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1 al consequences that follow injury to the L5 spinal nerve.
2 cord from single C-fiber afferents in the L4 spinal nerve.
3 taneous activity after transection of the L5 spinal nerve.
4 rve after ligation and transection of the L5 spinal nerve.
5 uting fibers come primarily from the injured spinal nerve.
6 e situated in characteristic regions of each spinal nerve.
7 uropathic pain induced by ligation of the L5 spinal nerve.
8 in the neural tube, or the fasciculation of spinal nerves.
9 ighboring, uninjured afferents from adjacent spinal nerves.
10 fasciculation of several cranial nerves and spinal nerves.
11 as induced by ligation of the left L(5)/L(6) spinal nerves.
12 itary chemoreceptor cells innervated only by spinal nerves.
13 nd the dorsal fin papillae are innervated by spinal nerves.
14 were removed with attached dorsal roots and spinal nerves.
15 located only on areas innervated by cervical spinal nerves.
16 duced increase in TH-IR fibres within lumbar spinal nerves.
17 pheral nerves by tight ligation of the L5/L6 spinal nerves.
18 c rats with tight ligations of the L5 and L6 spinal nerves.
19 2) that develop predominantly on cranial and spinal nerves.
20 ide, which receives both uninjured L4 and L5 spinal nerves.
21 d by conduction defects and demyelination in spinal nerves.
22 in the lumbar dorsal root ganglia and lumbar spinal nerves 14 days following continuous intrathecal i
23 oved along with the dorsal root (DR) and the spinal nerve 7-14 days after spinal nerve ligation in th
24 nd cut proximal to the previously ligated L5 spinal nerve -- a process which would transect the regen
25 trophy in brainstem, spinal cord tracts, and spinal nerves accompanied by cerebellar hypoplasia was o
27 nerve fiber recordings were made from the L4 spinal nerve after ligation and transection of the L5 sp
28 central processes of sensory neurons (in the spinal nerve and dorsal root), ganglionic transplantatio
29 diamidino yellow) were injected into the L5 spinal nerve and DRG, respectively, the number of double
31 ted in the dorsal root ganglion of the third spinal nerve and enter the brainstem through its dorsal
32 and requires neurogenic signaling involving spinal nerves and activation of cardiac sensory and symp
33 ed in the Schwann cell lineage in developing spinal nerves and in adult trigeminal and sciatic nerves
36 as sensory and motoneuron axons meet in the spinal nerves and travel into the limb, sensory axons re
37 pproach that targets peripheral (cranial and spinal) nerves and utilizes their afferent pathways as s
38 ung model (i.e., tight ligation of L5 and L6 spinal nerves) and a diabetic neuropathy model (i.e., st
39 of neuropathic pain (ligations of the L5/L6 spinal nerves) and explored the relative contributions o
40 atory changes in the central nervous system, spinal nerves, and dorsal root ganglia (DRG) of rhesus m
41 , at the nerve/CNS interfaces of cranial and spinal nerves, and in somitic/intersomitic regions along
42 ateral motor column (LMC) motor axons within spinal nerves are defasciculated as they grow toward the
46 he compound action potential recorded in the spinal nerves, as well as the paw withdrawal threshold.
47 hold afferents proximal to the axotomized L5 spinal nerve attenuated the spontaneous activities in L4
50 following groups of rats: (1) untreated; (2) spinal nerve axotomy (SNA), L5 SNA 1 week earlier; (3) m
51 avid lesions not only were found in impinged spinal nerves but also were associated with nonspinal ca
54 ells and other endoneurial components of rat spinal nerve contain serine racemase, and western blot a
55 directly supports the hypothesis that the L4 spinal nerve contributes to L5 ligation neuropathic pain
56 dystonia musculorum mouse, exhibiting rapid spinal nerve degeneration, dystonic movements, and sever
57 rimates which had a tight ligation of the L7 spinal nerve demonstrated a variety of neuropathic sympt
58 that uninjured C-fiber nociceptors in the L4 spinal nerve develop spontaneous activity after transect
59 gnathous pattern was not observed, such that spinal nerve development extends through the pygostyle r
61 initial position of a cutaneous axon in the spinal nerves does not strictly determine its subsequent
62 s nerves showed increased intermixing in the spinal nerves, due to errors in pathfinding and also to
64 nd found it important for the development of spinal nerve growth toward their muscle targets, suggest
66 fibers, but not C fibers, in the injured L5 spinal nerve have been shown to develop spontaneous acti
67 ombined bilateral transection of the 'genito-spinal' nerves (i.e. pelvic, hypogastric and pudendal).
