ライフサイエンスコーパス: STN

1 STN activity was rescued by NMDA receptor antagonism or

2 STN DBS did not protect against alpha-syn-mediated defic

3 STN DBS is neuroprotective against neurotoxicants in ani

4 STN gamma (60-90 Hz) increased most strongly when the ta

5 STN HFS inhibited key brain regions, including the subst

6 STN HFS prevented the re-escalation of heroin intake aft

7 STN neurons exhibited prolonged NMDA receptor-mediated s

8 STN synapses showed a decrease in calcium-permeable AMPA

9 ed, STN neurons are not hyperactive, and (4) STN activity opposes striatopallidal patterning.

10 esumably through homeostatic mechanisms, (4) STN neurons were not hyperactive, despite being disinhib

11 The fate mapped E11.5-12.5 STN neuronal population included 20% of neurons with pro

12 Long-term trkB blockade abolished STN DBS-mediated neuroprotection of SN neurons following

13 to the motor no-go response of the adjacent STN.

14 Depressive symptoms before and after STN-DBS surgery were documented in 116 patients with PD

15 ntion of neuropsychiatric side-effects after STN-DBS.

16 bstrate of neuropsychiatric impairment after STN-DBS and suggest that tractography could be used to p

17 crease lateral PFC-STN coherence and altered STN neuronal spiking.

18 to activity at prefrontal electrode Fz, and STN beta activity (13-30 Hz) coupled to electrodes C3/C4

19 correlated and temporally offset PV GPe and STN neuron activity is generated in part by elevated str

20 normal, temporally offset prototypic GPe and STN neuron firing results in part from increased striato

21 loss of dopamine, the activities of GPe and STN neurons become more temporally offset and strongly c

22 lar in duration and frequency in the GPi and STN, but GPi bursts were stronger and correlated to brad

23 nals within the striatum, thalamus, GPi, and STN were all associated with increases and decreases in

24 the release probability at DR-innervated and STN-innervated synapses, quantified by decreases in pair

25 w-frequency oscillatory activity in mPFC and STN before making a response have higher decision thresh

26 ressing prototypic GPe (PV GPe) neurons, and STN neurons.

27 ectrophysiology) in healthy participants and STN local field potentials in Parkinson's patients durin

28 We applied STN-DBS in an adeno-associated virus (AAV) 1/2-driven hu

29 At <2 and 6 months of age autonomous STN activity was impaired due to activation of KATP chan

30 The interstimulus intervals (ISIs) between STN-DBS and TMS that produced cortical facilitation were

31 l interaction deficits were not corrected by STN-HFS.

32 required to explore the circuitry engaged by STN-HFS, as well as other potential stimulation sites.

33 imb akinesia improvement normally induced by STN DBS.

34 response to cues prospectively triggered by STN beta bursts was slower than when responses were not

35 locomotor activity, which was unaffected by STN-HFS.

36 Over 4 h of continuous STN DBS, antidromic activation became less robust, where

37 based connectivity between the contralateral STN and motor cortex decreased.

38 N inputs in PD mice, reduced loss of cortico-STN transmission and patterning and improved motor funct

39 ion suggested that downregulation of cortico-STN transmission in PD mice was triggered by increased s

40 , in parkinsonian mice we found that cortico-STN transmission strength had diminished by 50%-75% thro

41 e generally to that of classically described STN neurons.

42 denervation or loss of SNpc neuron, nor did STN DBS elevate p-rpS6 levels further.

43 upregulated, (3) despite being disinhibited, STN neurons are not hyperactive, and (4) STN activity op

44 bution of antidromic activation of M1 during STN DBS in disrupting synchronization in cortical neuron

45 ic activation of M1 was only observed during STN DBS.

46 uency stimulation is necessary for effective STN DBS, or if low frequency stimulation can be effectiv

47 INTERPRETATION: Effective STN DBS for PD is associated with a specific connectivit

48 We found that electrical STN DBS relieved bradykinesia, as measured by movement v

49 ast reaction times were preceded by enhanced STN spike-to-cortical gamma phase coupling, indicating a

50 We evaluated STN DBS in a parkinsonian model that displays alpha-synu

51 ant between-group differences, all favouring STN-DBS, were found for NMSS, SCOPA-motor complications,

52 und to be narrow (E10.5-E14.5) with very few STN neurons born at E10.5 or E14.5.

