ライフサイエンスコーパス: GPe

1 GPe lesions resulted in increased discharge in STN and G

2 What was distinctive about GPe Na+ channels was a prominent resurgent gating mode.

3 recorded pairs of neurons within and across GPe and SNr shifted from the pathological low-frequency

4 , synchronous inhibition of tonically active GPe-STN neurons or phasic activity of GPe-STN neurons re

5 6, comprised approximately two-thirds of all GPe neurons, and were the major GPe cell type innervatin

6 Both GPi and GPe firing frequencies differed significantly with dysto

7 for dystonia and investigate whether GPi and GPe firing rates differ between dystonia types.

8 rnal segment of the globus pallidus (GPi and GPe, respectively) in two rhesus monkeys rendered parkin

9 Finally, the MSN and GPe response groups reorganized at the outcome epoch, as

10 MSNs and GPe neurons displayed sustained average activity to cue

11 We propose that the STN and GPe constitute a central pacemaker modulated by striatal

12 w-frequency rhythmic bursting in the STN and GPe is characteristic of PD.

13 Autonomous oscillation of STN and GPe neurons underlies tonic activity and is important fo

14 tum-STN-GPe cultures, neurons in the STN and GPe spontaneously produce synchronized oscillating burst

15 In contrast, arkypallidal GPe neurons originate from lateral/caudal ganglionic emi

16 here was a progressive decline in autonomous GPe pacemaking, which normally serves to desynchronize a

17 1.0-2.5, 4.5-5.5, and 7.0-9.0 msec for both GPe and GPi neurons.

18 However, unlike MSNs, neurons in both GPe response groups displayed prolonged and temporally o

19 lly pattern STN activity ex vivo, correlated GPe-STN activity is not normally observed in vivo.

20 Decreasing GPe and VP volumes were associated with poorer cognition

21 undamental biology and function of different GPe neuron classes.

22 y recorded pairs of high-frequency discharge GPe cells recorded from four monkeys during task-irrelev

23 ceive monosynaptic excitatory and disynaptic GPe-mediated inhibitory inputs from the STN.

24 ver that of Lim homeobox 6 (Lhx6)-expressing GPe neurons, restores movement in dopamine-depleted mice

25 the activity of parvalbumin (PV)-expressing GPe neurons over that of Lim homeobox 6 (Lhx6)-expressin

26 riatum, globus pallidus interna and externa (GPe), subthalamic nucleus (STN), and substantia nigra pa

27 nit activity in the globus pallidus externa (GPe) and substantia nigra reticulata (SNr) revealed that

28 s interna (GPi) and globus pallidus externa (GPe) in children undergoing deep brain stimulation (DBS)

29 ory inputs from the globus pallidus externa (GPe) that is reciprocally connected with the STN.

30 onnections from the globus pallidus externa (GPe) to striatum are substantially stronger onto fast-sp

31 cturally homologous to the primate external (GPe) and internal (GPi) pallidal segments.

32 ed inputs from the globus pallidus externus (GPe), a basal ganglia nucleus not previously known to pa

33 y decreased the firing rate of low-frequency GPe neurons, but did not alter the firing of high-freque

34 We performed patch-clamp recordings from GPe neurons and found that bath application of ethanol d

35 in vivo electrophysiological recordings from GPe showed that ethanol decreased the firing of a large

36 a network containing two types of GABAergic GPe projection neuron, so-called 'prototypic' and 'arkyp

37 A first population of prototypic GABAergic GPe neurons fire antiphase to subthalamic nucleus (STN)

38 the potential contributions of two GABAergic GPe cell types to voluntary action are fated from early

39 rsal learning task, we found that changes in GPe discharge rates predicted subsequent behavioral shif

40 average neuronal discharge rate decreased in GPe but increased in STN and GPi.

41 The disfacilitation in GPe is then amplified in basal ganglia circuitry and gen

42 te tonic inhibition and a disfacilitation in GPe.

43 ctivity, which accounted for the increase in GPe labelling.