72 iac ganglia, or on the rostral three somatic spinal nerves, in fixed specimens of the channel catfish
76 e (ODN) was administered intrathecally to L5 spinal nerve injured rats to reduce the expression of sp
77 features of MNs following different types of spinal nerve injury (i.e., axotomy and avulsion) in the
78 site for ectopic discharge generation after spinal nerve injury and separate mechanisms seem to be i
80 he study suggests that plasticity related to spinal nerve injury produces widespread alteration in gl
85 otor nerve guidance but is required to guide spinal nerves innervating the pectoral fins, equivalent
87 d number, respectively, and migration of the spinal nerves into the forelimb bud has been modified.
88 eration, and three types of ligation on left spinal nerve (L4, L4 and L5, L5) were performed in rats.
90 when DiI crystals were placed on the somatic spinal nerves, labeled primary afferents terminated in t
92 ically evoked responses of spinal neurons in spinal nerve ligated (SNL) rats or hindpaw levels of end
93 ked responses of spinal neurones in control, spinal nerve ligated and sham operated halothane-anaesth
94 es in control, hindpaw carrageenan inflamed, spinal nerve ligated and sham-operated rats were studied
97 d, significantly (P = 0.02) more neurones of spinal nerve-ligated (SNL) rats responded to brush compa
99 pression with or without dorsal rhizotomy in spinal nerve-ligated rats and its correlation with tacti
100 root ganglia (DRG) and dorsal spinal cord of spinal nerve-ligated rats with neuropathic pain, suggest
101 a in a variety of rat pain models including: spinal nerve ligation (ED(50) = 47 mg/kg, i.p.), sciatic
103 5-HT3 receptor antagonists in rats following spinal nerve ligation (SNL) but not sham operation.
105 rats and in rats that had received L5 and L6 spinal nerve ligation (SNL) immediately before injection
110 In this study, immunoblotting showed that spinal nerve ligation (SNL) induced a delayed and sustai
115 PPQ) model of acute visceral pain, and a rat spinal nerve ligation (SNL) model of neuropathic pain.
117 dependent flush as well as the hot plate and spinal nerve ligation (SNL) models of acute and neuropat
118 20 was also studied in the rat hot plate and spinal nerve ligation (SNL) models of acute and neuropat
119 ur present study, we examined the effects of spinal nerve ligation (SNL) on the number of neurons in
120 erve injury caused by the fourth lumbar (L4) spinal nerve ligation (SNL) or chronic constriction inju
122 lated from neuropathic rats induced by L5/L6 spinal nerve ligation (SNL) via electrophysiological and
123 ury models: sciatic nerve transection (SNT), spinal nerve ligation (SNL), and chronic constriction in
124 mized neurons from rats made hyperalgesic by spinal nerve ligation (SNL), basal K(ATP) channel activi
126 C-fiber-evoked potentials in rats receiving spinal nerve ligation (SNL), but not in uninjured rats.
127 verses neuropathic pain behavior after L5/L6 spinal nerve ligation (SNL), implicating a critical func
128 olving Sprague Dawley rats, we reported that spinal nerve ligation (SNL), in addition to causing allo
129 o rat model of neuropathy, unilateral lumbar spinal nerve ligation (SNL), to characterize the distrib
130 FA)-induced chronic inflammatory pain and L5 spinal nerve ligation (SNL)-induced neuropathic pain in
131 ed protein response (UPR) activation in a L5 spinal nerve ligation (SNL)-induced rat neuropathic pain
150 ing, and attenuated tactile allodynia in the spinal nerve ligation model of neuropathic pain (ED(50)=
151 reverse thermal hyperalgesia in vivo in the spinal nerve ligation model of neuropathic pain with exc
157 logical studies were performed 14-18 d after spinal nerve ligation or sham surgery, and the effects o
161 e (vector QHGAD67) 7 days after selective L5 spinal nerve ligation reversed mechanical allodynia and
162 Peripheral nerve injury in a rat model (spinal nerve ligation) of neuropathic pain triggers spro
164 utely isolated from normal rats (no previous spinal nerve ligation) responded to either mATP or ATP.
