ライフサイエンスコーパス: hypocretin-1

1 el immunofluorescence of FosB/DeltaFosB with hypocretin-1.

2 the input resistance was not affected after hypocretin-1.

3 to have a positive modulatory effect on CSF hypocretin-1.

4 ulation and the juxtacellular application of hypocretin-1.

5 modeling using the coordinates of the DQ0602-hypocretin 1-13 crystal structure.

6 pothalamus or after the local application of hypocretin-1; (5) the juxtacellular application of hypoc

7 ous EPSPs in NPO neurons increased following hypocretin-1 administration.

8 ocyte antigen typing and cerebrospinal fluid hypocretin-1 analysis are useful as adjuncts.

9 Hypocretin-1 and -2 depolarized hypocretin neurons by 15

10 In slices of the mature mouse and rat LC, hypocretin-1 and -2 increased spike frequency, with hypo

11 s using cultured LH cells revealed that both hypocretin-1 and -2 induced enhancement of neuronal acti

12 performed in all participants to measure CSF hypocretin-1 and GABA-A response.

13 Two hypocretin peptides, hypocretin-1 and hypocretin-2, are coded by a single gen

14 he levels of two hypothalamic neuropeptides, hypocretin-1 and melanin-concentrating hormone, measured

15 Hypocretins 1 and 2 (also called orexins A and B, respec

16 similar increase in activity was found with hypocretin-1 application to LH slices.

17 tin-1 and -2 increased spike frequency, with hypocretin-1 being an order of magnitude more potent.

18 ss hormone cortisol were not correlated with hypocretin-1 changes.

19 Determination of CSF hypocretin-1 concentration to diagnose narcolepsy might

20 When we lengthened the wake period by 4 hr, hypocretin-1 concentrations remained elevated, indicatin

21 activity did not significantly increase CSF hypocretin-1 concentrations, but did appear to have a po

22 Because 98% of patients with hypocretin-1 deficiency are positive for HLA DQB1*0602,

23 Although hypocretin-1 deficiency in narcolepsy might have therape

24 Hypocretin-1 depolarized the membrane potential, resulti

25 al diurnal rise in cerebrospinal fluid (CSF) hypocretin-1, despite an associated increase in CSF cort

26 pplication of vehicle (saline) and denatured hypocretin-1 did not produce changes in the preceding el

27 Concentrations of CSF hypocretin-1 (formerly orexin A) have been measured in m

28 The distribution of hypocretin-1 (hcrt-1) and hypocretin-2 (hcrt-2) immunore

29 We verified the orexogenic actions of hypocretin-1 (Hcrt-1) and hypocretin-2 (Hcrt-2) in an ad

30 that blockade of hypocretin transmission at hypocretin-1 (Hcrt-1; orexin-1) receptors decreases i.v.

31 ined the relationship between locomotion and hypocretin-1 in a wake-consolidating animal, the squirre

32 We examined the daily temporal pattern of hypocretin-1 in the cisternal CSF of the squirrel monkey

33 A role for hypocretin-1 in the generation of locomotor activity has

34 etin-1; (5) the juxtacellular application of hypocretin-1 induced motoneuron depolarization and, freq

35 hypocretin/orexin neurons is potentiated and hypocretin-1-induced action potential firing is facilita

36 signaling, MCH significantly attenuated the hypocretin-1-induced enhancement of spike frequency in h

37 Consistent with this effect, MCH attenuated hypocretin-1-induced enhancement of the frequency of min

38 Hypocretin-1 initiated strong regular membrane voltage o

39 wakefulness following the microinjection of hypocretin-1 into the LDT and a significant decrease in

40 Although hypocretin-1 is at least partially activated by a reacti

41 of the day, consistent with the premise that hypocretin-1 is involved in wake regulation.

42 Low CSF hypocretin-1 is most predictive of narcolepsy in patient

43 w/intermediate or normal cerebrospinal fluid hypocretin-1 is present in both diseases.

44 rast, the diagnostic significance of low CSF hypocretin-1 is unclear in the presence of acute CNS inf

45 nted low (</= 110 pg/mL) cerebrospinal fluid hypocretin-1 level.

46 We show that hypocretin-1 levels are maximal during positive emotion,

47 increased disease severity, and undetectable Hypocretin-1 levels in cerebrospinal fluid.

48 tent with a role in sleep induction, whereas hypocretin-1 levels increase at wake onset, consistent w

49 Hypocretin-1 levels peaked in the latter third of the da

50 e of TTX and glutamate receptor antagonists, hypocretin-1-mediated inward currents were blocked by su

51 ion with the juxtacellular microinjection of hypocretin-1 onto intracellularly recorded cells.

52 The hypothalamic peptides hypocretin-1 (orexin A) and hypocretin-2 (Hcrt-2; orexin

53 Hypocretin-1 (orexin-A) was administered to sleep-depriv

54 stent with recent studies which suggest that hypocretin 1/orexin A may be involved in modulating arou

55 o cocaine and alcohol via stimulation of the hypocretin-1/orexin-A (Hcrt-1/Ox-A) system.

56 Orexin A/hypocretin-1 (oxA/hcrt-1) is known to be a modulator of

57 d, frequently, high-frequency discharge; (6) hypocretin-1 produced a significant decrease in rheobase

58 3.3%); (7) in a small number of motoneurons, hypocretin-1 produced an increase in the synaptic noise;

59 icating a circadian-independent component to hypocretin-1 regulation.

60 Hypocretin-1 release peaks at the end of the active peri

61 QB1*06:02 positivity (no cerebrospinal fluid hypocretin-1 results available) or narcolepsy with docum

62 The application of hypocretin-1 significantly increased the mean amplitude

63 animal, locomotion is not necessary for CSF hypocretin-1 to increase throughout the daytime, but hig

64 nce and nuclear imaging, cerebrospinal fluid hypocretin-1, total tau, phosphorylated tau, amyloid-bet

65 Hypocretin-1 was dramatically decreased (<100 pg/ml) in

66 Hypocretin-1 was measurable (169 to 376 pg/ml) in all co

67 Accordingly, hypocretin-1 was microinjected into the LDT of chronic,

68 In the squirrel monkey, hypocretin-1 works in opposition to the accumulating sle