44 with autoimmunoradiography) was increased in GPe and GPi, likely reflecting increased striatal input

45 excitation followed by a weak inhibition in GPe neurons and a short-latency, very short-duration exc

46 Thus, modulations in GPe spiking activity are highest for attention-demanding

47 in the temporal firing pattern of neurons in GPe and GPi underlie the beneficial effect of HFS in the

48 This mode was significantly reduced in GPe neurons lacking functional Nav1.6 channels.

49 HFS) evoked powerful excitatory responses in GPe neurons.

50 terminants of pacemaking and fast spiking in GPe neurons are not fully understood, but voltage-depend

51 ight on the mechanisms underlying spiking in GPe neurons but also suggest that electrical stimulation

52 ored pacemaking and reduced burst spiking in GPe neurons.

53 We demonstrated that cocaine increased GPe neuron activity, which accounted for the increase in

54 s function makes it unlikely that individual GPe neurons, or even a single GPe cell type, could compu

55 organization applies to the dopamine-intact GPe.

56 tal to the operations of the dopamine-intact GPe.

57 Lhx6-GPe neurons, which do not express PV, are concentrated i

58 and anatomical differences suggest that Lhx6-GPe and PV-GPe neurons participate in different circuits

59 hirds of all GPe neurons, and were the major GPe cell type innervating the subthalamic nucleus (STN).

60 The median GPe firing frequency was higher in the NBIA group than i

61 number of functional GABAA receptor-mediated GPe-STN inputs.

62 lices at rates and in patterns that mimicked GPe activity in vivo.

63 HF-1 neurons, like most GPe neurons we examined, exhibited large firing rate mod

64 tic depression caused tonic, nonsynchronized GPe-STN activity to disrupt rather than abolish autonomo

65 active GPe-STN neurons or phasic activity of GPe-STN neurons reliably patterned STN activity through

66 gesting that GABA released from the axons of GPe neurons effectively activates GABA(B) receptors in t

67 urons are two distinct functional classes of GPe neurons.

68 hese findings warrant further exploration of GPe as a target for interventions for Parkinson's diseas

69 lication increased the spontaneous firing of GPe and GPi neurons, suggesting that GABA released from

70 r FoxP2, constituted just over one-fourth of GPe neurons, and innervated the striatum but not STN.

71 Inhibition of GPe activity revealed that it contributes to two forms o

72 acemaker modulated by striatal inhibition of GPe neurons.

73 three animals with ibotenic acid lesions of GPe.

74 gical, molecular, and anatomical measures of GPe-STN transmission were compared in the STN of control

75 Modeling of GPe cells as class 2 excitability neurons with common ex

76 These models suggest that a network of GPe and subthalamic nucleus (STN) neurons computes the n

77 physiological studies of single and pairs of GPe neurons have failed to fully disclose the physiologi

78 data argue that the frequency and pattern of GPe activity profoundly influence its transmission to th

79 ct temporal activities of two populations of GPe neuron in vivo are underpinned by distinct molecular

80 Thus, two populations of GPe neuron together orchestrate activities across all ba

81 tions (f-I curves) of the two populations of GPe neurons.

82 nections were stimulated at the mean rate of GPe activity in vivo (33 Hz).

83 he results indicate that a mere reduction of GPe activity does not produce parkinsonism.

84 ical excitation by adjusting the strength of GPe inhibition.

85 We also study the synchronization of GPe cells to synaptic input from the STN cell with depen

86 nel have a key role in the ethanol effect on GPe neurons, as the application of BK channel inhibitors

87 convergence of the MSN response groups onto GPe cells.

88 ring rate (0.78 +/- 0.136 spikes/s) in other GPe cells.

89 ernal and internal segments of the pallidum (GPe and GPi) receive heavy GABAergic innervations from t

90 nd internal segments of the globus pallidus (GPe and GPi, respectively).

91 onnected GABAergic external globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN) are clo

92 onnected GABAergic external globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN).

