ライフサイエンスコーパス: 5-HT(2) receptor

1 cently been unveiled and is mediated through 5-HT2 receptor.

2 ors, they overlap in their agonist action at 5-HT2 receptors.

3 involved in agonist binding in the serotonin 5-HT2 receptors.

4 can be induced by intermittent activation of 5-HT2 receptors.

5 rs, with some evidence of a weak affinity to 5-HT(2) receptors.

6 n-selective agonistic actions on 5-HT(1) and 5-HT(2) receptors.

7 ting that this effect of 5-HT is mediated by 5-HT(2) receptors.

8 and ketanserin, indicating the mediation by 5-HT(2) receptors.

9 (APDs) is their relatively high affinity for 5-HT(2) receptors.

10 5-HT) neurotransmission, acting primarily at 5-HT(2) receptors.

11 lower affinity than the corresponding 1a at 5-HT2 receptors, 3a and 3b had significantly greater aff

12 G-protein-coupled 5-HT(2) receptors (5-HT(2)Rs) also exist on vagal affere

13 The role of serotonin 5-HT2 receptors (5-HT2R) in the discriminative stimulus

14 In other brain regions, 5-HT2 receptors (5-HT2R) modify synaptic transmission di

15 and developmental profile of 5-HT(1A-1D) and 5-HT2 receptors, 5-HT1A receptors, and the serotonin (5-

16 or the previously characterized 5-HT(1A) and 5-HT(2) receptors, a proportion of layer V pyramidal neu

17 ynaptic, slow-onset inhibition attributed to 5-HT2 receptor activation exciting GABAergic interneuron

18 ith a role in facilitating tonic inhibition, 5-HT2 receptor activation increased the frequency of spo

19 at require the following: Gq-protein-coupled 5-HT2 receptor activation, new BDNF synthesis, and MEK/E

20 striatum elicited by MDMA appears to involve 5-HT2 receptor activation.

21 Episodic spinal serotonin-2 (5-HT2) receptor activation on or near phrenic motor neur

22 y cells, taurine and AL34662, a non-specific 5-HT(2) receptor activator, produced a similar regulatio

23 are primarily responsible for the effects of 5-HT2 receptor-active drugs on lordosis behavior.

24 s identified as a peripherally acting potent 5-HT(2) receptor agonist (EC(50) = 42.7 nM, E(max) = 89%

25 5-HT(2A) receptor activation by the 5-HT(2) receptor agonist DOI induced a transient increas

26 Compound 9 appears to be an excellent 5-HT(2) receptor agonist for conducting further studies

27 xyphenyl)-2-aminopropane (DOI, 50 microM), a 5-HT(2) receptor agonist, into the NACC produced greater

28 n of alpha-M-5-HT (100 microg kg(-1), LA), a 5-HT(2) receptor agonist, stimulated only two of the nin

29 t cholinergic interneurone firing, while the 5-HT2 receptor agonist alpha-methyl-5-HT (30 microm) mim

30 The 5-HT2 receptor agonist alpha-methyl-5-HT reduced the sAH

31 The nonselective 5-HT2 receptor agonist mCPP (0.0, 0.3, 1.0, or 3.0 mg/kg

32 Pretreatment of ganglia with the 5-HT2 receptor agonist R-(+)-dimethoxy-4-iodoamphetamine

33 Both the 5-HT2 receptor agonist, alpha-methylserotonin (100 micro

34 Serotonin 5-HT(2) receptor agonists have been identified as a pote

35 Recently, it has been reported that 5-HT2 receptor agonists effectively reduce intraocular p

36 Serotonin 5-HT2 receptor agonists have recently been shown to be e

37 ioral toxicity associated with non-selective 5-HT2 receptor agonists, targeting the 5-HT2C receptor m

38 a-methylserotonin, a nonselective agonist of 5-HT2 receptors, also blocked polysynaptic responses but

39 potent full agonist with selectivity for the 5-HT2 receptor and is anticipated to serve as a useful t

40 s a useful tool in exploring the role of the 5-HT2 receptor and its effector system in controlling in

41 itro at dopamine D2 and serotonin 5-HT1a and 5-HT2 receptors and in vivo for their ability to antagon

42 vary cell lines expressing each of the human 5-HT2 receptors and in vivo in animal models of obesity.

