Continuous telemetric recordings including E.K.G., E.O.G., and E.E.G. were carried out on two subjects during 4 working days: 1 day of "reference work" or classical clerical activities, 3 days of "data entry work". Although the time allowed for the task was not limited, the performance assessed from oculomotor patterns remained stable throughout the day, from one day to the next and from one subject to another. This stability was reflected on the stereotyped E.E.G. patterns recorded during the work period, the differences occurring between reading and typing were more acute in the left cortical hemisphere than in the right. As a result of these stable patterns, the ultradian oscillations of the behavioural and physiological parameters were less during data entry than during work reference. The only possible time adjustments were the interruptions or breaks between two document pages and their variations could be considered as indicators of work load.

The experiments were conducted to investigate changes occurring between maturity and old age in variations of the EEG when performing a series of mental tasks. Forty three normal male volunteers, divided in two age groups separated by 2 decades (52.9 +/- 0.2 yr, N = 22; 72.2 +/- 0.2 yr, N = 21), were continuously recorded by telemetry in 3 conditions: control, tests, questionnaires. Beta, alpha and theta rhythms and the number of slow waves were measured after visual EEG interpretation. The study showed that: (1) theta rhythms and slow waves were in higher proportions in men in their 70s; (2) variations induced by the various mental tasks were very similar at ages 50 and 70; (3) the two groups differed mostly in theta rhythm responses during tests with a coding task; (4) test performances and EEG indices were correlated only in the older group for theta rhythms.

A technique is described which permits glass micropipet recordings from the thalamus of undrugged, spontaneously breathing cats during waking and natural sleep. An inhibitory extrageniculate feed-back loop on lateral geniculate body (LGB) principal cells has been described from anatomical and electrophysiological experiments in acutely prepared animals. We identified the perigeniculate (PG) neurons and reevaluated their role in free-behaving animals. Four populations of units located above the LGB were classified according to their responses to optic tract (OT) and visual cortex (VC) stimulation and their spontaneous activity. Relay axons responded with a single action potential to OT and VC stimulation. Corticofugal axons responded with a burst of action potentials of longer latency to OT than to VC stimulation. Arguments are presented which suggest that their cell bodies are situated in the visual areas including the Clare and Bishop area. Thalamic reticularis neurons were unresponsive to OT and VC stimulation. Perigeniculate neurons responded with several action potentials to OT and VC stimulation (mean latencies: 2 ± 0.68 and 1.6 ± 0.61 ms, respectively) followed by a long-lasting (200 to 500 ms) negative shift of the membrane potential and a rebound discharge. Although anatomically the PG neurons belong to the thalamic reticularis nucleus they are readily identified by their responses to OT and VC stimulation and their firing patterns during natural sleep. Firing arrest and rebound discharge after OT and VC stimulation were absent in LGB principal cells during paradoxical sleep but not in PG neurons. The firing arrest of PG neurons when stimuli were applied during paradoxical sleep could lead to desinhibition of relay neurons and thus have facilitated transmission of afferent impulses.

(1) A chronic preparation is described in which it is possible to record juxtacellularly from identified thalamo-cortical relay (TCR) neurones in lateral geniculate body (LGB) of normally respiring, nonanaesthetized cats during natural sleep. (2) Cellular events were analyzed during and after focal electrical stimulation of homotopic visual cortex. (3) Projection of cortical epileptiform after-discharge (EAD) was strictly limited to functionally related areas of LGB. Of the 47 neurones tested only 30% were activated. (4) During the 2 sec, 50 c/sec tetanus the cortically evoked IPSPs in TCR cells were replaced by facilitation of cortico-thalamic transmission as demonstrated by the occurrence of a burst of action potentials (AP) following the antidromic AP. (5) During the ensuing EAD, high frequency AP discharges occurred in the cortico-thalamic axons during each cortical wave. This period was accompanied by prolonged (50-300 msec) low amplitude rhythmic depolarisations leading to temporary spike inactivation of TCR neurones. Comparable inactivating responses were recorded during paradoxical sleep. (6) Between paroxysmal bursts facilitation of synaptic transmission to the optic tract stimulation was observed. (7) Persistence of a positive collision test after a spontaneous AP indicates that AP are orthodromically propagated during the EAD.