93 nucleus (STN) and external globus pallidus (GPe) are associated with the operation of the basal gang

94 the external segment of the globus pallidus (GPe) are autonomous pacemakers that are capable of susta

95 indicate that the external globus pallidus (GPe) contains two main types of GABAergic projection cel

96 TN and inhibitory, external globus pallidus (GPe) form a feedback system that engages in synchronized

97 Neurons in the external globus pallidus (GPe) generate pacemaker activity that controls basal gan

98 striatum, and the external globus pallidus (GPe) in regulating RLS-like movements, in particular pal

99 d indirect pathway external globus pallidus (GPe) inhibition of the STN are critical for normal movem

100 The external globus pallidus (GPe) is a key contributor to motor suppressing pathways

101 The external globus pallidus (GPe) is a key nucleus within basal ganglia circuits that

102 The external segment of the globus pallidus (GPe) is one of the core nuclei of the basal ganglia, pla

103 We show how external globus pallidus (GPe) neuron is sensitive to the phase of the input from

104 on of labor in the external globus pallidus (GPe) of Parkinsonian rats, showing that the distinct tem

105 neurons within the external globus pallidus (GPe) was not fully appreciated.

106 the external segment of the globus pallidus (GPe), a downstream structure whose computational role ha

107 al activity of the external globus pallidus (GPe), a nucleus in the basal ganglia, contributes to the

108 the external segment of the globus pallidus (GPe), neuronal populations have been defined using molec

109 using on the mouse external globus pallidus (GPe), we demonstrate that the potential contributions of

110 n the striatum and external globus pallidus (GPe).

111 the external segment of the globus pallidus (GPe).

112 the external segment of the globus pallidus (GPe).

113 and the external segment of globus pallidus (GPe).

114 the external segment of the globus pallidus (GPe).

115 the external segment of the globus pallidus (GPe)], and one neuromodulator group [striatal tonically

116 se in the number of synaptic connections per GPe-STN axon terminal, to substantial strengthening of t

117 er of ultrastructurally defined synapses per GPe-STN axon terminal doubled with no alteration in term

118 lidus (GP in rodents, homolog of the primate GPe), pairs of neurons generally have uncorrelated firin

119 that exhibit activity similar to the primate GPe.

120 s knowledge gap by discovering two principal GPe neuron classes, which were identified by their nonov

121 Prototypic GPe neurons derive from the medial ganglionic eminence o

122 es, a network of arkypallidal and prototypic GPe neurons comprises a neural substrate capable of supp

123 cal differences suggest that Lhx6-GPe and PV-GPe neurons participate in different circuits with the p

124 In contrast, PV-GPe neurons are more concentrated in the lateral portion

125 stantia nigra pars compacta compared with PV-GPe neurons.

126 3 components of the GP-the external segment (GPe), internal segment (GPi), and ventral pallidum (VP)-

127 ing to the globus pallidus external segment (GPe).

128 d activity in the external pallidal segment (GPe) results in the abnormalities of neuronal discharge

129 imates these data were then used to simulate GPe-STN transmission.

130 Injection of simulated GPe-STN conductances revealed that synaptic depression c

131 hat individual GPe neurons, or even a single GPe cell type, could compute it.

132 itionally assumes that the feedback from STN-GPe circuit to cortex is important for maintaining the o

133 In mature organotypic cortex-striatum-STN-GPe cultures, neurons in the STN and GPe spontaneously p

134 by blocking different connections of the STN-GPe circuit.

135 tion are generated in the cortex and the STN-GPe circuits resonates at this frequency.

136 gle stimulation and during STN-BHFS, the STN-GPe excitatory response dominates over the STN-GPe-GPe r

137 e excitatory response dominates over the STN-GPe-GPe recurrent inhibition in the GPe, whereas the STN

138 rrent inhibition in the GPe, whereas the STN-GPe-GPi inhibitory response dominates over the STN-GPi e

139 DA-depletion, the spontaneous firing of Str-GPe neurons increases, and MC stimulation evokes a short

140 0.6 s) of complete silence, which are termed GPe pauses.

