Therapeutic Mechanisms Of High Frequency Stimulation In-Books Pdf

Therapeutic mechanisms of high frequency stimulation in
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that pattern regularization percolates straightforward from the The activity of the remaining BG nuclei was subsumed in the. target to the structures immediately downstream 34 36 input delivered to the GPi neurons and it varied in normal and. However this representation of the pattern regularization as PD conditions 64 The connections between neurons were. a local effect can hardly be reconciled with the fact that HFS of chosen consistently with the neuronal anatomy in NHPs and the. any structure of the cortico BG thalamo cortical loop is thera synaptic conductances were randomized across the entire net. peutic for at least some movement disorders 1 4 43 47 nor work to increase the pattern variability of the neurons at rest SI. does it explain why stimulation at frequencies above 160 180 Hz Notes 1 and 2. is not necessarily therapeutic despite the fact that the regularity DBS in the subthalamic area may elicit direct effects on the. of the axonal patterns may increase 48 49 Moreover co GPi monosynaptic orthodromic activation 17 putamen both. herence in the 8 30 Hz band among neurons across different monosynaptic orthodromic activation and antidromic activation. structures may decrease under HFS but not for lower frequen of striatonigral projections 5 65 67 cortex antidromic acti. cies 26 50 52 which suggests the emergence of diffused vation of cortico subthalamic projections 53 56 58 and. changes in neuronal activity that would be hardly accounted for thalamus antidromic activation of cortico subthalamic collater. with purely local effects als to the thalamus 31 We simulated these effects by applying. There is emerging evidence instead that HFS affects multiple a delayed depolarizing current pulse for each DBS pulse to the. structures simultaneously First it has been shown that deep PANs MSNs PYNs and TCNs The lag between current pulses. brain stimulation DBS may antidromically activate afferent and DBS input varied according to the depolarization mecha. axons and fibers of passage 53 59 thus reaching structures nism orthodromic vs antidromic and structure and the pulse. not immediately downstream Second studies 57 58 observed amplitudes were randomly distributed to simulate the stochastic. in 6 hydroxydopamine 6 OHDA intoxicated rats that the anti effects of both antidromic and orthodromic propagation 17 18. dromic effects increase with the stimulation frequency and peak 58 Fig S2 and SI Note 3. around 110 130 Hz Third it has been shown in 1 methyl 4 phenyl Regular DBS i e constant interpulse interval was applied at. 1 2 3 6 tetrahydropyridine MPTP intoxicated nonhuman primates 20 50 80 100 130 160 and 180 Hz Nonregular DBS i e. NHPs that STN DBS may evoke similar poststimulus responses interpulse intervals following a gamma distribution SI Note 3. NEUROSCIENCE, in different BG structures both downstream from and upstream with average frequency of 130 Hz was also applied For each. to the STN 5 27 28 30 60 Finally it has been reported that combination of disease condition and DBS setting three in. the cortico BG thalamo cortical system consists of multiple sets stances of the model were generated and each instance was. of reentrant interconnected and partially overlapping neuronal simulated for 32 000 ms The first 2 000 ms of each simulation. loops 5 42 61 62 which means that the structures upstream to were neglected to let the model reach steady state conditions. the target e g the striatum may play an important role in the and results were averaged across the model instances. therapeutic mechanisms of HFS, Altogether these results suggest that A pattern regulariza Normal vs Parkinsonian Conditions at Rest Figs 1 5 report the. tion is a global effect that exploits the closed loop nature of the population averaged results for the projecting neurons in the. cortico BG thalamo cortical system and selectively emerges only GPi PANs putamen MSNs cortex PYNs and thalamus. for specific HFS values