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1 self depending on a transient suppression of spike firing.
2  stress increases basolateral amygdala (BLA) spike firing.
3 ession of conditional increases in CS-evoked spike firing.
4 concentration, cells responded with sporadic spike firing.
5 in equal and independent of the frequency of spike firing.
6 nges in spike waveform during high-frequency spike firing.
7 ng while increasing the frequency of complex spike firing.
8  non-linear patterns in Purkinje cell simple-spike firing.
9 ose mediated by channelrhodopsins or natural spike firing.
10 y without altering the temporal precision of spike firing.
11 overshoot with robust sustained or transient spike firing.
12 ressions were the only significant change in spike firing.
13 entiation of the hump potential to full Ca2+ spike firing.
14 lic period, but which had little relation to spike firing.
15 on but not D2 receptor activation to enhance spike firing.
16 s-induced activation of the LC increases BLA spike firing and causes impairments in extinction learni
17 -mediated modulation of spontaneous neuronal spike firing and CB1R-mediated presynaptic inhibition of
18 reases the frequency of Purkinje cell simple spike firing and decreases the frequency of complex spik
19 sult from cellular depolarization, increased spike firing and enhanced NMDAR-mediated current charge
20 fter training and alters synaptically evoked spike firing and integrative properties of these neurons
21 onship between the learned changes in simple-spike firing and learning in eye velocity suggests an or
22 c HCN channels in pyramidal neurons modulate spike firing and synaptic potential integration by influ
23 reduce spike frequency and curtail sustained spike firing and that these effects entail protein kinas
24 tOH (11-66 mM) also decreased current-evoked spike firing and this was accompanied by a decrease in i
25 tionships, back-propagation-activated Ca(2+) spike firing, and a shift in the critical frequency by b
26 ion of synchronous GABA release, synchronous spike firing, and evoked-gamma power increase with lower
27 ctivity (increased responsiveness, irregular spike firing, and increased burst activity) in SNL rats.
28 eta frequency stimulation, decreased complex spike firing, and reduced the p42/44MAPK-mediated phosph
29 he distinction between synaptic activity and spike firing, and species differences encourage caution
30 evented EtOH's effect on holding current and spike firing, and western blotting revealed the presence
31                                  With simple-spike firing as observed in vivo, the presentation of a
32 e concentration, reflecting the abolition of spike firing at pre-pulse concentrations which still evo
33 threshold to spike and increases the gain of spike firing by 2- to 3-fold.
34 ata suggest that these pathways may increase spike firing by inhibition of a slow A-type potassium cu
35 ns, demonstrating that the changes in simple spike firing can be independent of climbing fiber input.
36 igated the intrinsic membrane properties and spike firing characteristics of rostral ipsi-lesional MV
37 lation on Kv4 channel control of the gain of spike firing depended on a signaling cascade leading to
38 , I(h); how I(h) influences excitability and spike firing depends primarily on channel distribution i
39 es, most fibers increased their frequency of spike firing due to an increase in spontaneous EPSC freq
40 GN and BLA exhibit associative plasticity of spike firing during auditory fear conditioning.
41 h is correlated with the amount of RD-evoked spike firing during the induction protocol.
42                                 Postsynaptic spike firing elicited fast mitochondrial Ca(2+) response
43  lobe vermis and hemisphere have high simple spike firing frequencies that precede complex spikes wit
44 esults indicate that mitochondria decode the spike firing frequency and the Hebbian temporal coincide
45 ts is the modulation of Purkinje cell simple spike firing frequency, which has implications for contr
46 urst firing into physiological tonic, single-spike firing in 6-OHDA rats in vivo.
47 lectrical synapses could promote coordinated spike firing in a cellular assemblage of GnRH1 neurons t
48 roxyglutarate, rapidly synchronized neuronal spike firing in a seizure-like manner, but only when non
49 iring and decreases the frequency of complex spike firing in adult behaving mice.