The number of episodes of intervening wakefulness, their duration and their sleep stage occurrence were analyzed in the sleep recordings of 19 young (19–23 years), good sleepers. There were 5 long sleepers (LS), 5 short sleepers (SS) and 9 regular sleepers (RS). The experimental protocol included 2 reference nights, a night sleep recovery (after 36 h of wakefulness) and a day sleep recovery (after 24 h). The night following the day sleep recovery was also recorded.

Summaryo(1)A chronic preparation is described in which it is possible to record juxtacellularly from identified thalamo-cortical relay (TCR) neurones in lateral geniculate body (LGB) of normally respiring, nonanaesthetized cats during natural sleep.(2)Cellular events were analyzed during and after focal electrical stimulation of homotopic visual cortex.(3)Projection of cortical epileptiform after-discharge (EAD) was strictly limited to functionally related areas of LGB. Of the 47 neurones tested only 30% were activated.(4)During the 2 sec. 50 c/sec tetamus the cortically evoked IPSPs in TCR cells were replaced by facilitation of cortico-thalamic transmission as demonstrated by the occurrence of a burst of action potentials (AP) following the antidromic AP.(5)During the ensuing EAD, high frequency AP discharges occurred in the cortico-thalamic axons during each cortical wave. This period was accompanied by prolonged (50–300 msec) low amplitude rhythmic depolarisations leading to temporary spike inactivation of TCR neurones. Comparable inactivating responses were recorded during paradoxical sleep.(6)Between paroxysmal bursts facilitation of synaptic transmission to the optic tract stimulation was observed.(7)Persistence of a positive collision test after a spontaneous AP indicates that AP are orthodromically propagated during the EAD. A chronic preparation is described in which it is possible to record juxtacellularly from identified thalamo-cortical relay (TCR) neurones in lateral geniculate body (LGB) of normally respiring, nonanaesthetized cats during natural sleep. Cellular events were analyzed during and after focal electrical stimulation of homotopic visual cortex. Projection of cortical epileptiform after-discharge (EAD) was strictly limited to functionally related areas of LGB. Of the 47 neurones tested only 30% were activated. During the 2 sec. 50 c/sec tetamus the cortically evoked IPSPs in TCR cells were replaced by facilitation of cortico-thalamic transmission as demonstrated by the occurrence of a burst of action potentials (AP) following the antidromic AP. During the ensuing EAD, high frequency AP discharges occurred in the cortico-thalamic axons during each cortical wave. This period was accompanied by prolonged (50–300 msec) low amplitude rhythmic depolarisations leading to temporary spike inactivation of TCR neurones. Comparable inactivating responses were recorded during paradoxical sleep. Between paroxysmal bursts facilitation of synaptic transmission to the optic tract stimulation was observed. Persistence of a positive collision test after a spontaneous AP indicates that AP are orthodromically propagated during the EAD. Résuméo(1)Une technique d'enregistrement juxtacellulaire, chez le chat respirant spontanément et non anesthésié, est décrite.(2)Les activités cellulaires des neurones relais thalamo-corticaux du corps genouillé latéral (GL) ont été analysées pendant la stimulation électrique répétitive du cortex visuel homotopique et la post-décharge épileptique (PDE) qui suit.(3)La zone de projection, dans le GL, de la PDE est très limitée: seuls, 30% de 47 neurones testés ont été activés.(4)La stimulation à 50 c/sec s'accompagne d'une facilitation de la transmission cortico-thalamique. Celle-ci est mise en évidence par la suppression des IPSP, qui font normalement suite au potentiel d'action (PA) antidromique, et leur remplacement par des PA répétitifs.(5)Pendant les ondes corticales de la PDE, des bouffées de PA à haute fréquence sont enregistrées dans les axones cortico-thalamiques. Cette période s'accompagne, dans les neurones relais, de dépolarisations rythmiques prolongées (50 à 300 msec), associées à une inactivation temporaire du générateur de PA. Des dépolarisations inactivantes similaires sont également enregistrées pendant le sommeil paradoxal.(6)Pendant les silences séparant les bouffées paroxystiques, la transmission synaptique des influx afférents du tractus optique est facilitée.(7)L'origine orthodromique des PA, pendant la PDE, a été vérifiée par des tests de collision. Une technique d'enregistrement juxtacellulaire, chez le chat respirant spontanément et non anesthésié, est décrite. Les activités cellulaires des neurones relais thalamo-corticaux du corps genouillé latéral (GL) ont été analysées pendant la stimulation électrique répétitive du cortex visuel homotopique et la post-décharge épileptique (PDE) qui suit. La zone de projection, dans le GL, de la PDE est très limitée: seuls, 30% de 47 neurones testés ont été activés. La stimulation à 50 c/sec s'accompagne d'une facilitation de la transmission cortico-thalamique. Celle-ci est mise en évidence par la suppression des IPSP, qui font normalement suite au potentiel d'action (PA) antidromique, et leur remplacement par des PA répétitifs. Pendant les ondes corticales de la PDE, des bouffées de PA à haute fréquence sont enregistrées dans les axones cortico-thalamiques. Cette période s'accompagne, dans les neurones relais, de dépolarisations rythmiques prolongées (50 à 300 msec), associées à une inactivation temporaire du générateur de PA. Des dépolarisations inactivantes similaires sont également enregistrées pendant le sommeil paradoxal. Pendant les silences séparant les bouffées paroxystiques, la transmission synaptique des influx afférents du tractus optique est facilitée. L'origine orthodromique des PA, pendant la PDE, a été vérifiée par des tests de collision.

