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1 tagonists, kainate lowered the threshold for antidromic action potential generation, suggesting that
2           The dorsal root reflex (DRR) is an antidromic action potential originating in the spinal co
3 ould be recorded at the granule cell soma as antidromic action potentials and from the axons with a n
4                                     However, antidromic action potentials are recruited at lower thre
5 ilaments were determined either by recording antidromic action potentials from the tooth or by using
6 creased and both postsynaptic potentials and antidromic action potentials propagated farther.
7 we observed that postsynaptic potentials and antidromic action potentials propagated less far within
8 on was demonstrated by somatic recordings of antidromic action potentials.
9 Kainate application also induced spontaneous antidromic action potentials.
10                                     However, antidromic activation (mossy fiber stimulation) evoked a
11    Recorded neurons were classified by their antidromic activation and by their changes in firing rat
12              Over 4 h of continuous STN DBS, antidromic activation became less robust, whereas therap
13 ivity over time, and differences in observed antidromic activation between animals and target sites w
14 phase of STN DBS, the difference in observed antidromic activation between animals, and target sites,
15             Neurons were identified by their antidromic activation from contralateral facial and acce
16             Neurons were identified by their antidromic activation from facial nucleus (FN) or red nu
17  latencies to trigeminal ganglion shocks and antidromic activation from thalamus or cerebellum were a
18                     Neurones were tested for antidromic activation from the contra- and ipsilateral v
19                  Neurones were identified by antidromic activation from the contralateral thalamus, a
20   The rmPFC neurons were identified by their antidromic activation from the mediodorsal nucleus and/o
21 vation between animals and target sites with antidromic activation not observed during GPi DBS, raise
22 ) deep brain stimulation (DBS) may depend on antidromic activation of cortex via the hyperdirect path
23 ially by driving recurrent inhibition though antidromic activation of corticostriatal axon collateral
24 ations in the orbitofrontal cortex (OFC) via antidromic activation of corticostriatal recurrent inhib
25                                 Furthermore, antidromic activation of electrical activity in the cell
26                                              Antidromic activation of ganglion cell axons also increa
27        Our results suggest a contribution of antidromic activation of M1 during STN DBS in disrupting
28        This study tested the hypothesis that antidromic activation of M1 is a prominent feature under
29 et had similar therapeutic effects, however, antidromic activation of M1 was only observed during STN
30 tablished inflammation, a consequence of the antidromic activation of nociceptor peripheral terminals
31                   Previous studies show that antidromic activation of sensory fibers is an important
32 s mediated by peripheral release of CGRP via antidromic activation of sensory fibers.
33 lation through sympathetic inhibition and/or antidromic activation of sensory fibers.
34 sodilation at >or=90% of MT may also involve antidromic activation of some unmyelinated C-fibers.
35  cartwheel cells were recorded to ortho- and antidromic activation of the granule cells (i.e., by sti
36 r were further identified as mitral cells by antidromic activation of the lateral olfactory tract and
37 s remain unclear, it has been suggested that antidromic activation of the primary motor cortex (M1) p
38 e if SCS produces cutaneous vasodilation via antidromic activation of the unmyelinated C-fibers and/o
39 ere located and identified by the electrical antidromic activation of their constituent motoneurons.
40               Our previous studies show that antidromic activation of transient receptor potential va
41      Retrograde and anterograde labeling and antidromic activation of vBNST neurons by VTA stimulatio
42                                           In antidromic activation studies, mu-opioids inhibited a su
43 ic tract (STT) neurons were identified using antidromic activation techniques and examined for their
44  this projection in rats using the method of antidromic activation to map the axon terminals of neuro
45                                     Although antidromic activation waned over time, synchronization o
46 entified as NTS or DMN using orthodromic and antidromic activation, respectively, following vagal sti
47 injured neuronal circuits is the same during antidromic activation, stimulation of granule cell axons
48 ated STN activity, rather than inhibition or antidromic activation.
49 urons were identified as septohippocampal by antidromic activation.
50  reflex (DRR) and the axonal reflex (AR) are antidromic activities in primary afferents and are invol
51 l neuronal populations; however, diminishing antidromic activity over time, and differences in observ
52 striatal stimulus current necessary to evoke antidromic activity.
