ライフサイエンスコーパス: postsynaptic receptor

1 , whereas the D2 long isoform is primarily a postsynaptic receptor.

2 transmitter, and they establish ASICs as the postsynaptic receptor.

3 which two neurotransmitters act on the same postsynaptic receptor.

4 e presynaptic plasma membrane and opposed to postsynaptic receptors.

5 presynaptic mechanisms or saturation of the postsynaptic receptors.

6 ed and the manner by which it interacts with postsynaptic receptors.

7 ing postsynaptic signals upon recognition by postsynaptic receptors.

8 n the synapse with a resultant activation of postsynaptic receptors.

9 that the transmitters can activate the same postsynaptic receptors.

10 g neurotransmitters produce their effects on postsynaptic receptors.

11 ke of neurotransmitter efficiently activates postsynaptic receptors.

12 portionally through changes in the number of postsynaptic receptors.

13 scape the cleft and activate presynaptic and postsynaptic receptors.

14 es, in part because they likely contain more postsynaptic receptors.

15 tic plasticity elicited by acute blockage of postsynaptic receptors.

16 acts on, and can be photoincorporated into, postsynaptic receptors.

17 a vesicle is much larger than the number of postsynaptic receptors.

18 amate release may lead to desensitization of postsynaptic receptors.

19 transmitter release or increased opening of postsynaptic receptors.

20 ther unitary packets of transmitter saturate postsynaptic receptors.

21 se to direct iontophoresis of glutamate onto postsynaptic receptors.

22 ed synapse-organizing molecule that clusters postsynaptic receptors.

23 and/or a reduction of the desensitization of postsynaptic receptors.

24 has a potent effect at both presynaptic and postsynaptic receptors.

25 ly segregated and pharmacologically distinct postsynaptic receptors.

26 ration profile of neurotransmitter acting on postsynaptic receptors.

27 operating on a separate functional group of postsynaptic receptors.

28 of synaptic vesicles, or desensitization of postsynaptic receptors.

29 utamate transients and from the diversity of postsynaptic receptors.

30 ion of dendritic proteins, including several postsynaptic receptors.

31 lease is assumed to activate the same set of postsynaptic receptors.

32 ite; and (2) the GluR4 AMPA receptors as the postsynaptic receptors.

33 vesicle mobilization and by the response of postsynaptic receptors.

34 eHg on transmitter release or sensitivity of postsynaptic receptors.

35 n composition and functional contribution of postsynaptic receptors.

36 a reduction of available functional GABA(A) postsynaptic receptors.

37 l release events engage a high proportion of postsynaptic receptors (62%), revealing a larger compone

38 This increase in postsynaptic receptor abundance is not accompanied by ot

39 on and stabilization, synaptic transmission, postsynaptic receptor abundance, axonal degeneration and

40 transmission depends, to a large extent, on postsynaptic receptor abundance.

41 ransmitter released, as well as the class of postsynaptic receptors activated by their firing remain

42 what is known about glutamate signaling and postsynaptic receptor activation is based on experiments

43 concentration time course and ensuring that postsynaptic receptor activation remains brief and prima

44 , consequently, the duration and location of postsynaptic receptor activation.

45 including presynaptic vesicle tethering and postsynaptic receptor aggregation.

46 re there is a high probability of opening of postsynaptic receptors, all of which are occupied by the

47 the context of years of work characterizing postsynaptic receptor and signaling functions of learnin

48 elopmental stages occurs independent of both postsynaptic receptor and synaptic responses in zebrafis

49 Thus, both postsynaptic receptor and transmitter release properties

50 tine, but not muscarinic agonists, activates postsynaptic receptors and a depolarizing inward current

51 s function like high efficacy agonists at D2 postsynaptic receptors and autoreceptors (i.e., tergurid

52 at released neurotransmitter acts locally on postsynaptic receptors and is cleared from the synaptic

53 ic plasticity: changes in both the number of postsynaptic receptors and loading of synaptic vesicles

54 s responsible for limiting the activation of postsynaptic receptors and maintaining low levels of amb

55 antagonist-like effects at normosensitive D2 postsynaptic receptors and synthesis modulating autorece

56 ntent is increased, yet the abundance of the postsynaptic receptors and the amplitude of miniature ex

57 tamate spillover to adjacent presynaptic and postsynaptic receptors and the consequent induction of p

