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1 unclear how sleep influences the associated arousal response.
2 ivated transcription factor, greatly reduced arousal responses.
3 d and were not usually associated with other arousal responses.
4 cortex, indicating spatial heterogeneity of arousal responses.
5 before optical VTA stimulation inhibited the arousal responses and restoration of righting in 6/6 ChR
6 ia, i.e., the heart rate and ventilatory and arousal responses, and abolishes the normal decrease in
7 ripheral theories of emotion was that bodily arousal responses are too undifferentiated to account fo
8 precise relationship between discomfort (or arousal) responses as a function of distance from an obs
9 -conditioned stimuli reinstated the acquired arousal response, as reflected in pupil and EEG alpha-be
10 duced spontaneous recovery of threat related arousal responses, as compared to the waitlist control g
11 and autonomic function as well as stress and arousal responses attributed to EM-1 in the central nerv
13 nction, we hypothesized that blunted hypoxic arousal responses during sleep Stage 3/4 would be presen
15 MRI signal is a substantial component of the arousal response governed by the autonomic nervous syste
19 models we performed a behavioral screen for arousal responses including emotionality, locomotor, and
22 t appropriately transcoded into somato-motor-arousal responses normally associated with an aversive m
24 atory autonomic, respiratory, somatomotor or arousal responses that limit the extent of blood pressur
27 that Lmx1b(f/f/p) mice completely lacked any arousal response to inhalation of 10% CO(2) (with 21% O(
29 sizable number of individuals displaying no arousal response to the visual or auditory stimuli, rega
30 creased threat sensitivity may interact with arousal responses to alter hippocampal reactivity, and f
31 and physiologic evidence points to impaired arousal responses to hypercarbia and hypoxia, which ulti
33 ), we evaluated the muscle, ventilatory, and arousal responses to negative-pressure challenges during
34 C1 neurons orchestrate cardiorespiratory and arousal responses to somatic stresses, whereas RTN selec
36 nt inputs control the gain of LC-NA-mediated arousal responses, whereas non-coincident inputs, such a