53 on changes in depressive symptoms following STN-DBS, which have been reported to improve, worsen, or

54 We tested various models for STN drug screening with the aim of identifying the most

55 approach revealed a distinct sweet spot for STN DBS in PD.

56 hanges in oscillatory activity recorded from STN between ultradian sleep states to determine whether

57 surprise signals occur, and that the fronto-STN circuits for doing this, at least for stopping and c

58 Furthermore, STN burst-firing and beta oscillations are two independe

59 the idea that the reciprocally connected GPe-STN network plays a key role in disease symptomatology a

60 s models, abnormal rates and patterns of GPe-STN network activity are linked to motor dysfunction.

61 ctivity was not present in the cortex or GPe-STN network.

62 ne the causal roles of VP --> VTA and VP --> STN pathways in context-induced reinstatement and reacqu

63 at silencing either the VP --> VTA or VP --> STN pathways is sufficient to reduce both reinstatement

64 work suggests that LFP recordings from human STN differentiate between sleep cycle states, and sleep-

65 2) receptor subunits within the normal human STN.

66 del recapitulated several hallmarks of human STN DBS, including rapid onset and offset, frequency dep

67 ts for the discovery of broad-spectrum human STN drugs.

68 opulations of principal neurons in the human STN.

69 disrupted beta band oscillatory activity in STN and SNr.

70 urther, after controlling for differences in STN volumes within or between groups, the PD group had l

71 creases in firing rates of single neurons in STN, globus pallidus externa (GPe), and substantia nigra

72 ed that these dynamics were recapitulated in STN, but also in external globus pallidus and striatum.

73 are regulated by different NMDA receptors in STN.

74 , suggesting a noncanonical role for trkB in STN DBS-mediated behavioral effects.

75 azole and mebendazole, are currently used in STN mass drug administration, with many instances of low

76 e, we show that trial-by-trial variations in STN low-frequency oscillatory activity predict adjustmen

77 This could result from intra-STN feedback excitation.

78 decision making by recording intraoperative STN and prefrontal cortex (PFC) electrophysiology as par

79 Our results suggest that for the left STN-DBS lead, placement impacting fibers to left prefron

80 sion and that compensatory plasticity limits STN hyperactivity and cortical entrainment.

81 ling occurred independent of changes in mean STN firing rates, and the relative timing of STN spikes

82 In preclinical models, STN DBS provides neuroprotection for substantia nigra (S

83 After 36 months, STN-DBS significantly improved NMSS, PDQ-8, SCOPA-motor

84 ed optogenetics to activate or inhibit mouse STN to test its putative causal role.

85 uence of the medial prefrontal cortex (mPFC)-STN pathway on decision thresholds during high cautiousn

86 oscillatory activity and corresponding mPFC-STN coupling are involved in determining how much eviden

87 In the Spare-the-Nephron (STN) Study, kidney transplant recipients randomized abou

88 ency stimulation of the subthalamic nucleus (STN HFS) for heroin addiction.

89 djustments by recording subthalamic nucleus (STN) activity and electroencephalography in 11 Parkinson

90 om the isocortex to the subthalamic nucleus (STN) adjacent to the PSTN.

91 on (DBS), targeting the subthalamic nucleus (STN) and globus pallidus interna, is a surgical therapy

92 evidence implicates the subthalamic nucleus (STN) and globus pallidus internus (GPi) in reward and pu

93 timulation (DBS) of the subthalamic nucleus (STN) and globus pallidus internus (GPi) is an effective

94 field potentials in the subthalamic nucleus (STN) and scalp EEG (modified 10/20 montage) during sleep

95 of effective DBS to the subthalamic nucleus (STN) and test its ability to predict outcome in an indep

96 TEMENT It is known that subthalamic nucleus (STN) beta activity is linked to symptom severity in Park

97 The striatum and the subthalamic nucleus (STN) constitute the input stage of the basal ganglia (BG

98 onhuman primates during subthalamic nucleus (STN) DBS and globus pallidus internus (GPi) DBS.

