Technical comment: an automatic hatch detector for birds.
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Biomedical subjects
Publications and source records attributed to M Corner.
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Multiple-unit activity was recorded from residual neurons in the gigantocellular field ( FTG ) of the pontine reticular formation in young rats after extensive contralateral FTG lesions. Epochs of normal appearing active sleep continued to occur but were characterized by abnormally low FTG neuronal firing rates. In contrast, during epochs of active sleep with exaggerated motility, the FTG discharge frequencies approximated those observed during active wakefulness.
The neocortical EEG was quantified during sleep, while under light chloral hydrate anaesthesia, in rats ranging from 9 to 20 days of postnatal age. Continuous amplitude modulation at 0.5-1.0 min per cycle, synchronously over all frequency bands, was observed in 9- and in 10-day-old pups. By day 13, the mean amplitude had risen considerably in each of the frequency bands, and a slow fluctuation in delta-wave activity began to be discernible. Sodium glutamate injections induced EEG changes at 10 days which mimicked certain aspects of normal maturation (viz., large stereotyped potentials at irregular intervals, along with a selective increase in delta-wave activity). Natural as well as experimentally induced EEG changes were paralleled by a rise in neocortical amino acid concentrations, including glutamic acid and GABA. Delta wave amplitudes during quiet sleep increased still further between 13 and 14 days, while beta activity remained at a constant level. Between days 14 and 15 a precipitous decline in delta-wave activity was found, attributable to greater inhibition of slow waves during active sleep. No further developmental changes were noted, except for a gradual rise in the time spent in quiet sleep relative to active sleep.
Hippocampal EEG and neck EMG activity were recorded in restrained as well as in unrestrained rat pups following treatment with drugs which selectively suppress wakefulness and active sleep, respectively. Chloral hydrate did not affect active sleep but eliminated the bursts of coordinated total-body movements which were seen during sleep, especially under conditions of restraint. Chlorimipramine, in contrast, suppressed active sleep while sparing the coordinated total-body motility. It is concluded that these latter movements represent an episodic arousal phenomenon, against a background of quiet sleep, which becomes intensified under certain postural conditions.
Spontaneous action potentials were recorded at 1 mm depth (layer IV/V) in the occipital cortex of free moving rats between 8 and 60 days of postnatal age. Neuronal firing rates during quiet sleep (QS) increased sharply around day 11-12, parallel with an increase in the amplitude of EEG slow waves. The QS discharge pattern at all ages consisted of intermittent action potentials interspersed with short bursts. Active sleep (AS) from day 11-12 was characterized by longer lasting and more frequent bursts, and by a 2-3 X higher mean neuronal discharge rate than during QS. A peculiarity in 12-day-old rats was the presence of large fluctuations in overall firing rate continuously throughout sleep. Clomipramine completely abolished AS (for several hours) at all ages studied, during which time the cortical firing rates during sleep remained at (or lower than) the QS level prior to drug injection.
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