58 In the vSt, 5-HT1A (a postsynaptic receptor) and 5-HT1B (a presynaptic recepto

59 e volume, ultrafast fusion pore closure, the postsynaptic receptor, and the location between release

60 neous trains, do not require the function of postsynaptic receptors, and are all-or-none overshooting

61 modulation of striatal inputs is mediated by postsynaptic receptors, and that of globus pallidus-evok

62 ary to delineate the exact properties of the postsynaptic receptors, and their role in transmission a

63 pecific vesicular trafficking route taken by postsynaptic receptors appears to depend on the stimulus

64 in the mammalian brain, in which the primary postsynaptic receptors are alpha-bungarotoxin-sensitive

65 or chick ciliary ganglion neurons, where the postsynaptic receptors are concentrated on somatic spine

66 Neuropeptides acting on pre- and postsynaptic receptors are coreleased with GABA by inter

67 r PNMT-containing dendrites, suggesting that postsynaptic receptors are more readily available for li

68 n synaptic physiology is the extent to which postsynaptic receptors are saturated by the neurotransmi

69 It is not well understood how postsynaptic receptors are selectively enriched in dendr

70 e agonistic effects of terguride at pre- and postsynaptic receptors are short-lived, but terguride ma

71 bitory synapses with large and gephyrin-rich postsynaptic receptor areas are likely indicative of hig

72 Quinpirole acted on postsynaptic receptors as it reversed the reduced prolif

73 IPSG neither by changing the sensitivity of postsynaptic receptors, as tested by iontophoretically e

74 cells might be presynaptic autoreceptors or postsynaptic receptors at afferent or efferent synapses.

75 receptors of a putative efferent system, or postsynaptic receptors at synapses with other taste cell

76 ity can determine the subunit composition of postsynaptic receptors at this synapse.

77 ow clearance of glutamate is likely to limit postsynaptic receptor availability through desensitizati

78 blocks fast IPSCs by acting directly on the postsynaptic receptors, because it reduces the amplitude

79 covered from restricting-type AN, the 5-HT1A postsynaptic receptor binding in mesial temporal and sub

80 Tetrodotoxin (TTX), but not postsynaptic receptor blockade, reversed depolarization-

81 during train stimulation in the presence of postsynaptic receptor blockers.

82 nically blocking action potential firing and postsynaptic receptors but was markedly reduced on DG de

83 d not be totally eradicated, suggesting that postsynaptic receptor changes may also play a role in th

84 ariability were considered: stochasticity of postsynaptic receptors ("channel noise"), variations of

85 ng the role of the loss of responsiveness of postsynaptic receptor channels to neurotransmitter owing

86 eneral anesthetics exert their action on the postsynaptic receptor channels.

87 lts in rapid and near-synchronous opening of postsynaptic receptor channels.

88 ations between presynaptic release sites and postsynaptic receptor/channels.

89 or, and the location between release and the postsynaptic receptor cluster at glutamatergic, calyx of

90 in this model precede structural changes on postsynaptic receptor cluster density.

91 We concluded that postsynaptic receptor cluster dissolution seemed more di

92 er distance between the release site and the postsynaptic receptor cluster.

93 he effects of long-term synaptic blockade on postsynaptic receptor clustering at central inhibitory g

94 Postsynaptic receptor clustering is induced in a highly

95 Postsynaptic receptor clustering is thought to be of cri

96 We propose that presynaptic terminals induce postsynaptic receptor clustering through the action of b

97 bute to efficient recruitment of gephyrin to postsynaptic receptor clusters and are essential for res

98 tic neurofilament bundles do not overlap the postsynaptic receptor clusters but do codistribute with

99 tory interneurons) were also associated with postsynaptic receptor clusters of variable shapes and co

100 presynaptic specializations, align them over postsynaptic receptor clusters, and increase synaptic fu

101 of synaptic vesicles in nerve terminals and postsynaptic receptor clusters.

102 alcium entry, of presynaptic release, and of postsynaptic receptors combine to produce a postsynaptic

103 uts onto Pyr and FS neurons also differed in postsynaptic receptor composition and organization of pr

104 cells is developmentally regulated, with the postsynaptic receptor composition established during syn

105 lts demonstrate precise input specificity of postsynaptic receptor composition via differential activ

106 SC responses are thought to be determined by postsynaptic receptor composition.

107 demonstrating that both GABA(A) and GABA(B) postsynaptic receptors contribute to seizure-induced enh

108 azide (CTZ) revealed that desensitization of postsynaptic receptors contributed to synaptic depressio

109 C to accumbens shell and local dopamine D(1) postsynaptic receptors contributes to context-induced re

110 ease in conductance and number of functional postsynaptic receptors contributing to single quanta.