99 eloped a mouse model of subthalamic nucleus (STN) DBS for PD, to permit investigation using cell type

100 therapeutic effects of subthalamic nucleus (STN) deep brain stimulation (DBS) in Parkinson's disease

101 timulation (DBS) of the subthalamic nucleus (STN) has been reported to improve sleep architecture in

102 ronal population of the subthalamic nucleus (STN) has the ability to prolong incoming cortical excita

103 eld potentials from the subthalamic nucleus (STN) in 15 PD patients of both genders OFF-medication, d

104 t-firing pattern of the subthalamic nucleus (STN) in a feed-forward, or efferent-only, mechanism.

105 ies have implicated the subthalamic nucleus (STN) in decisions that involve inhibiting movements.

106 T We tested whether the subthalamic nucleus (STN) in humans is causally involved in controlling stepp

107 ities recorded from the subthalamic nucleus (STN) in patients with deep brain stimulation (DBS) elect

108 The subthalamic nucleus (STN) is a critical excitatory signaling center within th

109 timulation (DBS) of the subthalamic nucleus (STN) is a highly effective symptomatic therapy for motor

110 NIFICANCE STATEMENT The subthalamic nucleus (STN) is a pivotal element of the basal ganglia and serve

111 cies has shown that the subthalamic nucleus (STN) is activated by scenarios involving stopping or pau

112 timulation (DBS) of the subthalamic nucleus (STN) is an effective therapy for the motor symptoms of P

113 The subthalamic nucleus (STN) is an element of cortico-basal ganglia-thalamo-cort

114 The subthalamic nucleus (STN) is hypothesized to play a central role in the rapid

115 The subthalamic nucleus (STN) is the main target for neurosurgical treatment of m

116 timulation (DBS) of the subthalamic nucleus (STN) is the most common neurosurgical treatment for Park

117 timulation (DBS) of the subthalamic nucleus (STN) is the most commonly used surgical treatment for Pa

118 Gamma activity in the subthalamic nucleus (STN) is widely viewed as a pro-kinetic rhythm.

119 making assume that the subthalamic nucleus (STN) mediates this function by elevating decision thresh

120 the rhythmic output of subthalamic nucleus (STN) neurons and synchronization with the mesial cortex.

121 at a network of GPe and subthalamic nucleus (STN) neurons computes the normalization term in Bayes' e

122 (GPe) and glutamatergic subthalamic nucleus (STN) neurons form a key network within the basal ganglia

123 (GPe) and glutamatergic subthalamic nucleus (STN) neurons form a key, centrally positioned network wi

124 characterization in the subthalamic nucleus (STN) of PD patients undergoing deep brain stimulation (D

125 nges are present in the subthalamic nucleus (STN) of people with mild-to-moderate severity of Parkins

126 The subthalamic nucleus (STN) of the basal ganglia appears to have a potent role

127 s, which project to the subthalamic nucleus (STN) of the basal ganglia, play a key role in inhibiting

128 ity, ostensibly via the subthalamic nucleus (STN) of the basal ganglia.

129 spiking activity in the subthalamic nucleus (STN) to frontal electroencephalograms preceded the onset

130 analysed human ECoG and subthalamic nucleus (STN) unit activity during hand gripping.

131 l tegmental area (VTA), subthalamic nucleus (STN), lateral hypothalamus, among others, and the roles

132 he basal ganglia is the subthalamic nucleus (STN), which serves as a therapeutic target for deep brai

133 hat repeated pairing of subthalamic nucleus (STN)-DBS and M1-TMS at specific time intervals will lead

134 the cerebral cortex and subthalamic nucleus (STN).

135 ivity in the cortex and subthalamic nucleus (STN).

136 cally attributed to the subthalamic nucleus (STN).

137 tine nucleus (PPN), and subthalamic nucleus (STN).

138 tal gyrus, caudate, and subthalamic nucleus (STN).

139 ucleus accumbens or the subthalamic nucleus (STN).

140 tic influences from the subthalamic nucleus (STN).

141 timulation (DBS) of the subthalamic nucleus (STN).

142 At 12 months of age approximately 30% of STN neurons had been lost, as in HD.

143 , and thus the contribution of activation of STN neurons to the therapeutic effects of DBS remains un

144 cluded that direct optogenetic activation of STN neurons was neither necessary nor sufficient for rel

145 ition of the STN and increased activation of STN NMDA receptors.

146 Next we showed that brief activation of STN projection neurons was sufficient to interrupt or pa

147 to a particular function of the activity of STN neurons.