141 We conclude that GPe exhibits several core components of a dichotomous or

142 Our results demonstrate that GPe, commonly studied in motor contexts, takes part in c

143 arning-related neural activity and show that GPe discharge rates closely matched across-trial learnin

144 These results suggest that GPe may play a central role in propagating abnormal circ

145 The GPe is comprised of a heterogeneous population of neuron

146 The GPe neurons provide another major GABAergic innervation

147 ed, indicative of reduced activity along the GPe-STN pathway.

148 Because the GPe powerfully regulates the frequency, pattern, and syn

149 nent of a positive feedback loop between the GPe and striatum that promotes synchronization and rhyth

150 In order to perform such computation, the GPe needs to send feedback to the STN equal to a particu

151 We suggest that common inputs decrease the GPe discharge rate and lead to a bifurcation phenomenon

152 ticular pallidocortical projections from the GPe to the motor cortex.

153 revised framework for understanding how the GPe relates to behavior in both health and disease.

154 -sensitive responses differed greatly in the GPe ( approximately 400 ms long) and in the GPi (60 ms l

155 fectively activates GABA(B) receptors in the GPe and GPi and contributes significantly to the control

156 BA(B) antagonist)-sensitive responses in the GPe and GPi.

157 +/- 3% of labeled elements), whereas, in the GPe and SNr, the labeling was mainly presynaptic (71% +/

158 In vivo, most neurons in the GPe are characterized by high firing rates (50-100 spike

159 neurons and Npas1-expressing neurons in the GPe represent two nonoverlapping cell classes, amounting

160 genetically distinct cell populations in the GPe that differ molecularly, anatomically, and electroph

161 tility of cell-specific interventions in the GPe to target functionally distinct pathways, with the p

162 activity of two neuronal populations in the GPe, elevating the activity of parvalbumin (PV)-expressi

163 In the GPe, the average sustained response was composed of two

164 the STN-GPe-GPe recurrent inhibition in the GPe, whereas the STN-GPe-GPi inhibitory response dominat

165 synchronized rhythmic burst activity in the GPe-STN loop, which may be relevant to the resting tremo

166 ion of an NBQX/CPP/gabazine mixture into the GPe.

167 ifurcation phenomenon (pause) in some of the GPe neurons.

168 This work revises our understanding of the GPe, and provides the foundation for future studies of i

169 erminal, to substantial strengthening of the GPe-STN pathway.

170 concentrated in the lateral portions of the GPe.

171 re concentrated in the medial portion of the GPe.

172 he motor-suppressing "indirect-pathway," the GPe consists of a number of distinct cell types and anat

173 Relative to controls, in the HD patients the GPe showed a 54% overall volume decline, 60% neuron loss

174 In idiopathic and experimental PD, the GPe and STN exhibit hypoactivity and hyperactivity, resp

175 projections from the STN and potentially the GPe.

176 nt studies have challenged the idea that the GPe comprises a single, homogenous population of neurons

177 To test the hypothesis that the GPe's influence is constrained by short-term synaptic de

178 e another major GABAergic innervation to the GPe itself and GPi.

179 In contrast to the GPe, STN-BHFS evoked a predominantly inhibitory response

180 he diversity of the neurons that make up the GPe.

181 the origin of the GABA(B) responses was the GPe, not the Put.

182 In simulated dopamine-depletion, this GPe-FSI activity is necessary for the emergence of stron

183 allidal types are functionally homologous to GPe and GPi neurons, we recorded from neurons in area X

184 18.9 s) was also longer than pauses in tonic GPe activity in vivo.

185 asses, amounting to 55% and 27% of the total GPe neuron population, respectively.

186 al activation of STN NMDA receptors triggers GPe-STN inputs to strengthen abnormally, contributing to

187 Unitary GPe-STN synaptic connections initially generated large c

188 d by short-term synaptic depression, unitary GPe-STN inputs were stimulated in rat and mouse brain sl

189 Although phasic, unitary GPe-STN inputs powerfully pattern STN activity ex vivo,

190 Our circuit model suggests that when GPe spikes are synchronous, this pallidostriatal pathway

191 ring periods of synchronized activity within GPe.