43 staminergic (H3) and serotonergic (5-HT1 and 5-HT2) receptors, and sigma binding sites.

44 Ketanserin, a 5-HT(2) receptor antagonist prevented sensory LTF but no

45 glutamate receptors, but was blocked by the 5-HT(2) receptor antagonist ritanserin.

46 5-HT were sensitive to 10 microm-ketanserin (5-HT(2) receptor antagonist) and strongly inhibited by a

47 The 5-HT(2) receptor antagonist, ritanserin, and the 5-HT(2B

48 A combination of a 5-HT2 receptor antagonist and TXA2 synthase inhibitor/re

49 Consistently, the 5-HT2 receptor antagonist ketanserin (10 microm) fully b

50 Similar treatment with the 5-HT2 receptor antagonist ketanserin (3 microM) had no s

51 ged increase in MPC phospho-ERK, whereas the 5-HT2 receptor antagonist ketanserin (3-[2-[4-(4-fluorob

52 Pretreatment with the select 5-HT2 receptor antagonist Ketanserin blocked DOI-induced

53 opamine receptor antagonist SCH 23390 or the 5-HT2 receptor antagonist ketanserin.

54 TXA2 on SMC proliferation was abolished by a 5-HT2 receptor antagonist, LY281067, without affecting t

55 PAG), and that such effects are blocked by a 5-HT2 receptor antagonist.

56 e reuptake inhibitor, but a potent serotonin 5-HT2 receptor antagonist.

57 ological roles of serotonin in tissues where 5-HT2 receptors are co-expressed.

58 Since 5-HT2 receptors are known to utilize protein kinase C (P

59 5-HT2 receptors are potential candidates because activat

60 sport into platelets and decreased serotonin 5-HT2 receptor binding.

61 agonists with greater affinity for D2 DA and 5-HT2 receptors, blocked the development of locomotor se

62 he rhythmic activity of olivary neurones via 5-HT2 receptors by inhibition of the T-type calcium curr

63 ory control on cholinergic interneurones via 5-HT2 receptors, by suppressing the AHPs associated with

64 These data demonstrate that 5-HT2 receptors can form functionally asymmetric heterod

65 We report that 5-HT2 receptors can form homo- and heterodimers when exp

66 cted ligands for the examined members of the 5-HT2 receptor class.

67 CIH required 5-HT release and activation of 5-HT(2) receptors coupled to PKC signaling.

68 Experiment 2 compared 5-HT(2) receptor densities across these mice and cocaine

69 ation (LTF) is characterized by a persistent 5-HT2 receptor-dependent increase in respiratory motor o

70 [3H]Ketanserin binding to cortical 5-HT2 receptors did not differ among the lines, except i

71 Expression of 5-HT2 receptors did not increase binding of JCPyV to cel

72 le of 5-HT in behavior and the regulation of 5-HT(2) receptor function.

73 s, supporting the physiological relevance of 5-HT2 receptor heterodimerization in vivo Accordingly, e

74 ogether, our results show that activation of 5-HT(2) receptors in PFC pyramidal neurons inhibits GABA

75 Moreover, activation of 5-HT(2) receptors in PFC slices increased the in vitro k

76 a group, despite equivalent upregulation of 5-HT(2) receptors in the lumbar ventral horn of lesioned

77 suggesting a relationship between IL-1RI and 5-HT2 receptors in the medial hypothalamus that is consi

78 anatomical relationship between IL-1beta and 5-HT2 receptors in the medial hypothalamus.

79 Furthermore, stimulation of 5-HT2 receptors increases the phosphorylation state of S

80 demonstrate that GLYX-13 does not influence 5-HT2 receptor induced head twitch response or impulsivi

81 ) = 1 nM for both) and moderate affinity for 5-HT(2) receptors (K(i) = 73 and 75 nM, respectively).