165 ivo studies in a rat neuropathic pain model (spinal nerve ligation) showed dose-dependent antiallodyn
166 cally characterized neurons in the RVM after spinal nerve ligation, a model of neuropathic pain that
168 G was extensive as early as 2 days after the spinal nerve ligation, and the sprouted fibers were almo
169 dorsal horn was dramatically increased after spinal nerve ligation, and this was abolished by saporin
171 vity was lost in the hind paw ipsilateral to spinal nerve ligation, but maintained in the contralater
172 in-43 (GAP-43) in the L5 DRG 1 week after L5 spinal nerve ligation, indicated sprouting of sympatheti
174 ion in naive, sham-operated and neuropathic (spinal nerve ligation, SNL) rats using in vivo electroph
176 nglionic neurons was greatly increased after spinal nerve ligation, suggesting the increased number o
189 ; AXO, partial sciatic nerve ligation; PSNL, spinal nerve ligation; SNL or chronic constriction injur
190 bset of animals also underwent unilateral L5 spinal nerve ligature to induce sustained neuropathic pa
191 dy suggests that treating uninjured adjacent spinal nerves may be used to manage chronic neuropathic
192 bundles as the axons course distally in the spinal nerves; more distally, some bundles join to again
200 ligation of the left fifth and sixth lumbar spinal nerves or streptozotocin-induced diabetic neuropa
201 ems may use the neural crest, the developing spinal nerves, or both, to establish this segmental patt
208 ther (1) a ventral dural leak, (2) a leaking spinal nerve root diverticulum, or (3) a direct CSF-veno
209 ved by MRI imaging which demonstrated lumbar spinal nerve root enhancement and clumping or lesions.
211 obability of generating true tracts for each spinal nerve root of the brachial plexus, at different f
212 een identified in myelinated axons of lumbar spinal nerve roots in rabbit and rat on the basis of RNa
216 focal axonal damage to the brainstem and the spinal nerve roots, found in 11 cases but not in control
232 aphy (EMG) can be used to predict whether C5 spinal nerve stumps are healthy and eligible for graftin
233 city, respectively, in predicting healthy C5 spinal nerve stumps eligible for grafting were 93% (233
235 st in the prediction of healthy graftable C5 spinal nerve stumps in acute adult brachial plexus injur
236 t, and rhomboid EMG in predicting healthy C5 spinal nerve stumps that are eligible for grafting.
237 functional magnetic stimulation (FMS) of the spinal nerves (T1-L5) to obtain maximum expiratory funct
239 ugh grafts were invaded by branches of local spinal nerves, these neurites were rarely found near ect
241 ge spatial coverage and high resolution from spinal nerve to ankle level: four slabs per leg, each wi
242 ting along the blood vessels and cranial and spinal nerves to various parts of the meninges surroundi
243 hed a new passive transfer mouse model by L5 spinal nerve transection (L5SNT; modified Chung's model)
244 at microglial Gi DREADD activation inhibited spinal nerve transection (SNT)-induced microglial reacti
247 and proportion of FAAH-IR DRG occurred after spinal nerve transection injury but not after chronic in
248 histochemistry, we performed a unilateral L5 spinal nerve transection on male Wistar rats and measure
253 above the known level of entry of the genito-spinal nerves was combined with bilateral vagotomy.
254 ber of TH-IR fibres within the L3, L4 and L5 spinal nerves was significantly higher in LIF-treated an
255 ligation of the left fifth and sixth lumbar spinal nerves, we found a >17-fold, time-dependent incre
256 trast agent-enhanced spinal vasculature, and spinal nerves were all well rendered alongside surroundi
259 ery, the DRGs with attached dorsal roots and spinal nerves were removed and ectopic discharges were r
260 , SNA plus loose ligation of the adjacent L4 spinal nerve with inflammation-inducing chromic gut; and