111 c inputs to shape the subunit composition of postsynaptic receptors could be an important mechanism f

112 Therefore, reductions in postsynaptic receptor density and compromised presynapti

113 of muscle cells and thus the maintenance of postsynaptic receptor density and synaptic function.

114 Our findings indicate that the reduced postsynaptic receptor density resulting from defective r

115 astoid muscles with shRNA, we found that the postsynaptic receptor density was dramatically reduced,

116 in quantal efficacy associated with reduced postsynaptic receptor density.

117 s) is critical for the maintenance of a high postsynaptic receptor density.

118 een neighboring synapses, thereby minimizing postsynaptic receptor desensitization and improving sens

119 lls (HBC(R)s) in the salamander retina evade postsynaptic receptor desensitization by using (1) multi

120 ime how a tonic glutamatergic synapse avoids postsynaptic receptor desensitization, a strategy that m

121 n unitary quantal size, which was not due to postsynaptic receptor desensitization.

122 y was increased, suggesting that it reflects postsynaptic receptor desensitization.

123 ransmitter neurons extends beyond actions on postsynaptic receptors, due in part to differential spat

124 glutamate is a strong negative regulator of postsynaptic receptor field size and function during dev

125 onsible for initiation or maintenance of the postsynaptic receptor field.

126 dulation of the presynaptic active zones and postsynaptic receptor fields mediating synaptic function

127 on that prevents activity-induced changes in postsynaptic receptor fields.

128 (2) What is the occupancy of postsynaptic receptors following the release of a synapt

129 onstrains DA availability at presynaptic and postsynaptic receptors following vesicular release and i

130 GABAA receptors (GABAARs), the main postsynaptic receptors for GABA, have been recently demo

131 perates through an increase in the number of postsynaptic receptors for the excitatory neurotransmitt

132 Postsynaptic receptors formed alpha1/beta-containing clu

133 rmally triggered as a result of reduction in postsynaptic receptor function at the Drosophila larval

134 her in retrograde signaling or in regulating postsynaptic receptor function or both, contribute to LT

135 in neurotransmitter release probability and postsynaptic receptor function, remodeling of GABAergic

136 lity, Ca2+-triggered presynaptic release, or postsynaptic receptor functions.

137 nsmitter diffusion and its interactions with postsynaptic receptors have been used to study propertie

138 on of DA synthesis-a possible consequence of postsynaptic receptor hypersensitivity, or increased ext

139 sts (e.g., terguride) may not affect D2-like postsynaptic receptors in an adult-typical manner during

140 it contribution in the molecular assembly of postsynaptic receptors in cerebellar glomeruli is respon

141 mission such as presynaptic transporters and postsynaptic receptors in living human brains.

142 d subunit composition of GABA(A) and glycine postsynaptic receptors in one example of gephyrin-rich s

143 ) in the terminals of nociceptors as well as postsynaptic receptors in spinal neurons regulate the tr

144 g between neurotransmitter release sites and postsynaptic receptors in synaptic transmission.

145 olves presynaptic protein kinases as well as postsynaptic receptor insertion.

146 tamate receptor field, and that the level of postsynaptic receptors is closely dependent on presynapt

147 The maintenance of a high density of postsynaptic receptors is essential for proper synaptic

148 The spatial organization of postsynaptic receptors is likely to determine many funct

149 ntaneous release, indicating a population of postsynaptic receptors is uniquely activated by this mod

150 for the tonic current changes and can affect postsynaptic receptor kinetics with a loss of paired-pul

151 Thus, a decrease in postsynaptic receptors leads to an increase in presynapt

152 r a potential link between AChE function and postsynaptic receptor lifetime.