148 eta oscillations entrain spiking activity of STN, striatal cholinergic interneurons and BG downstream

149 Spectral analysis of STN local field potentials revealed elevated beta power

150 expectedly reduced the functional benefit of STN DBS on a short timescale that is inconsistent with c

151 ifferent temporal relationships to bursts of STN beta activity.

152 feature underlying the therapeutic effect of STN and GPi DBS.

153 roprotective and disease-modifying effect of STN-DBS in a mechanistically relevant model of PD.

154 n mediating the symptom-relieving effects of STN DBS using cell type-specific optogenetic stimulation

155 ssion is impaired, resembling the effects of STN lesioning or inactivation.

156 Class IIb evidence for beneficial effects of STN-DBS on NMS at 36-month follow-up which also correlat

157 neuroprotective and symptomatic efficacy of STN DBS.SIGNIFICANCE STATEMENT Subthalamic nucleus deep

158 These findings provide further evidence of STN involvement in impulsive behaviour in the PD populat

159 from the Dbx1 microdomain, at the expense of STN and PM populations.

160 Optogenetic activation and inactivation of STN-projecting neurons reduced and increased inappropria

161 Increases of STN LFO power preceding the response predicted increased

162 We propose that the involvement of STN in reactive control is restricted to its ventromedia

163 Knockdown of STN NMDA receptors, which also suppresses proliferation

164 um imaging showed that the great majority of STN-projecting neurons were preferentially active in no-

165 Within-subject measures of STN volume and fractional anisotropy (FA) were derived f

166 Repeated pairing of STN-DBS and M1-TMS at short ( approximately 3 ms) and me

167 imulation could alter the spiking pattern of STN neurons, there was no net effect on firing rate, sug

168 as stimulation altered the firing pattern of STN spiking without changing overall rate.

169 M1 activation at least in the acute phase of STN DBS, the difference in observed antidromic activatio

170 efficacy and disease-modifying potential of STN DBS.

171 nstructions, while cue-induced reductions of STN beta power decreased thresholds irrespective of inst

172 ictly segregated to a ventromedial region of STN.

173 o neuroprotection in the SNpc as a result of STN-DBS.

174 Our results highlight the pivotal role of STN divergent projections in BG physiology and pathophys

175 physiological evidence for the exact role of STN during adjustment of decision thresholds is lacking.

176 We re-examined the role of STN local cells in mediating the symptom-relieving effec

177 xpression and produced a robust silencing of STN neurons as measured using whole-cell recording ex vi

178 Direct optogenetic stimulation of STN neurons was effective in treating the symptoms of pa

179 This suggests that a subpopulation of STN neurons forms a local glutamatergic network, which t

180 We found that specific subsets of STN neurons have activity consistent with causal roles i

181 erate plateau potentials, similar to that of STN neurons without local axon collaterals and more gene

182 a dendritic arbor that differed from that of STN neurons without local axon collaterals.

183 STN firing rates, and the relative timing of STN spikes was offset by half a gamma cycle for ipsilate

184 ecordings, allowed identifying a new type of STN neurons that possess a highly collateralized intrins

185 itionally, we found a selective weakening of STN inputs to PV(+) neurons in the chronic 6-hydroxydopa

186 and three weeks later received four weeks of STN DBS or electrode implantation that remained inactive

187 Optogenetic STN DBS at 130 pulses per second (pps) reduced pathologi

188 As with electrical DBS, optogenetic STN DBS exhibited a strong dependence on stimulation rat

189 havioral and neuronal effects of optogenetic STN DBS in female rats following unilateral 6-hydroxydop

190 High-rate optogenetic STN DBS can indeed ameliorate parkinsonian motor symptom

191 milarly to electrical DBS, while optogenetic STN DBS with ChR2 did not produce behavioral effects.

192 that VP neurons projecting to either VTA or STN are recruited during context-induced reinstatement o

193 uppresses proliferation of GABAergic pallido-STN inputs in PD mice, reduced loss of cortico-STN trans

194 val since baseline (completion of the parent STN study at 24 months posttransplant).

195 tential recordings from 19 (15 participants) STN and 26 (22 participants) GPi nuclei.

196 ching applied on the cohort of 151 patients (STN-DBS n=67, MED n=84) resulted in a well-balanced sub-

197 potentiation, and less effectively patterned STN activity.

198 es were associated with increase lateral PFC-STN coherence and altered STN neuronal spiking.

199 sion, while compensatory plasticity prevents STN hyperactivity and limits cortical entrainment.