and that B the therapeutic merit of TCNs respectively under normal and PD conditions at rest. pattern regularization has to deal with the restoration of a more Each population was N 600 neurons i e total number of. normal functionality of the entire cortico BG thalamo cortical neurons across three model instances The multifarious effects. loop rather than with variations in the information content of of the PD elicited loss of dopamine on the D1 5 dopaminergic. one specific structure receptors on the MSNs and on the interneurons in the putamen. We explored hypotheses A and B and assessed the system 68 were simulated by varying the maximal conductance of the. wide effects of DBS by constructing a computational model of M type potassium currents in the MSNs and the activity of the. the cortico BG thalamo cortical loop in both normal and parkin PPIs We also changed the stochastic distribution of the inputs. sonian conditions and by simulating the effects of STN DBS both at delivered to the GPi neurons thus simulating the effects of the loss. low 20 80 Hz and high 100 180 Hz frequencies The model of dopamine on the GPe STN subsystem SI Note 2. includes populations of single compartment neurons and inter As a result the simulated PANs showed a 56 increment of. neurons from motor cortex striatum GPi and thalamus according the population averaged pairwise cross correlation at the tran. to a network topology derived from the NHP anatomy and it sim sition from normal to PD conditions SI Note 4 and 5 26. ulates both the orthodromic and antidromic effects of DBS As increment in the average firing rate Fig 1E and an increased. a result this model reproduced both average activity and discharge incidence of the bursting mode thus reproducing experimental. patterns of single units in NHP and rats under normal and parkin results in refs 17 and 69 71 for NHPs A comparison between. sonian conditions with and without DBS for all modeled structures simulated and actual NHP single units from ref 17 is reported in. We show through numerical simulation that hypothesis A is Fig 1 A and C. significantly contributed by reinforcement mechanisms in the The percentage of time spent by PANs in bursts raised from. striatum These mechanisms are selectively elicited by HFS fa 9 1 2 3 normal to 22 3 4 0 PD the percentage of GPi. cilitate the percolation of regularized discharge patterns from spikes belonging to bursts raised from 13 9 3 4 to 58 5. the striatum to the GPi and have a primary role in B because 16 0 mean S D and the population average rates firing. the percolated striato pallidal input combines with the local and burst rate were comparable to the values in refs 17 23 and. effects of STN DBS to restore the thalamic relay function 63 71 for both normal and MPTP treated NHPs Fig 1 E and F. Furthermore the spectral analysis of the spiking patterns showed. Results that under PD conditions the PANs had exaggerated oscillations. We modeled the direct pathway in the cortico BG thalamo cor either in the 4 to 8 Hz band tremor band 60 of the population. tical loop 7 8 a schematic is shown in Fig S1 by using single or in the 10 to 15 Hz band beta band 40 of the population. compartment neurons from the motor cortex 200 pyramidal neu Fig 2 A and B These oscillations were caused by a combination. rons PYNs and 20 fast spiking interneurons FSIs dorsolateral of the input from putamen 72 and the input from the GPe. striatum i e putamen 200 medium spiny neurons MSNs and 20 STN subsystem 73 The frequency bands of the oscillations and. parvalbumin positive interneurons PPIs GPi 200 pallidal neu the ratio between the number of neurons with tremor and. rons PANs and ventrolateral thalamus 200 thalamocortical beta band oscillations were consistent with experiments in refs. neurons TCNs and 40 reticular neurons RENs 51 52 69 and 70 Fig 2C. Santaniello et al PNAS Published online January 26 2015 E587. A NHP Recordings E 150 Model NHP, firing rate spikes s. 100 A3 B C, B 50 2 2 2, Model NHP 1 1, burst rate bursts min. 0 5 10 15 20 25 5 10 15 20 25 30 5 10 15 20 25 30, frequency Hz frequency Hz frequency Hz.