153 Postsynaptic receptor localization is crucial for synaps

154 initial step in synapse disassembly involves postsynaptic receptor loss rather than dendritic retract

155 The presynaptic and postsynaptic receptors may prove to be future targets in

156 ty to alpha3-nAChR targeting due to a unique postsynaptic receptor microheterogeneity - under one pre

157 We demonstrate a unique postsynaptic receptor microheterogeneity on chick parasy

158 mechanisms underlying the establishment of a postsynaptic receptor mosaic on CNS neurons are poorly u

159 al motoneuron soma number or in serotonergic postsynaptic receptor mRNA copy numbers within single-ce

160 that during an IPSC, a substantial number of postsynaptic receptors must be exposed to subsaturating

161 nhibition is determined by the properties of postsynaptic receptors, neurotransmitter release, and cl

162 The heated debate over the level of postsynaptic receptor occupancy by transmitter has not b

163 We conclude that the level of postsynaptic receptor occupancy can depend on the probab

164 In contrast, mGluR1a appears to be a postsynaptic receptor of neurons in the neostriatum, glo

165 might be autoreceptors at afferent synapses, postsynaptic receptors of a putative efferent system, or

166 that an increased alpha1 subunit assembly in postsynaptic receptors of cerebellar inhibitory synapses

167 synapse, ELFN1 binds in trans to mGluR6, the postsynaptic receptor on rod ON-bipolar cells.

168 ed by enhancement of release, enhancement of postsynaptic receptors, or both.

169 revealed that endocytosis and exocytosis of postsynaptic receptors play a major role in the regulati

170 resynaptic vesicular release of transmitter, postsynaptic receptor populations and clearance/inactiva

171 ptic release probability, demonstrating that postsynaptic receptor properties can contribute to facil

172 remaining axon did not reoccupy a site, the postsynaptic receptors rapidly disappeared.

173 three classes may reflect different types of postsynaptic receptor rather than dendritic location.

174 dominant interactors play important roles in postsynaptic receptor recycling.

175 Postsynaptic receptor saturation also accelerates recove

176 2+) influx, initial release probability, and postsynaptic receptor saturation and desensitization.

177 These findings establish that MVR and postsynaptic receptor saturation can influence transmiss

178 Thus, postsynaptic receptor saturation interacts with presynap

179 the univesicular release constraint and the postsynaptic receptor saturation lead to a limited amoun

180 We find that postsynaptic receptor saturation makes it difficult to d

181 As MVR increases the likelihood of postsynaptic receptor saturation, it is of interest to c

182 easable vesicle per active zone, and (3) the postsynaptic receptor saturation.

183 ltivesicular release (MVR) in the absence of postsynaptic receptor saturation.

184 e in excitatory neurons was accounted for by postsynaptic receptor saturation.

185 mechanisms of neurotransmitter exocytosis or postsynaptic receptor sensitivity did not contribute to

186 ltiple low-probability release sites, robust postsynaptic receptor sensitivity, and efficient transmi

187 ue to increased dopamine release or enhanced postsynaptic receptor sensitivity.

188 correlated with compensatory adaptations of postsynaptic receptor sensitivity.

189 ction may serve as an important modulator of postsynaptic receptor sensitivity.

190 ns to control muscle cells, without altering postsynaptic receptor sensitivity.

191 Surface diffusion of postsynaptic receptors shapes synaptic transmission.

192 ce a relatively low concentration of GABA at postsynaptic receptors, similar to slow IPSCs in mature

193 of schizophrenia involves blocking dopamine postsynaptic receptor sites, the authors investigated th

194 lso tested the hypothesis that variations in postsynaptic receptor subtype distribution between speci

195 ortical neurons as a result of variations in postsynaptic receptor subtypes as well as the types of n

196 e is controlled by the type of glutamatergic postsynaptic receptor that is expressed on their dendrit

197 male mice results in part from GIRK2-coupled postsynaptic receptors that are activated by endogenous

198 acts as a negative regulator of its cognate postsynaptic receptor to sculpt receptor field size.

199 em, moment-to-moment communication relies on postsynaptic receptors to detect neurotransmitters and c

200 eptors to regulate synaptic transmission and postsynaptic receptors to hyperpolarize neurons.

201 Postsynaptic receptor trafficking plays an essential rol

202 l reference, and smaller contacts with fewer postsynaptic receptors were also modeled.

203 At birth postsynaptic receptors were localized in irregular patch

204 hitecture, and the densities of synapses and postsynaptic receptors were normal at the neuromuscular

205 rally insufficient to activate all available postsynaptic receptors, whereas the sum of transmitter f

206 onses is determined by the scatter of target postsynaptic receptors, which in turn depends on recepto

207 involves crosstalk between NMDA and GABA(A) postsynaptic receptors, whose strength is controlled by

208 quires activation of NMDA-type and AMPA-type postsynaptic receptors within the abdominal ganglion, be

209 5, suggesting a high response probability of postsynaptic receptors, without an unusually high releas