200 g the same time period when conflict-related STN-to-M1 communication is increased, cortico-spinal exc

201 rtical plasticity can be induced by repeated STN and M1 stimulation at specific intervals.

202 values were averaged over the left and right STN separately for each subject.

203 p with the STN (R(2) = 21%) and sensorimotor STN (R(2) = 19%).

204 Our data show STN-HFS suppresses excessive self-grooming in two autism

205 lia in patients with PD who underwent staged STN DBS.

206 Subthalamic nucleus deep brain stimulation (STN DBS) is increasingly used in mid- to late-stage Park

207 Subthalamic nucleus deep brain stimulation (STN DBS) protects dopaminergic neurons of the substantia

208 Subthalamic deep brain stimulation (STN-DBS) for Parkinson's disease treats motor symptoms a

209 Subthalamic nucleus deep brain stimulation (STN-DBS) in Parkinson's disease (PD) not only stimulates

210 subthalamic nucleus deep-brain stimulation (STN-DBS) with motor cortical transcranial magnetic stimu

211 subthalamic nucleus deep brain stimulation (STN-DBS), while they performed an instrumental learning

212 Dbx1 microdomain gives rise to subthalamic (STN), premammillary (PM) and posterior hypothalamic (PH)

213 In summary, STN gamma activity may support flexible motor control as

214 trate that stimulation of three DBS targets (STN, subthalamic nucleus; GPi, globus pallidus internus;

215 ts during a perceptual decision-making task; STN low-frequency oscillatory (LFO) activity (2-8 Hz), c

216 undergoing neurosurgery, we demonstrate that STN beta oscillations can be suppressed when consecutive

217 These results demonstrate that STN DBS does not protect the nigrostriatal system agains

218 We demonstrate that STN DBS in male rats activates signaling downstream of t

219 Together, our results demonstrate that STN low-frequency oscillatory activity and corresponding

220 tion to examine the therapeutic effects that STN HFS may have on relapse in humans with heroin addict

221 We found that STN LFP activities in the gamma (55-90 Hz) and beta (13-

222 We found that STN-HFS significantly suppressed excessive self-grooming

223 The findings indicate that STN and GPi evoke a similar motor network pattern, while

224 These results show that STN-DBS can modulate cortical plasticity.

225 s used to interrupt licking, and showed that STN inhibition reduced the disruptive effect of surprise

226 Linear effects models showed that STN volume was significantly smaller in the PD subjects

227 These results suggest that STN DBS increases BDNF-trkB signaling to contribute to t

228 rvation with low divergence, suggesting that STN neurons operate as independent processing elements d

229 simultaneous recordings from cortex and the STN in humans, single-unit recordings in humans, high-re

230 cillations between prefrontal cortex and the STN, which may provide a preferential "window in time" f

231 hic and clinical characteristics between the STN-DBS and MED groups.

232 vation interrupts behavior, and blocking the STN blunts the interruptive effect of surprise.

233 Crucially, the STN and lateral PFC beta decrease was significantly atte

234 ndividual neurons was recorded in either the STN (n=100) or the GPi (n=100).

235 We compared beta power in the STN and GPi during rest and movement in 37 people with P

236 r objective was to compare beta power in the STN and GPi during rest and movement in people with PD u

237 s with PD diagnosed with ICD, neurons in the STN and GPi would be more responsive to reward-related s

238 ta band (15-30 Hz) activity decreased in the STN and PFC, and this decrease was progressively enhance

239 ups, the PD group had lower FA values in the STN compared to controls (corrected p <= 0.008).

240 epping-related modulation of activity in the STN could entrain patients' stepping movements as eviden

241 Previous work has shown that activity in the STN is modulated in a rhythmic pattern when Parkinson's

242 he unexpected action-related activity in the STN region was the more detrimental was the effect on re

243 Hence, synchrony in the STN, a hallmark of motor processing, exclusively depends

244 s of loss responsive neurons (p<0.05) in the STN, but not in the GPi.

245 of synaptic excitation and inhibition in the STN, which contributes to parkinsonian activity and moto

246 rate that morphological changes occur in the STN, which likely impact the function of the hyperdirect

247 tion of abnormal oscillatory activity in the STN-associated neural circuit, and these results highlig

248 monstration of associative plasticity in the STN-M1 circuits in PD patients using this novel techniqu

249 To investigate the STN microcircuitry, we combined multiple simultaneous pa

250 To explore this potential linkage, the STN was studied in BAC transgenic and Q175 knock-in mous

251 ransmission, leading to disinhibition of the STN and increased activation of STN NMDA receptors.