50                              Rates of simple spike firing in both on-beam and off-beam Purkinje cell
51 in, a selective SK channel blocker, affected spike firing in hippocampal neurons in different ways.
52          The results demonstrate that simple spike firing in lobules IV-VI is significantly correlate
53 e show that dopamine-mediated enhancement of spike firing in NAcb shell medium spiny neurons was prev
54  The two optoXRs exerted opposing effects on spike firing in nucleus accumbens in vivo, and precisely
55  show that a dopamine-induced enhancement of spike firing in nucleus accumbens neurons in brain slice
56 s of odorant receptors, inhibiting the basal spike firing in olfactory sensory neurons.
57  mice showed increased sensory-evoked simple spike firing in positively modulating PCs, consistent wi
58                                  Synchronous spike firing in previously silent neurones could be driv
59             In this manner, I(h) can enhance spike firing in response to an EPSP when spike threshold
60 cal blockade of I(h) significantly increased spike firing in RTN neurons and large spontaneous IPSC f
61 ransmission and the consequent STN-triggered spike firing in SNr neurons.
62                     Contextual modulation of spike firing in the amygdala is a putative mechanism for
63  (LC)-NE regulates stress-induced changes in spike firing in the BLA and consequent extinction learni
64 periments that dissociate auditory CS-evoked spike firing in the lateral amygdala (LA) and both condi
65 d a substantial increase in both CS-elicited spike firing in the MGN and conditional freezing behavio
66 onditioning-related increases in CS-elicited spike firing in the MGN and conditional freezing to the
67  attenuates the ability of the vSub to drive spike firing in the NAc.
68 ppear to mediate dopaminergic enhancement of spike firing in the NAcb shell, and may therefore play a
69 oscillations were suppressed, while thalamus spike firing increased, associated with rapid mouse whis
70 ruleus mimics this shift in reciprocal IL-PL spike firing, increases the expression of conditioned fr
71 g, and immunohistochemistry, we find that 1) spike firing is inhibited by dopamine and SKF 83959 (an
72  of the cerebellar cortex, changes in simple spike firing likely reflect the contribution of the cere
73 wed modulation of synaptic potentials and/or spike firing locked to the oscillation produced by venti
74 a concise model of the synaptic input driven spike firing mechanism that gives a close quantitative m
75 slices, by combining patch-clamp analysis of spike firing, membrane currents and synaptic inputs with
76 lative physiological importance of different spike-firing modes remains unclear.
77 e microscope films oxygen-carrying blood and spike-firing neurons across the mouse cortex in real tim
78                      In contrast, the simple spike firing of 91.0% of the Purkinje cells was not sign
79           Two sets of analyses of the simple spike firing of 97 Purkinje cells examined the effects o
80 r the expression of plasticity in the simple-spike firing of cerebellar Purkinje cells during trial-o
81 ll three monoamines decreased current-evoked spike firing of lOFC neurons and this action required Gi
82 hat ethanol inhibits persistent activity and spike firing of PFC neurons and that the degree of ethan
83 s occur in both the simple spike and complex spike firing of Purkinje cells.
84 id not yield increases in either CS-elicited spike firing or freezing to the tone CS.
85 urons in model networks may exhibit periodic spike firing or synchronized membrane potentials that gi
86  show that intrinsic plasticity enhances the spike firing output of Purkinje cells and persists over
87 voked, as well as the depolarization-induced spike firing pattern of ganglion cells.
88 lates On and Off EPSPs, and the light-evoked spike firing pattern of On-Off ganglion cells.
89 s of neuropeptide Y (NPY) and exhibit a late-spiking firing pattern, with extensive local connectivit
90 ble of supporting a diversity of multineuron spike firing patterns from overlapping sets of neurons.
91  constant-velocity motion produces irregular spike firing patterns, and spike counts typically have a
92 gating to regulate membrane excitability and spike firing patterns.
93 ns were not simply movement-related in their spike-firing patterns but instead were selectively modul
94 tex, and they also had similar accommodating spike-firing patterns.
