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1 minae, especially the substantia gelatinosa (lamina II).
2 s and appear prominent in lamina I and inner lamina II.
3 al neuron population in lamina I and 7.0% in lamina II.
4 three groups of neurons between lamina I and lamina II.
5 ed 11% of the neurons in lamina I and 41% in lamina II.
6 y slightly more numerous in lamina I than in lamina II.
7 dorsal horn that extended from lamina I into lamina II.
8 emical staining were coordinately reduced in lamina II.
9 , a major class of inhibitory interneuron in lamina II.
10  heterogeneous population of interneurons in lamina II.
11 3 of these had somata in lamina I and 157 in lamina II.
12 total neuron population in both lamina I and lamina II: 55% and 52%, respectively.
13 ve neurons are located in lamina I and outer lamina II, a region strongly innervated by nociceptors.
14 wo types of glomerular afferent terminals in lamina II also are immunopositive for VR1.
15             However, the immunoreactivity in lamina II also is prominent in dendrites that are contac
16 eus, in the ventral horn and occasionally in lamina II and III.
17 e neurons were located in the dorsal part of lamina II and in lamina I.
18 the dorsal horn, besides KChIP3 in the inner lamina II and lamina III, we detected DPP10 in most proj
19 ctivity maintains inhibitory transmission in lamina II and reduces pain hypersensitivity.
20  revealed long-latency synaptic responses in lamina II and short-latency responses in lamina III.
21 calized PTH2 receptor protein to spinal cord lamina II and showed that it is synthesized by subpopula
22     Dorsal dendrites that clearly penetrated lamina II and that could receive a direct C-afferent inp
23  HRP labeling in lamina I was expanding into lamina II and there was a shrinking gap between lamina I
24 l cord superficial dorsal horn (lamina I and lamina II) and in DRG.
25 the spinal cord was found in lamina I, inner lamina II, and laminae III/IV.
26 slet cells arose almost entirely from within lamina II, and these local inputs included both excitato
27                We found that interneurons of lamina II are at the origin of the major ascending circu
28 uction slowed in lamina I and accelerated in lamina II as local circuit neurons and the remaining pro
29 a-2 is associated with AMPARs at synapses in lamina II but excluded from those at C-fiber inputs, a v
30 ced greater inhibition of eEPSC amplitude in lamina II but not lamina I of the spinal cord dorsal hor
31 eactive neurons were concentrated in ventral lamina II, but were also present in lamina III.
32 ve lamina I projection neurons, and includes lamina II calretinin neurons, which we show also convey
33           Vertical, radial and tonic central lamina II cells consistently expressed outward current t
34 nated primary afferents and connect to other lamina II cells that have input from a different set of
35                                              Lamina II central neurons, with dorsal root (DR) C-fiber
36                                   Inhibitory lamina II connections appear arranged to modulate activi
37 GluR5/6/7 in perikarya and fine processes in lamina II, especially its inner part (IIi).
38 ceptor (MOR) can be visualized in individual lamina II excitatory interneurons and internalizes into
39 ed from the somata of nociceptors and spinal lamina II excitatory interneurons, which sense and modul
40 with Kv4.3 in the cell bodies of a subset of lamina II excitatory interneurons, while KChIP1, KChIP2,
41 bunits are found in two large populations of lamina II excitatory interneurons.
42 ociceptors and Kv4.2/Kv4.3 in certain spinal lamina II excitatory interneurons.
43 Excitatory interneuronal connectivity within lamina II exhibited a pronounced sagittal orientation, i
44                           In contrast, inner lamina II has a sparser distribution of cobalt-positive
45 he SDH, including its substantia gelatinosa (lamina II), has an explicit organization in which partic
46  region of spinal substantia gelatinosa (SG; lamina II(i)) is a heterogeneous sublamina important for
47 ntrated in interneurons in the inner part of lamina II (IIi ) of the dorsal horn, has been implicated
48 ergic C-fiber synapses in the deeper half of lamina II (IIi) contain E-cadherin but mostly lack N-cad
49  suggested that neurons in the inner part of lamina II (IIi), onto which IB(4)-positive sensory neuro
50 gly, we found that inhibitory neurons at the lamina II/III border are under tonic glycinergic control
51 3 was evident only in neurons located within lamina II/III starting at 24 hr after injury and in micr
52 onpyramidal neurons located predominantly in lamina II/III, 30% (33/109) of which were also GABA immu
53 labeled for enkephalin were also abundant in lamina II/III.