The number of episodes of intervening wakefulness, their duration and their sleep stage occurrence were analyzed in the sleep recordings of 19 young (19-23 years), good sleepers. There were 5 long sleepers (LS), 5 short sleepers (SS) and 9 regular sleepers (RS). The experimental protocol included 2 reference nights, a night sleep recovery (after 36 h of wakefulness) and a day sleep recovery (after 24 h). The night following the day sleep recovery was also recorded. The duration of waking episodes was very stable and was independent both of type of sleeper and of situation. The histogram of these durations seemed to follow an exponential law. The number of awakenings varied according to the individual, the habitual sleep length (SS had very few) and the situation (such as length of prior wakefulness or circadian factors).

(1) The sleep pattern of 23 children, aged 5-12 years, with episodic nocturnal phenomena (night-terrors, somnambulism, rhythmic movements) was recorded during two successive nights. It was compared with that of a group of 21 normal children of the same age. (2) In the pathological group, slow wave sleep (SLP, stages 3 and 4) was significantly shortened during the 2 nights. This deficit mainly involved the first 3h of sleep. (3) As for the slow wave sleep, REM sleep (SP) modifications prevailed during the first hours of sleep. The first REM period was delayed and preceded by more numerous and atypical partial REM periods. The duration of the first REM period increased faster as a function of its latency than in the normal child. (4) In contrast with this difficulty for REM sleep to occur during the first part of the night, the subsequent REM sleep pattern was similar in the 2 groups (total REM sleep duration, mean REM period duration, mean REM cycle duration). For equal latencies, REM periods had similar duration. Finally, the total REM sleep amount was a linear function of the total sleep time, with more or less identical coefficients for the two groups. (5) The part played by these modifications during the first hours of sleep in the occurrence of night terrors and somnambulism is discussed.

1.(1) Le sommeil de 23 enfants, âgés de 5 à 12 ans présentant des manifestations épisodiques du sommeil (terreurs nocturnes, somnambulisme, rythmies) a été enregistré deux nuits consécutives. Il a été comparé à celui d'un groupe de 21 enfants normaux de même âge.2.(2) Dans le groupe pathologique lors des deux nuits, le sommeil lent profond (SLP, stades 3 et 4) est significativement diminué. Ce déficit porte surtout sur les trois premières heures de sommeil.3.(3) Comme pour le SLP, les modifications du sommeil paradoxal (SP) prédominent dans les premières heures de sommeil. Le premier stade SP est retardé, il est précédé d'ébauches de SP plus nombreuses et plus atypiques. La durée du SP1 s'accroît plus vite en fonction de sa latence que chez l'enfant normal.4.(4) Contrastant avec cette difficulté d'installation du sommeil paradoxal en début de nuit, l'organisation ultérieure du SP est comparable dans les deux groupes, (quantité totale de SP, durée moyenne des stades SP, durée moyenne des cycles).A latence égale, les stades SP ont des durées comparables. Enfin la quantité totale de SP est une fonction linéaire du temps de sommeil dont les coefficients sont sensiblement les mêmes pour les deux groupes.5.(5) Le rôle de ces modifications de l'organisation du début du sommeil dans la survenue des terreurs nocturnes et de somnambulisme est discuté.