53 ycles in the extended network (heterodromic, antidromic and homodromic), which represents a unifying
54 linked micropipette-microwire recording, and antidromic and orthodromic activation from the ventral t
55 ey rats demonstrated reciprocal interinsular antidromic and orthodromic activation, elicited with sim
56 ical stimulation of the reuniens evoked both antidromic and orthodromic intracellular mPFC responses,
57 ypoxia and 1 hour wash-out of the inhibitors antidromic and orthodromic responses were still blocked
58                                              Antidromic block can cause acceleration due to double-wa
59 riod, and was associated with unidirectional antidromic block of the paced impulse.
60                                              Antidromic CAPs of C-fibers in dorsal roots were evoked
61                               In Protocol 3, antidromic CAPs of the dorsal root were measured in resp
62 al electrode simultaneous down and upstream (antidromic) capture of a confined isthmus of slow conduc
63                                              Antidromic (centrifugal) conduction of these spikes may
64 h participate with substrate glutamine in an antidromic circular arrangement of hydrogen bonds, cause
65 imilar beneficial effects, the proportion of antidromic-classified cells in each differed, 30 versus
66                               In Protocol 2, antidromic compound action potentials (CAPs) of the tibi
67 p junctions between AVA and A-MNs only allow antidromic current, but, curiously, disrupting them inhi
68 ger at shorter V1V2 intervals, but a shorter antidromic delay in the area of unidirectional block for
69                        Bursts of spontaneous antidromic dorsal root action potentials, and evoked dor
70  nerve to block both orthodromic signals and antidromic DRRs without affecting ARs.
71                                      We used antidromic electrical stimulation to identify V1 neurons
72                                   Capture of antidromic electrophysiological responses to thalamic st
73                                 Finally, the antidromic ERG recordings obtained in our implanted volu
74 were recorded using 16 scalp electrodes, and antidromic ERGs were obtained using DTL electrodes while
75 ese responses could not be attributed to the antidromic firing of corticothalamic cells, intrathalami
76                      The possible effects of antidromic firing on synaptic strength are unknown.
77         Synaptic stimulation delivered after antidromic firing, which was otherwise too weak to induc
78 glutamate released from its own dendrites by antidromic impulse invasion, or/and lateral excitation b
79  this site was likely to produce block of an antidromic impulse, which may initiate double-wave reent
80 us motoneurons were also smaller, had longer antidromic latencies and a lower synaptic coverage than
81       There was no significant difference in antidromic latencies between Type I (m = 1.47 msec) and
82                                     The mean antidromic latency from the L1 level was 42.8 +/- 4.4 ms
83 t discount the potential therapeutic role of antidromic M1 activation at least in the acute phase of
84 on site and distally through orthodromic and antidromic mechanisms for several stimulation frequencie
85 ng neuroendocrine GABA neurons identified by antidromic median eminence stimulation.
86                                 Here, we use antidromic methods to identify corticotectal neurons in
87                                              Antidromic (n=35), monosynaptic (n=2), di-or tri-synapti
88     Both during normal bursting activity and antidromic nerve stimulation, the conduction delay over
89  sites adjacent to infection that depends on antidromic neuron activation.
90                               A mechanism of antidromic passage of depolarizing current from a neuron
91                                              Antidromic population events in subiculum were single sp
92 for 35 min after trauma injury, improved CA1 antidromic population spike (PS) recovery to 91 +/- 2%,
93                                              Antidromic population spikes confirmed projections from
94                                              Antidromic potentials are larger if the afferent is clos
95 epending on the injury level), 1-2 ms before antidromic potentials were elicited in motor neurons by
96 pagation of V2 around the line of block, and antidromic propagation through the original location of
97 ion of the lateral olfactory tract evoked an antidromic pulse followed by a short EPSP, which could a
98                                   The use of antidromic-rectifying gap junctions to amplify chemical
99 generated to locomotion interneurons through antidromic-rectifying gap junctions.
100 so released from sensory-motor nerves during antidromic reflex activity, to produce relaxation of som
101 of nociceptors mediates inflammation through antidromic release of neuropeptides into infected or inj
102 flammation is believed to originate with the antidromic release of substance P, and of other neurokin
103                            The proportion of antidromic responses consisting of full spikes from anti
104 hose neurons projecting to MT, identified by antidromic responses to electrical stimulation of MT.