54 t fibers that terminate in the outer part of lamina II (IIo) and dorsal part of lamina IIi, whereas t
55 dergic C-fiber synapses in the outer half of lamina II (IIo) contain N-cadherin but lack E-cadherin.
56 med on visualized dorsal horn neurons in the lamina II in the spinal cord slice preparation of rats.
57 on microscopy analysis of ENT1 expression in lamina II indicated its presence within pre- and post-sy
58                                      Certain lamina II inhibitory cells were found to connect to one
59 st whether endogenous opioids modulate these lamina II interneurons during noxious stimulation, we ne
60 he spinal cord and that postsynaptic MORs on lamina II interneurons likely participate in the analges
61 c glomeruli, suggesting that GIRK-containing lamina II interneurons receive prominent input from C fi
62 as boosted to the adapting-firing excitatory lamina II interneurons while GABAergic and glycinergic i
63               In the tonic-firing inhibitory lamina II interneurons, glutamatergic drive was reduced
64 ociceptive messages via postsynaptic MORs on lamina II interneurons.
65        The spinal substantia gelatinosa (SG; lamina II) is a major synaptic zone for unmyelinated (C)
66  frequency but not amplitude in spinal outer lamina II (lamina IIo) neurons, and this increase is abo
67 munoreactivity was the most intense in inner lamina II, lamina III, and lamina X, and it was the leas
68  are lost from their target region in spinal lamina II, leading to reduced thermal hyperalgesia.
69   Ultrastructurally the dorsal part of inner lamina II (LIIid) harbors a mix of glomeruli that either
70     mGluR2/3 was mainly in the inner part of lamina II; mGluR5 was mainly in laminae I and II.
71 rm-sap (500 ng) produced (1) partial loss of lamina II MOR-expressing dorsal horn neurons, (2) no eff
72  transgenic mouse in which certain GABAergic lamina II neurones are labelled with green fluorescent p
73                       One hundred and twenty lamina II neurones fitted one of five morphological cate
74 l voltage-clamp recordings were performed on lamina II neurones in the rat spinal cord slices.
75 th GABA(A) and strychnine-sensitive GlyRs in lamina II neurones of juvenile (P15-21) rats.
76  fibre-evoked EPSCs were observed in 24 % of lamina II neurones, monosynaptic A delta fibre EPSCs wer
77 sity for eliciting A fibre-mediated EPSCs in lamina II neurones.
78  83 of 139 cells), but only in a minority of lamina II neurons (6 of 53 cells).
79       The majority of low-threshold EPSPs in lamina II neurons after axotomy displayed properties sim
80  a functional increase in A1R sensitivity in lamina II neurons after nerve injury.
81 ression and intracellular dynamics of VR1 in lamina II neurons are controlled by presynaptic input.
82          Excitatory inputs to all classes of lamina II neurons arose from a wider rostrocaudal area t
83         Inhibition of glutamate release onto lamina II neurons by presynaptic muscarinic and GABA(B)
84 rease in inhibitory postsynaptic currents of lamina II neurons coincides with the induction of apopto
85   We demonstrate that MOR internalization in lamina II neurons correlates precisely with the extent o
86                                              Lamina II neurons expressed low levels of mGluR1b immuno
87 1, attenuated synaptically evoked EPSCs onto lamina II neurons in a concentration-dependent manner.
88 rded with intracellular microelectrodes from lamina II neurons in control slices were elicited by hig
89 beta-S included in the internal solution) on lamina II neurons in rat spinal cord slices.
90 citatory postsynaptic currents (sEPSCs) from lamina II neurons in spinal cord slices from wild-type (
91 II-IV neurons and the ventral input zones of lamina II neurons occurring at the II/III border.
92 ry, we have studied synaptic transmission in lamina II neurons of an isolated adult rat spinal cord s
93                    Patch-clamp recordings in lamina II neurons of isolated spinal cord slices showed
94              Using patch-clamp recordings in lamina II neurons of isolated spinal cord slices, we com
95 e amplitude of spontaneous EPSCs (sEPSCs) in lamina II neurons of spinal cord slices is reduced.
96 ermore, these observations indicate that the lamina II neurons receive inappropriate sensory informat
97  AMPA and NMDA receptor-mediated currents in lamina II neurons requires coactivation of both PKC and
98  amplitude, of spontaneous EPSCs (sEPSCs) in lamina II neurons that also responded to mustard oil (al
99 inhibits the glutamatergic synaptic input to lamina II neurons through presynaptic muscarinic recepto
100 nd miniature IPSCs (mIPSCs) were recorded in lamina II neurons using whole-cell recordings in spinal
101                                  A sample of lamina II neurons was also studied for comparison.
102 are evoked in a subpopulation of spinal cord lamina II neurons, a region known to receive strong inpu
103  Type I TARPs, evoked whole-cell currents in lamina II neurons, but such currents were severely atten
104  versus control animals in both lamina I and lamina II neurons.
