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Mapping of Cortical Avalanches to the Striatum
KTH, Skolan för datavetenskap och kommunikation (CSC), Beräkningsbiologi, CB. KTH, Skolan för datavetenskap och kommunikation (CSC), Beräkningsvetenskap och beräkningsteknik (CST). University of Freiburg, Germany.
National Institute of Mental Health, Bethesda, USA.
National Institute of Mental Health, Bethesda, USA.
KTH, Skolan för datavetenskap och kommunikation (CSC).ORCID-id: 0000-0002-0550-0739
2015 (engelsk)Inngår i: Advances in Cognitive Neurodynamics, Springer Netherlands, 2015, 4, s. 291-297Kapittel i bok, del av antologi (Fagfellevurdert)
Abstract [en]

Neuronal avalanches are found in the resting state activity of the mammaliancortex. Here we studied whether and how cortical avalanches are mappedonto the striatal circuitry, the first stage of the basal ganglia. We first demonstrate using organotypic cortex-striatum-substantia nigra cultures from rat that indeed striatal neurons respond to cortical avalanches originating in superficial layers. We simultaneously recorded spontaneous local field potentials (LFPs) in the cortical and striatal tissue using high-density microelectrode arrays. In the cortex, spontaneous neuronal avalanches were characterized by intermittent spatiotemporal activity clusters with a cluster size distribution that followed a power law with exponent 1.5. In the striatum, intermittent spatiotemporal activity was found to correlate with cortical avalanches. However, striatal negative LFP peaks (nLFPs) did not showavalanche signatures, but formed a cluster size distribution that had a much steeper drop-off, i.e., lacked large spatial clusters that are commonly expected for avalanche dynamics. The underlying de-correlation of striatal activity could have its origin in the striatum through local inhibition and/or could result from a particular mapping in the corticostriatal pathway. Here we show, using modeling, that highly convergent corticostriatal projections can map spatially extended cortical activity into spatially restricted striatal regimes.

sted, utgiver, år, opplag, sider
Springer Netherlands, 2015, 4. s. 291-297
Emneord [en]
Neuronal avalanches, Striatum, Cortico-striatal network, Cortex, Basal ganglia
HSV kategori
Identifikatorer
URN: urn:nbn:se:kth:diva-168104DOI: 10.1007/978-94-017-9548-7_41ISI: 000380362800041ISBN: 978-94-017-9547-0 (tryckt)OAI: oai:DiVA.org:kth-168104DiVA, id: diva2:814424
Merknad

QC 20150623

Tilgjengelig fra: 2015-05-27 Laget: 2015-05-27 Sist oppdatert: 2018-02-09bibliografisk kontrollert
Inngår i avhandling
1. Untangling Cortico-Striatal Circuitry and its Role in Health and Disease - A computational investigation
Åpne denne publikasjonen i ny fane eller vindu >>Untangling Cortico-Striatal Circuitry and its Role in Health and Disease - A computational investigation
2018 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

The basal ganglia (BG) play a critical role in a variety of regular motor and cognitive functions. Many brain diseases, such as Parkinson’s diseases, Huntington’s disease and dyskinesia, are directly related to malfunctions of the BG nuclei. One of those nuclei, the input nucleus called the striatum, is heavily connected to the cortex and receives afferents from nearly all cortical areas. The striatum is a recurrent inhibitory network that contains several distinct cell types. About 95% of neurons in the striatum are medium spiny neurons (MSNs) that form the only output from the striatum. Two of the most examined sources of GABAergic inhibition into MSNs are the feedback inhibition (FB) from the axon collaterals of the MSNs themselves, and the feedforward inhibition (FF) via the small population (1-2% of striatal neurons) of fast spiking interneurons (FSIs). The cortex sends direct projections to the striatum, while the striatum can affect the cortex only indirectly through other BG nuclei and the thalamus. Understanding how different components of the striatal network interact with each other and influence the striatal response to cortical inputs has crucial importance for clarifying the overall functions and dysfunctions of the BG.

    In this thesis I have employed advanced experimental data analysis techniques as well as computational modelling, to study the complex nature of cortico-striatal interactions. I found that for pathological states, such as Parkinson’s disease and L-DOPA-induced dyskinesia, effective connectivity is bidirectional with an accent on the striatal influence on the cortex. Interestingly, in the case of L-DOPA-induced dyskinesia, there was a high increase in effective connectivity at ~80 Hz and the results also showed a large relative decrease in the modulation of the local field potential amplitude (recorded in the primary motor cortex and sensorimotor striatum in awake, freely behaving, 6-OHDA lesioned hemi-parkinsonian rats) at ~80 Hz by the phase of low frequency oscillations. These results suggest a lack of coupling between the low frequency activity of a presumably larger neuronal population and the synchronized activity of a presumably smaller group of neurons active at 80 Hz.

    Next, I used a spiking neuron network model of the striatum to isolate the mechanisms underlying the transmission of cortical oscillations to the MSN population. I showed that FSIs play a crucial role in efficient propagation of cortical oscillations to the MSNs that did not receive direct cortical oscillations. Further, I have identified multiple factors such as the number of activated neurons, ongoing activity, connectivity, and synchronicity of inputs that influenced the transfer of oscillations by modifying the levels of FB and FF inhibitions. Overall, these findings reveal a new role of FSIs in modulating the transfer of information from the cortex to striatum. By modulating the activity and properties of the FSIs, striatal oscillations can be controlled very efficiently. Finally, I explored the interactions in the striatal network with different oscillation frequencies and showed that the features of those oscillations, such as amplitude and frequency fluctuations, can be influenced by a change in the input intensities into MSNs and FSIs and that these fluctuations are also highly dependent on the selected frequencies in addition to the phase offset between different cortical inputs.

    Lastly, I investigated how the striatum responds to cortical neuronal avalanches. Recordings in the striatum revealed that striatal activity was also characterized by spatiotemporal clusters that followed a power law distribution albeit, with significantly steeper slope. In this study, an abstract computational model was developed to elucidate the influence of intrastriatal inhibition and cortico-striatal interplay as important factors to understand the experimental findings. I showed that one particularly high activation threshold of striatal nodes can reproduce a power law-like distribution with a coefficient similar to the one found experimentally. By changing the ratio of excitation and inhibition in the cortical model, I saw that increased activity in the cortex strongly influenced striatal dynamics, which was reflected in a less negative slope of cluster size distributions in the striatum.  Finally, when inhibition was added to the model, cluster size distributions had a prominently earlier deviation from the power law distribution compared to the case when inhibition was not present. 

sted, utgiver, år, opplag, sider
Stockholm: KTH Royal Institute of Technology, 2018. s. 88
Serie
TRITA-EECS-AVL ; 2018:9
Emneord
cortico-striatal circuits, levodopa-induced dyskinesia, Parkinson’s disease, effective connectivity, cross-frequency coupling, corticostriatal network, network oscillations, GABAergic transmission. basal ganglia, striatum, cortex, fast spiking interneurons, medium spiny neurons, neuronal avalanches
HSV kategori
Identifikatorer
urn:nbn:se:kth:diva-222467 (URN)978-91-7729-676-8 (ISBN)
Disputas
2018-03-05, F3, Lindstedtsvägen 26, KTH Campus, Stockholm, 13:15 (engelsk)
Opponent
Veileder
Merknad

QC 20180209

Tilgjengelig fra: 2018-02-09 Laget: 2018-02-09 Sist oppdatert: 2018-06-12bibliografisk kontrollert

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