105                                   Reciprocal antidromic responses were absent.
106                         We hypothesized that antidromic spike failure contributes to the cortical des
107                   These findings reveal that antidromic spike failure plays a critical role in mediat
108                                              Antidromic spike failure shaped the parabolic relationsh
109                        We modeled stochastic antidromic spike failure to determine how spike failure
110 h could also be elicited independently of an antidromic spike in the recorded cell.
111                                 Although the antidromic spike latency of the single-spiking and burst
112 m depression between synaptically evoked and antidromic spike trains emphasize that the properties of
113 s was compared quantitatively to that during antidromic spike trains evoked by electrical stimulation
114 naptic spike width that did not occur during antidromic spike trains under physiological calcium conc
115 kes in a burst could be made to collide with antidromic spike.
116 generated rhythmic barrages (up to 25 Hz) of antidromic spikes during BMPs.
117                During BMPs the soma received antidromic spikes generated in processes in the buccal g
118 , we used optogenetic stimulation to trigger antidromic spikes in a local region of primary visual co
119 lation of the medial forebrain bundle evoked antidromic spikes in both burst-firing neurones and in s
120 firing neurones and classical 5-HT neurones, antidromic spikes made collisions with spontaneously occ
121                 Plateau potentials after the antidromic spikes or local cerebral inputs will locally
122                        During the barrage of antidromic spikes, high-frequency firing will produce st
123 curred spontaneously (53%) or in response to antidromic stimulation (81%).
124 ses in Ca(2+) transients evoked by light and antidromic stimulation are blocked by the purinergic ant
125 r pharmacological gap junction blockade, but antidromic stimulation could not drive activity in contr
126  in a small number of burst-firing neurones, antidromic stimulation evoked spike doublets, similar to
127 ioid, GABA(A), and NK1 receptor antagonists, antidromic stimulation of a population of striatal proje
128                                              Antidromic stimulation of cardiac sensory C fibers relea
129 rneurons in the medial prefrontal cortex via antidromic stimulation of cortico-accumbal afferents.
130         Skin blood flow was monitored during antidromic stimulation of identified cutaneous C fibres
131 dromic stimulation of the olfactory nerve or antidromic stimulation of mitral and tufted (M/T) cells.
132                           Here, we show that antidromic stimulation of motor axons evokes depolarizin
133  and recorded recurrent IPSPs in response to antidromic stimulation of motor axons.
134 ntial [total motor activity (TMA)] evoked by antidromic stimulation of the distal ventral root.
135  In bicuculline (10 microM) and 6 mM [K +]o, antidromic stimulation of the granule cells evoked burst
136 ith extracellular field potentials following antidromic stimulation of the lateral olfactory tract (L
137 es on granule cells that can be activated by antidromic stimulation of the lateral olfactory tract (L
138 ing bursts of action potentials generated by antidromic stimulation of the mossy fibers.
139                     They can be activated by antidromic stimulation of the trigeminal nerve, as well
140 furcating axon collaterals in the chicken by antidromic stimulation of two sites along each branch an
141 ctivation of sensory nerve fibers, either by antidromic stimulation or capsaicin, depolarized these n
142 ive green fluorescent protein expression and antidromic stimulation or retrograde Evans blue dye trac
143 ptic to local glutamatergic neurons, we used antidromic stimulation to reveal that many of these cell
144                            Furthermore, such antidromic stimulation was adequate to rescue "tagged" s
145                                Additionally, antidromic stimulation-induced intracellular [Na(+)] inc
146 eutic NAc-DBS might exert its effect through antidromic stimulation.
147 s activation of a pool of identified SPNs by antidromic stimulation.
148 he contralateral thalamus were determined by antidromic stimulation.
149 +) activity were recorded in area CA3 during antidromic stimulation.
150 ic transmission are much more effective than antidromic stimuli that do not.
151                                           In antidromic studies, NA dose-dependently increased firing
152 e refractoriness followed by resetting of an antidromic tachycardia (AT) in patients with decremental
153 rats was significantly greater, and the mean antidromic threshold was significantly lower than in con
154 tion requires a sufficient excitable gap and antidromic unidirectional block of the paced impulse in
155 res were tested for their ability to produce antidromic vasodilatation.
156   These effects were potent: the area of the antidromic volley evoked in the sural nerve by intraspin

 
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