105  inhibitory postsynaptic currents (IPSCs) of lamina II neurons.
106 but not AMPA currents, are reduced 86-88% in lamina II neurons.
107  and the amplitude of monosynaptic eEPSCs in lamina II neurons.
108   Within the nociceptive afferent pathway to lamina II, nonpeptidergic C-fiber synapses in the deeper
109  eliminated AMP hydrolysis in DRG and spinal lamina II of dKO mice.
110 t to trigeminal primary afferent profiles in lamina II of rat subnucleus caudalis.
111 resent on C-fiber-type neurons projecting to lamina II of spinal cord dorsal horn.
112    The latencies of synaptic FPs recorded in lamina II of the dorsal horn after sciatic nerve section
113 f axonal fibres and terminals was evident in lamina II of the dorsal horn and throughout the cord.
114 nt fibers were observed to be sprouting into lamina II of the dorsal horn, as indicated by cholera to
115 ntrated in interneurons of the inner part of lamina II of the dorsal horn, has been implicated in inj
116 horn termination of unmyelinated C fibers in lamina II of the dorsal horn, using nerve injections of
117 itatory synaptic transmission to neurones in lamina II of the dorsal horn.
118 ections from either tracer were localized to lamina II of the ipsilateral subnucleus caudalis.
119 g potassium (GIRK) channels are expressed in lamina II of the mouse spinal cord and that pharmacologi
120             Thus, excitatory interneurons in lamina II of the mouse spinal cord can be subdivided int
121 ng specific neurotransmitter patterns within lamina II of the pars caudalis/medullary dorsal horn.
122  suggest that ATP-activated P2X receptors in lamina II of the rat spinal cord may play a role in tran
123 rs and spinal neurons terminals in the inner lamina II of the spinal cord where they inhibit glutamat
124 erent fibers and their abnormal sprouting in lamina II of the spinal dorsal horn.
125 TB-labeled terminals appeared to sprout into lamina II of the spinal dorsal horn.
126 uncular nucleus, paratrigeminal nucleus, and lamina II of the spinal trigeminal nucleus and entire sp
127 ation of presynaptic axonal terminals within lamina II of the subnucleus caudalis.
128 ype I TARP gamma-2 (stargazin) is present in lamina II of the superficial dorsal horn, an area involv
129 bres terminate in the substantia gelatinosa (lamina II) of the spinal cord, virtually all of the neur
130  epidermis to the substantia gelatinosa (SG, lamina II) of the spinal cord.
131                   The substantia gelatinosa (lamina II) of the spinal dorsal horn contains inhibitory
132 n ceased simultaneously in both lamina I and lamina II on E16.
133                                              Lamina II outer vertical neurons with DR Adelta input mo
134                    Neurones located in outer lamina II, particularly radial and vertical cells, were
135 d 11 neurons in lamina I and 42.6 neurons in lamina II per 10-microm transverse section.
136 ganization of the intrinsic circuitry within lamina II remains poorly understood.
137 (A) receptor-mediated synaptic inhibition in lamina II spinal cord neurons.
138  These results indicate that reoccupation of lamina II synapses by sprouting Abeta fibers normally te
139 1.22 neurons in lamina I and 0.24 neurons in lamina II that had supraspinal projections per 10-microm
140 on controls the inhibitory circuitry deep in lamina II that is likely to be responsible for separatin
141  root ganglia (DRG) and on axon terminals in lamina II (the substantia gelatinosa) of spinal cord.
142 rved patchy immunostaining in cell bodies in lamina II, this unexpected result may reflect synthesis
143 t of their soma, but in lamina I neurons and lamina II vertical cells this ventral displacement of th
144 (DR) C-fiber input, monosynaptically excited lamina II vertical neurons with DR Adelta input.
145 resent at high levels in the ventral part of lamina II we have limited information concerning the typ
146 ma (PKCgamma)-immunoreactive interneurons in lamina II, we found that around one-third of the VGAT bo
147 ve section, 31 of 57 (54%) EPSPs recorded in lamina II were elicited by low-threshold stimulation.
148 ory cells had axonal projections confined to lamina II whereas excitatory vertical cells projected to
149 oject to lamina I and the innermost layer of lamina II, which has previously been implicated in persi

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