ライフサイエンスコーパス: autaptic

1 meostasis was unperturbed, demonstrated that autaptic activity has significant inhibitory effects on

2 Here we report that GABAergic autaptic activity is present in fast-spiking, but not in

3 ects of synaptic transmission differ between autaptic and dissociated cultures, and the synaptic tran

4 te and gamma-aminobutyric acid (GABA) act as autaptic and heterosynaptic presynaptic inhibitory trans

5 nd mIPSC frequencies did not deviate between autaptic and synaptic connections, the frequency of mEPS

6 receptor ligands exhibited 3.8 +/- 1.9 close autaptic appositions.

7 in pyramidal neurons by artificial GABAergic autaptic conductances, suggesting that tightly coupled s

8 ing model of neuronal activity, we study how autaptic connections affect activity patterns, and evalu

9 isolation on glial islands formed functional autaptic connections and continued to elaborate new syna

10 Therefore, in the hippocampus autaptic connections contribute to spike AHPs in many in

11 These results suggest a role of autaptic connections in controlling network-wide bursts

12 pairs formed both interneuronal synaptic and autaptic connections indiscriminately.

13 ns are self-innervated by powerful GABAergic autaptic connections reliably activated after each spike

14 Adding more autaptic connections to excitatory neurons increased the

15 Results show autaptic connections to excitatory neurons with high ave

16 gnificantly affects changes in bursting from autaptic connections.

17 arge numbers of conventional synaptic and/or autaptic contacts that can be easily visualized, making

18 naptic currents were dramatically reduced in autaptic cultures from MALS triple knockout mice due to

19 o different hippocampal neuron preparations: autaptic cultures in which a single isolated cell innerv

20 DSE in autaptic cultures is both more robust and elicited with

21 ed that CB1-dependent DSE can be elicited in autaptic cultures of excitatory hippocampal neurons of t

22 that CB1-dependent DSE can be elicited from autaptic cultures of excitatory mouse hippocampal neuron

23 BDNF) on excitatory synaptic transmission in autaptic cultures of hippocampal CA1 neurons.

24 In autaptic cultures, the total extent of evoked release, s

25 and ABHD6 and determined their expression in autaptic cultures.

26 tatory glutamatergic synapses in hippocampal autaptic cultures.

27 This change occurred without a change in autaptic current kinetics.

28 The autaptic current was abolished by GABA(A) receptor antag

29 epulses reversibly increased fast excitatory autaptic currents (eacs) mediated by alpha-amino-3-hydro

30 ure glia were rendered nonviable, excitatory autaptic currents (EACs) were prolonged in the presence

31 acid (AMPA) receptor component of excitatory autaptic currents (EACs) with an EC50 of 3.8 microM.

32 ak NMDA receptor-mediated (NMDAR) excitatory autaptic currents (EACs) with no effect on the NMDAR EAC

33 aspartate receptors (NMDARs), and inhibitory autaptic currents (iacs) mediated by gamma-aminobutyric

34 Compared to glycine, NMDAR-mediated autaptic currents decayed faster with sarcosine suggesti

35 izing prepulses did not significantly reduce autaptic currents in any neuron studied.

36 d the effect of hyperpolarizing prepulses on autaptic currents in cultured postnatal rat hippocampal

37 An additional requirement for autaptic DSE is filled internal calcium stores.

38 knockdown of DAGLalpha substantially reduces autaptic DSE, shifting the "depolarization-response curv

39 t have a role in determining the duration of autaptic DSE.

40 Autaptic endocannabinoid signalling is rich, robust and

41 dopamine neurons evoked a fast glutamatergic autaptic EPSC that showed presynaptic inhibition caused

42 ls of InsP(6) and occluded the inhibition of autaptic EPSCs by exogenous InsP(6).

43 also decreased paired pulse facilitation of autaptic EPSCs evoked by depolarization, indicating that

44 The InsP(6)-induced inhibition of autaptic EPSCs was effectively abolished by coapplicatio

45 ntibody on the InsP(6)-induced inhibition of autaptic EPSCs.

46 -Astrocyte autaptic evoked EPSCs, but not IPSCs, displayed an alter

47 used a concentration-dependent inhibition of autaptic excitatory postsynaptic currents (EPSCs) in cul

48 me neuron significantly inhibited the evoked autaptic GABA release.

49 itatory postsynaptic currents (EPSCs) in rat autaptic hippocampal cultures.

50 Here, using rat autaptic hippocampal microcultures, we show that memanti

51 N1/GluN2A and GluN1/GluN2B receptors and rat autaptic hippocampal microisland cultures, we show that

52 subunits modulate the synaptic plasticity of autaptic hippocampal neurons (i.e., Ca(v)beta(2a) induce

53 natomical evidence that MGL regulates DSE in autaptic hippocampal neurons and, taken together with ot

54 Cultured autaptic hippocampal neurons exhibit robust DSE.

55 Cultured autaptic hippocampal neurons from S426A/S430A mice showe

56 Finally, in cultured autaptic hippocampal neurons, CRIP1a overexpression atte

57 idine-1-carboxylate (JZL184)] prolong DSE in autaptic hippocampal neurons, whereas inhibition of ABHD

58 e retrograde inhibition via CB1 receptors in autaptic hippocampal neurons.

59 To determine whether autaptic inhibition plays a functional role in the adult

60 y postsynaptic current (IPSC) in a PN and an autaptic IPSC.

61 rons and significantly prolongs the decay of autaptic IPSCs and miniature IPSCs in our cultures.

62 D6 is expressed in two distinct locations on autaptic islands, including a prominent localization in

63 eurons of mouse hippocampal brain slices and autaptic microcultures did not, per se, significantly af

64 Using patch-clamp electrophysiology of autaptic neuronal cultures from Rab3-deficient mouse hip

65 otocol makes it possible to transfect single autaptic neurons as well as mature neurons (15-82 days i

66 estion, we analyzed synaptic transmission in autaptic neurons cultured from RIM1alpha-/- mice.

67 was strongly depressed compared with either autaptic neurons or glutamatergic pairs.

68 ct mEPSC frequencies in either glutamatergic autaptic neurons or in glutamatergic pairs.

69 When expressed in Snap-25-null mouse autaptic neurons, region I mutations reduced the size of

70 ng in vitro assays and rescue experiments in autaptic neurons, we show that interactions within regio

71 otypic" glutamatergic or GABAergic pairs and autaptic neurons.

72 ponsible for a portion of 2-AG production in autaptic neurons.

73 hment rate of the readily releasable pool in autaptic neurons.

74 same drug or one of the others in individual autaptic neurons.

75 Peak autaptic NMDA responses were potentiated to 178.9 +/- 22

76 Thus, well-timed inhibition, whether autaptic or synaptic, facilitates precise spike timing a

77 pocampal neurons in culture, the size of the autaptic readily releasable pool before and after stimul

78 The formation of new cholinergic synapses in autaptic single-cell microcultures is inhibited by SPARC

79 We discovered that autaptic synapses are optimized for maximal transmission

80 ot only interneuronal synapses, but also the autaptic synapses on itself exhibited a trend toward enh

81 ted higher rates of spontaneous release than autaptic synapses.

82 Indeed, blockade of autaptic transmission degraded temporal precision in mul

83 ecise self-inhibition mediated by inhibitory autaptic transmission.

84 These two classes displayed distinct autaptic transmission.