252 The functional connectivity of the STN at the microcircuit level, however, still requires r

253 ts into the microcircuit organization of the STN by identifying its neurons as parallel processing un

254 ht explain why deep-brain stimulation of the STN can impair subjects' ability to slow down responses

255 inhibited, (5) optogenetic inhibition of the STN exacerbated abnormal GPe activity, and (6) exaggerat

256 nstrated that optogenetic stimulation of the STN excited its major projection targets.

257 ism for fast yet transient decoupling of the STN from synchronizing afferent control.

258 sights into the synaptic organization of the STN identifying its neurons as parallel processing units

259 connectivity and synaptic properties of the STN in acute brain slices obtained from rats of both sex

260 ping rhythm, suggesting a causal role of the STN in dynamic gait control.

261 We argue that a major function of the STN is to broadly pause behavior and cognition when stop

262 t cortical inputs and synchronization of the STN neuronal population.

263 The influence of the STN on continue-evoked activity in the pre-SMA was predi

264 While increased oscillatory activity of the STN predicts elevated decision thresholds during high le

265 Manual segmentation of the STN was performed on 0.4 mm in-plane resolution images.

266 t in a rapid yet transient decoupling of the STN when stimulated at high frequencies.

267 ients' stepping movements as evidence of the STN's involvement in stepping control.

268 rtly through their direct innervation of the STN, but manipulating LH-projecting neurons had the oppo

269 esided around the dorsolateral border of the STN.

270 s described for anatomic subdivisions of the STN.

271 iques to firstly, visualize and quantify the STN neurochemical organization based on neuronal markers

272 each implanted with DBS leads targeting the STN and GPi.

273 y of the basal ganglia that also targets the STN.

274 g stopping or pausing, yet evidence that the STN causally implements stops or pauses is lacking.

275 ese results provide strong evidence that the STN is both necessary and sufficient for such forms of b

276 Our study suggests that the STN is causally involved in dynamic control of step timi

277 inputs from the motor cortex directly to the STN and that rescuing this loss alleviates Parkinsonian

278 ation, the GPe needs to send feedback to the STN equal to a particular function of the activity of ST

279 ontal cortical areas directly project to the STN via so-called hyperdirect pathways.

280 Relative to the STN, beta power in the GPi may be readily detected, modu

281 Our results show that, relative to the STN, beta power in the GPi may be readily detected, modu

282 This bundle connected frontal regions to the STN.

283 movements, raising the question whether the STN is involved in the dynamic control of stepping.

284 o the variance explained by overlap with the STN (R(2) = 21%) and sensorimotor STN (R(2) = 19%).

285 riple what was explained by overlap with the STN (R(2) = 9%) and its sensorimotor subpart (R(2) = 10%

286 these data argue that dysfunction within the STN is an early feature of HD that may contribute to its

287 first order dynamic linear model with these STN LFP features as inputs can be used to decode the tem

288 ntromedial portion, further implicating this STN subdivision in impulse control disorders.

289 Thus STN activation interrupts behavior, and blocking the STN

290 n and Yahr stage 2.6) were assessed prior to STN-DBS and 3 months postoperatively.

291 on and response inhibition networks prior to STN-DBS was not associated with postoperative impulsivit

292 , when the overlap of bursts between the two STN was high, slowing was more pronounced.

293 as linked to depressive symptom change under STN-DBS.

294 Although both animals undergoing STN DBS had similar beneficial effects, the proportion o

295 l (LFP) recordings in PD subjects undergoing STN-DBS over the course of a full-night's sleep.

296 ergic deficits had developed, rats underwent STN-DBS electrode implantation ipsilateral to the vector

297 Whether STN DBS can be protective in other models of synucleinop

298 c stimulation.SIGNIFICANCE STATEMENT Whether STN local cells contribute to the therapeutic effects of

299 logy and pathophysiology and may explain why STN is such an effective site for invasive treatment of

300 A training dataset of 51 PD patients with STN DBS was combined with publicly available human conne

301 Ten PD human patients with STN-DBS were studied in the on-medication state with DBS