol (CAP), reduced neuronal unit discharge, particularly discharge bursts, within the perfused area, and reduced the incidence of sustained REM periods. During transitions to "aborted" as compared to sustained REM episodes. RF unit discharge was reduced, under all conditions. In 72-hour sleep deprived cats, systemic injections of both atropine (ATR) and CAP attenuated REM rebound, but with different patterns. CAP reduced REM episode frequency. ATR reduced REM duration. ATR also reduced PGO wave frequency. Combined CAP and ATR treatment produced additive REM depressant effects. These data suggest that cholinergic mechanisms regulate PGO activity and maintenance of REM episodes and that protein synthesis-dependent mechanisms regulate RF unit discharge bursts, and REM triggering.

Animals↗
PubMed1982

Sleep related breathing disorders in older men: a search for underlying mechanisms.

The incidence of sleep-related breathing disorders (SRBDs) associated with hemoglobin desaturation was determined by nocturnal polygraphic evaluations in 26 healthy men, aged 55-70 years. Sixteen subjects (62%) had abnormal rates of at least 12 episodes per hour of sleep: 8 had occlusive, and 8 had central apnea or hypopnea. During waking ten of 16 SRBD subjects and only one subject without SRBDs exhibited either an elevated nasopharyngeal airway resistance (n = 4) or a reduced ventilatory response to hypercapnia (n = 4) and/or hypoxia (n = 3). However, these abnormalities were not related to the type or severity of SRBDs, and 6 subjects with SRBDs demonstrated no respiratory defect. We conclude that SRBDs have a very high incidence in older males and are not usually secondary to pulmonary cardiac, neurological, or behavioral disorders. Additionally, we hypothesize that abnormalities in ventilatory control or upper airway resistance contribute to SRBDs, but depression of brain stem reticular formation activity during sleep plays a primary role in these disorders. Factors related to both aging and SRBDs are reviewed. These include reduced chemoreceptor responses, altered steroid hormone metabolism, and use and metabolism of hypnotic drugs and alcohol.

Aged↗
PubMed1982

Respiratory behavior in near-miss sudden infant death syndrome.

Seventeen infants with unexplained prolonged apnea that has been designated near-miss sudden infant death syndrome were monitored for sleep and cardiorespiratory variables during a 12-hour, all-night recording session. Infants were matched for gestational age, sex, and age at recording with control infants. Respiratory variables studied included respiratory rate, respiratory variability, apnea duration, apnea density, and periodic breathing. No statistically significant differences were found in sleep state or respiratory variables between near-miss and control infants. Eight infants (47%) had no recurrence of prolonged apnea, whereas three (17.6%) had recurrent apneic episodes for six weeks to eight months following the original episode. No clinical or polygraphic finding predicted which infant would exhibit recurrent apnea. None of the infants was monitored at home. All infants were developing normally when examined at 1 to 2 years of age.

Apnea↗
PubMed1980

Sudden infant death syndrome: sleep apnea and respiration in subsequent siblings.

Subsequent siblings of infants who died of the Sudden Infant Death Syndrome are at a four- to six-times increased risk to die of this syndrome. This study compares the respiratory development during sleep state of this epidemiologic high risk group with that of normal infants during the first six months of life. Subsequent siblings exhibited higher respiratory rates in all states at 3 months of age. Quiet sleep and indeterminate respiratory rates were elevated at 1 week of age compared to control infants. Indeterminate respiratory rates remained higher at 6 months of age. These differences were accompanied by a reduced incidence of total breathing pauses of two to five seconds and six to nine seconds duration in siblings. Study groups could not be differentiated on the basis of either breathing pauses of more than ten seconds of central apnea of six seconds or more. Obstructive and mixed apnea (6 seconds or more) were infrequently observed in these study groups. A high degree of intersubject variability characterized all data on breathing pauses.

Computers↗
PubMedDate not supplied

Sleep-waking discharge of neurons in the posterior lateral hypothalamic area of cats.

Damage to the posterior hypothalamic area produces a syndrome of EEG synchrony and behavioral somnolence. Cells of a recently described projection system within the posterior lateral hypothalamic area (PLHa) are potential candidates for mediating this area's influences on EEG and behavioral arousal. We examined PLHa neuronal activity during sleep and wakefulness in freely moving cats, identifying projection neurons by antidromic activation from stimulation sites in the external capsule, anterior cingulate bundle, or mesencephalic reticular formation. Orthodromic response evoked from these sites were also investigated. Twenty-two cells were found to send axons outside the PLHa; 9 with ascending projections and 13 with descending projections. Projection cells were found to discharge phasically in relation to waking movements. Most seemed to be related to complex head movements, although specific movement correlates were difficult to ascertain. Discharge rates during periods of waking immobility were similar to those occurring during slow-wave sleep. Rates during phasic REM sleep were generally similar to peak waking rates. Cells with ascending and descending projections displayed similar discharge profiles, although the former had somewhat higher rates in all conditions. Seventy-four cells were orthodromically driven from external capsule or anterior cingulate bundle. Responses evoked from these two sites were similar; an initial brief period of excitation, followed by a sustained (mean greater than 100 msec) episode of discharge suppression. Twenty-four cells exhibited orthodromic excitation from the mesencephalic reticular formation, but the duration of the subsequent discharge suppression was comparatively brief (mean less than 30 msec). With few exceptions, the discharge correlates of orthodromically driven cells were identical to those described above for identified projection neurons. These results do not support a role for neurons within the PLHa in the control of tonic EEG arousal. They are consistent with a possible involvement in either motor function, or phasic movement-related aspects of EEG activation.

Action Potentials↗