0 200 400 600 800 1000 Fig 2 A and B Population average normalized power spectrum density PSD. of tremor band oscillatory A and beta band oscillatory B GPi neurons in our. model under normal black dots PD blue line and PD HFS red line con. ditions C Population average normalized PSD of beta band oscillatory GPi. 0 200 400 600 800 1000 0, time ms Model NHP neurons from a NHP under PD blue line and PD HFS red line conditions HFS is. 130 Hz in A and B and 125 Hz in C C is modified with permission from ref 51. Fig 1 A D Raster plot of a GPi neuron under PD conditions at rest A and. C and with STN HFS B and D A and B are from an MPTP treated NHP. modified with permission from ref 17 C and D are from a pallidal neuron the trend reported in ref 78 On the other hand the loss of do. in our model Red bars in C denote estimated bursts E Population average. pamine had an effect on the oscillations of the TCN discharge. firing rate mean SD of the GPi neurons under normal white PD. black and PD with STN HFS PD HFS gray conditions in our model and. pattern 224 out of 600 TCNs had a significant change in the. NHPs F Population average burst rate mean SD of the GPi neurons interspike interval ISI histogram t test P 0 05 with an en. under PD black and PD HFS gray conditions in our model and NHPs hanced bimodal distribution of the ISIs in PD conditions and. Population average burst rate of the GPi under normal condition is 20 9 peaks around 3 ms and 30 ms Fig 6 A and B consistently with. 4 7 bursts per minute mean SD Rates for NHPs in E and F are reported in data from MPTP treated NHPs 31 Correspondingly the dif. refs 17 and 71 and ref 23 respectively Asterisks squares show significant ference between the power spectrum of the spike trains under. differences normal vs PD and PD HFS PD vs PD HFS one way ANOVA normal and PD conditions mean square error MSE in the. with Tukey Kramer post hoc test P 0 001 HFS is 136 Hz in the NHPs B E. 3 100 Hz band was significant Fig 7A P 0 001, and F and 130 Hz in our model D F. Direct Effects of STN DBS on the GPi Thalamus Cortex and Putamen. Under PD conditions the modulation of M type potassium STN DBS at 130 Hz range 125 136 Hz has been reported to. currents and the reduced GABAergic input from the striatal restore movement disorders in MPTP treated NHPs and 6 OHDA. interneurons affected the activity of the MSNs Overall 72 of treated rats 5 15 17 23 28 31 51 57 80. the MSNs 490 out of 600 increased the average firing rate In our model under PD conditions 130 Hz STN DBS affected. t test P 0 05 which is consistent with refs 74 and 75 whereas the GPi PANs by inducing more regular firing patterns higher av. the remaining neurons decreased it As a result even though the erage firing rates and lower burstiness Fig 1 B E and F with. mean firing rate increased there was a larger variability of the results matching experimental observations in refs 17 and 23 Fig 1. spiking patterns across the population Fig 3 A and B and an D F The percentage of time spent in bursts and the percentage. increased level of pairwise cross correlation SI Note 5 of spikes belonging to bursts dropped to 14 8 6 7 and. Overall the changes in the striato pallidal subsystem had mi 27 7 15 5 mean SD respectively and the oscillations in the. nor effects on the average activity of the cortical and thalamic tremor and beta band were significantly attenuated Wilcoxon rank. neurons In cortex the percentage of PYNs with random regu sum test P 0 001 consistently with results in ref 51 Fig 2. lar or bursty patterns mildly changed at the transition from STN DBS at 130 Hz also affected the remaining structures in. normal to PD conditions random 270 vs 290 regular 97 vs the model under PD conditions The population average firing. 121 bursty 231 vs 184 normal vs PD definition of the patterns rate significantly increased t test P 0 001 for the MSNs Fig 3. is given in ref 76 and SI Note 4 and nonsignificant changes C and D and PYNs Fig S3 and it mildly decreased for the. Wilcoxon rank sum test P 0 05 were reported for the distri TCNs Fig 5 C and F whereas individual TCNs either signifi. bution of the firing rates across the PYNs Fig 4 A B D and E cantly increased 77 out of 600 or decreased 339 out of 600 the. the population average firing rate Fig 4C and the percentage firing rate t test P 0 05 consistently with experiments in refs. of time spent in burst activity Fig 4F consistently with ref 76 31 57 and 80 Furthermore the ISI histogram for the TCNs. M1 group We measured the fraction of power allocated in the moved from a continuous distribution to a multimodal distribution. 8 30 Hz band for each PYN and we found that this fraction with peaks corresponding to multiples of the DBS interpulse in. increased in 331 out of 600 PYNs when under PD conditions terval Fig 6 A and B whereas the spectral content of the TCN. which is consistent with the increment of oscillations in that band spike trains was affected in a way that compensated for the changes. reported by ref 76 The average increment in the 8 30 Hz power induced by the PD conditions and returned to a value close to. across these 331 PYNs was 5 9 6 0 mean SD range normal conditions MSE was minimal and 0 Fig 7A. 0 53 9 and resulted in no prominent oscillation in that band The firing pattern of the TCNs however remained significantly. which is consistent with the analysis of single unit recordings of different from normal when 130 Hz STN DBS was applied These. to treat parkinsonian movement disorders but its mechanisms remain elusive Current hypotheses suggest that the therapeutic merit of HFS stems from increasing the regularity of the firing patterns in the basal ganglia BG Although this is consistent with experiments in humans and animal models of Parkinsonism it is

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