95 and a larger DAP amplitude, and enhanced the spike-firing precision and reliability of the calyx term
96                                 However, the spike firing properties of individual cortical neurons f
97 lectrodes, cell resting potential (V(m)) and spike firing properties were unaffected over 10-15 min r
98 Purkinje cells uncovered an increased simple spike firing rate and decreased modulation of firing dur
99 hways; 2) complex-spike responses and simple-spike firing rate are correlated across the Purkinje cel
100  the Purkinje cell population; and 3) simple-spike firing rate at the time of an instruction for lear
101 epetitions of a learning instruction, simple-spike firing rate becomes progressively depressed in Pur
102 e found to increase or decrease their simple spike firing rate during microsaccades.
103 onse to a learning instruction causes simple-spike firing rate of Purkinje cells in the floccular com
104 nesthetized adult rats demonstrated that the spike firing rate was increased by the GluN2C/D potentia
105 on, resulting in a nonlinear increase in the spike firing rate, particularly at temperatures above ap
106 hich information is contained in the average spike firing rate.
107 ciated with a subsequent reduction in simple spike firing rate.
108 nce always reflected a significant change in spike firing rate.
109 consistently increased the action potential (spike) firing rate of oxytocin neurones in urethane-anae
110 lation of Purkinje cell membrane current and spike-firing rate.
111 s of spikelets are preceded by higher simple spike firing rates but, following the complex spike, sim
112  greater pressure-dependent increases in ACC spike firing rates in EA rats compared with controls.
113 se including sound evoked potentials and the spike firing rates of AC neurons were recorded right aft
114 position of the cursor was controlled by the spike firing rates recorded from the same site.
115 in primary visual cortex, V1, increase their spike firing rates to signal image segmentation and atte
116 ed increases in contrast by decreasing their spike firing rates, two types of inhibitory neurons in t
117 oth K+ channel blockers increased average CS spike-firing rates.
118 report that modulation targets properties of spike firing rather than action potential shape, involve
119      In a majority of Purkinje cells, simple spike firing recorded before and during adaptation demon
120 ynaptic mechanisms that enable this accurate spike firing remain poorly understood.
121 owed by an intact post-burst pause of single spike firing, resulting in a temporal discoordination of
122            Analysis of Purkinje cell complex spike firing revealed that feedback in the cerebellar nu
123               The dose-response relation for spike firing rose at lower odour concentrations than the
124 ty of LA neurons exhibited context-dependent spike firing; short-latency spike firing was greater to
125 aneously recorded neurons synchronized their spike firing similarly during both the high-gamma-band a
126 GDP-beta-S, DA induced a further decrease in spike firing, suggesting the involvement of a non-GIRK c
127 ptors mediate stress-induced changes in mPFC spike firing that contribute to extinction impairments.
128 sistently decreased ( approximately 22%) and spike firing threshold (V(th)) was raised ( approximatel
129  EPSPs and bringing the neuron closer to the spike-firing threshold than the callosal pathway.
130 )-mediated Ca(2+) signals strongly inhibited spike firing through activation of K(+) membrane conduct
131 ngle BLA neurons exhibit robust increases in spike firing to both recent and remote conditioned stimu
132 til, at the highest pre-pulse concentrations spike firing was abolished despite the continued presenc
133 ontext-dependent spike firing; short-latency spike firing was greater to both CSs when they were pres
134  In this regard, dopaminergic enhancement of spike firing was prevented by inhibitors of protein kina
135                           EtOH inhibition of spike firing was prevented by the GABAA antagonist picro
136                       Thus, the structure of spike firing was reorganized during learning in relation
137 r, conditioning-related changes in CS-evoked spike firing were solely determined by the associative h
138 eptors (D1R and D2R), and that MCH increases spike firing when both D1R and D2R are activated.
139  responses, as well as in action potential ("spike") firing, wherein all mitral cells affiliated with
140 eases the regularity of Purkinje cell simple spike firing while increasing the frequency of complex s

 
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