82 splacement of radioligand from rat and human 5-HT2 receptors, making it one of the most potent halluc

83 This study suggests that 5-HT(2) receptors mediate genetic sensitivity to cocaine

84 owever, in experiment 3 we demonstrated that 5-HT(2)-receptor mediated phosphoinositide hydrolysis wa

85 This data suggests that the 5-HT2 receptor-mediated depolarization and increase in R

86 serotonergic facilitation of TRPV1 function; 5-HT2 receptor-mediated facilitation was also inhibited

87 al motoneurones as a result of activation of 5-HT2 receptors, microinjection of 5-HT2 antagonists int

88 erotonin (5-Hydroxytryptamine, 5-HT) and the 5-HT2 receptor modulate cardiovascular and autonomic fun

89 herefore, supports a pronociceptive role for 5-HT2 receptors, most likely through modulation of 5-HT2

90 In myometrium, 5-HT2 receptors not only play a role in contraction but

91 AADC cells, together with an upregulation of 5-HT2 receptors, offers a partial explanation of hyperre

92 requires mast cell-derived 5-HT to activate 5-HT(2) receptors on parasympathetic cholinergic neurons

93 om intestinal EC cells activated 5-HT(3) and 5-HT(2) receptors on vagal afferent fibers to mediate lu

94 ous, activation of postsynaptic 5-HT type 2 (5-HT(2)) receptors on hypoglossal (XII) motoneurons lead

95 on: indirect inhibition mediated through the 5-HT2 receptors on GABAergic interneurons and direct inh

96 ffects may also be linked to the presence of 5-HT2 receptors on the same groups of neurons in this re

97 ffinity and selectivity (>1000-fold) for the 5-HT(2) receptor relative to other 5-HT receptors.

98 E(max) = 89%) with high selectivity for the 5-HT(2) receptors relative to other serotonergic recepto

99 5-HT(2) receptor stimulation is known to cause fibroblas

100 mine and its metabolite norfenfluramine with 5-HT(2) receptor subtypes and examined the expression of

101 wo directly acting agonists for serotonergic 5-HT(2) receptor subtypes, quipazine and (+/-)-1-[2, 5]-

102 e indole nucleus of tryptamines that bind to 5-HT2 receptor subtypes and possess LSD-like behavioral

103 tention that within the VMN, both 5-HT1A and 5-HT2 receptor subtypes contribute to the modulation of

104 The differences in the 5-HT2 receptor synaptic and behavioral responses may be

105 a greater affinity for 5-hydroxytryptamine2 (5-HT2) receptors than for D2 dopamine receptors; its eff

106 ults suggest that serotonin acts at separate 5-HT2 receptors to facilitate the acquisition and expres

107 neonatal 6-OHDA lesions involves coupling of 5-HT2 receptors to the ERK1/2/MAP Kinase cascade, a path

108 6-OHDA lesions result in a novel coupling of 5-HT2 receptors to the ERK1/2/MAP Kinase pathway, a sign

109 HT release or direct stimulation of striatal 5-HT2 receptors via the 5-HT2 agonist DOI, produced robu

110 q-coupled M3-muscarinic, thromboxane-A2, and 5-HT2 receptors was desensitized in airway smooth muscle

111 ut effect at 5-HT7 but has high affinity for 5-HT2 receptors, was also effective in attenuating the p

112 ulsions despite the fact that they have more 5-HT(2) receptors, we hypothesized that these mice may e

113 Only 5-HT2 receptors were found to support infection by JCPyV

114 leus, but became critical when alpha1 NE and 5-HT2 receptors were pharmacologically blocked.

115 cal methods to demonstrate that IL-1beta and 5-HT2 receptors were present on the same neurons within

116 ry LTF of the carotid body via activation of 5-HT(2) receptors, which involves a novel signalling mec

117 These include the 5-HT2 receptor, which is further sub classified into 5-H

118 Most emphasis has been placed on 5-HT1A and 5-HT2 receptors, which inhibit and facilitate the behavi

119 ide evidence that activation of 5-HT(1A) and 5-HT(2) receptors within the medial hypothalamus exert d

120 whether pharmacological treatments targeting 5-HT2 receptors would alter the acquisition and expressi