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1  blockade likely increased excitability by a postsynaptic action.
2 ppears to be a more important determinant of postsynaptic action.
3 een the morphology of an interneuron and its postsynaptic action.
4 yperpolarized the cells, suggesting a direct postsynaptic action.
5 in a Ca2+-free solution, indicating a direct postsynaptic action.
6 tetrodotoxin (1 microm), indicating a direct postsynaptic action.
7 sting that this inhibition was mediated by a postsynaptic action.
8  by mechanistically distinct presynaptic and postsynaptic actions.
9 ease glutamate transmission by both pre- and postsynaptic actions.
10 l documented, little is known about possible postsynaptic actions.
11  influences of release yet have antagonistic postsynaptic actions.
12 ic synthesis, vesicular storage, release and postsynaptic actions.
13 released from multiple sites has independent postsynaptic actions.
14 , including those of dynorphin A release and postsynaptic actions, and of CGRP secretion.
15       The convergence or divergence of these postsynaptic actions awaits further investigation.
16 findings provide evidence for segregation of postsynaptic actions between two targets of RT cells and
17 3 receptor activation may be partly a direct postsynaptic action but part may also be due to facilita
18                                      Lack of postsynaptic action currents in the mutants suggests tha
19 hin inhibits the hypocretin system by direct postsynaptic actions (hyperpolarization, decreased spike
20                           Noc has inhibitory postsynaptic actions in CA1, CA3, and the dentate and se
21  have therapeutic effects through unexpected postsynaptic actions in dlPFC, strengthening synaptic co
22 e release of serotonin (5HT) or increase the postsynaptic action of 5HT.
23            While much is now known about the postsynaptic action of neurosteroids, far less is known
24 orporation of synaptic NMDARs and document a postsynaptic action of this major SNARE protein relevant
25 alyze the relative contributions of pre- and postsynaptic actions of a particular gene product in neu
26 ession during hypoxia/cerebral ischemia, but postsynaptic actions of A1Rs are less clear.
27 les to differentiate between presynaptic and postsynaptic actions of BDNF.
28 ese mice, GABAB activity and presynaptic and postsynaptic actions of ethanol were investigated.
29 ynaptic potential blockade demonstrated that postsynaptic actions of Hcrt/Orx alone could evoke prolo
30                                              Postsynaptic actions of NPY, mediated by both Y1- and Y2
31         GAL has been shown to antagonize the postsynaptic actions of other cosecreted neurotransmitte
32 erally for discriminating presynaptic versus postsynaptic actions of other neurotransmitters and neur
33 h pharmacological studies have described the postsynaptic actions of vestibular efferent stimulation
34  however, the ability of GAL to modulate the postsynaptic actions of VP has not been assessed.
35                             We also studied 'postsynaptic' actions of these drugs through their modul
36 gic dendrites and, thus, implicates abundant postsynaptic action on GABAergic neurons via M(2).
37 ind that ACh produces significant excitatory postsynaptic actions on young MGB neurons, probably medi
38                                        mGluR postsynaptic actions over spinal neurons display the pha
39        In knockout mice, the speed of pre-to-postsynaptic action potential (AP) transmission was redu
40 nt neurotransmitter is released to trigger a postsynaptic action potential (AP).
41 electrically compact granule cells, a single postsynaptic action potential can retard escape of gluta
42 of the amygdala (LA) is only modified when a postsynaptic action potential closely follows a synaptic
43 ited high probability of firing a well timed postsynaptic action potential during high-frequency stim
44  synaptic potentiation that does not require postsynaptic action potential firing in the axon.
45 wn whether LTP can be induced by patterns of postsynaptic action potential firing that occur in these
46  drive day/night differences in constitutive postsynaptic action potential firing.
47  of presynaptic activity properly timed with postsynaptic action potential output can not only increa
48 o prevented synaptic potentiation induced by postsynaptic action potential trains.
49 r some conditions, information regarding the postsynaptic action potential, carried by backpropagatin
50 ity exploiting the time relationship between postsynaptic action potentials (APs) and EPSPs.
51               Repeated induction of pre- and postsynaptic action potentials (APs) at a fixed time dif
52                    Ca2+ signals triggered by postsynaptic action potentials (APs) drive the induction
53 y postsynaptic potentials (EPSPs) led single postsynaptic action potentials (APs) within a narrow tem
54 chanisms that link glutamatergic signalling, postsynaptic action potentials and inhibitory synaptic s
55 larized (LTP) or hyperpolarized (LTD) and no postsynaptic action potentials are evoked.
56 lso show that coincident individual pre- and postsynaptic action potentials are only capable of induc
57 n re-established the effectiveness of single postsynaptic action potentials at inducing LTP in adult
58 ring single presynaptic activity with single postsynaptic action potentials at low stimulation freque
59   Presynaptic stimulation paired with single postsynaptic action potentials became progressively less
60 ong-term potentiation (LTP), indicating that postsynaptic action potentials can modulate synaptic pla
61 ptic potentials (EPSPs) were paired with two postsynaptic action potentials in a theta-burst pattern,
62 tem inputs can be recorded concurrently with postsynaptic action potentials in inferior colliculus (I
63  postsynaptic MNTB neurons and induced extra postsynaptic action potentials in response to presynapti
64 lying oscillatory somatic [Ca2+]i by evoking postsynaptic action potentials in SCN neurons during a p
65                   Near coincidental pre- and postsynaptic action potentials induce associative long-t
66  STDP rule in which pairs of single pre- and postsynaptic action potentials induce synaptic modificat
67     Initially, the timing of presynaptic and postsynaptic action potentials must be translated into s
68  mainly contribute to variable delays in the postsynaptic action potentials of PCs while modulated by
69 ned by the precise timing of presynaptic and postsynaptic action potentials on a millisecond timescal
70 thermore, coincident synaptic activation and postsynaptic action potentials rapidly restrict diffusio
71 z and that the timing of individual pre- and postsynaptic action potentials relative to one another i
72  and a step increase in the number of evoked postsynaptic action potentials, both consistent with a r
73               When glutamate was paired with postsynaptic action potentials, however, the NMDA-recept
74 synaptic glutamate receptors, and 26% was on postsynaptic action potentials, in approximate accord wi
75 tion rate; however, pairs of presynaptic and postsynaptic action potentials, repeated at frequencies
76 nearby synapses and activity coincident with postsynaptic action potentials, respectively.
77 llowed 30 ms later by depolarization-induced postsynaptic action potentials.
78  critically on the timing of presynaptic and postsynaptic action potentials.
79 ptic stimulation, and the timing of pre- and postsynaptic action potentials.
80 fficacy can depend on the timing of pre- and postsynaptic action potentials.
81 modified according to the timing of pre- and postsynaptic action potentials.
82 , depends on the relative timing of pre- and postsynaptic action potentials.
83 by STDP compete for control of the timing of postsynaptic action potentials.
84 ly increased likelihood of firing well-timed postsynaptic action potentials.
85 o the rate and the timing of presynaptic and postsynaptic action potentials.
86 ugh glutamate and GABA have clearly distinct postsynaptic actions, we are just beginning to appreciat
87                         Both presynaptic and postsynaptic actions were specific because they were not
88 atergic transmission through a CRF1-mediated postsynaptic action, whereas Ucn I facilitated synaptic