| 2. |
- Klaus, A., et al.
(författare)
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The influence of subthreshold membrane potential oscillations and GABAergic input on firing activity in striatal fast-spiking neurons
- 2009
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Ingår i: BMC Neuroscience. - 1471-2202. ; 10:Suppl.1, s. P244-
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Tidskriftsartikel (refereegranskat)abstract
- The striatum is the main input stage of the basal ganglia system, which is involved in executive functions of the forebrain, such as the planning and the selection of motor behavior. Feedforward inhibition of medium-sized spiny projection neurons in the striatum by fast-spiking interneurons is supposed to be an important determinant of controlling striatal output to later stages of the basal ganglia[1]. Striatal fast-spiking interneurons, which constitute approximately 1–2% of all striatal neurons, show many similarities to cortical fast-spiking cells. In response to somatic current injection, for example, some of these neurons exhibit spike bursts with a variable number of action potentials (so called stuttering)[2-4]. Interestingly, the membrane potential between such stuttering episodes oscillates in the range of 20–100 Hz[3,5]. The first spike of each stuttering episode invariably occurs at a peak of the underlying subthreshold oscillation. In both cortex and striatum, fast-spiking cells are inter-connected by gap junctions[6,7]. In vitro measurements as well as theoretical studies indicate that electrical coupling via gap junctions might be able to promote synchronous activity among these neurons[6,8]. Here we investigate the possible role of subthreshold oscillations on the synchronization of sub- and suprathreshold activity in a model of electrically coupled fast-spiking neurons. We use the model of Golomb et al.[3], which we extended with a dendritic tree so as to be able to simulate distal synaptic input. We show that gap junctions are able to synchronize subthreshold membrane potential fluctuations in response to somatic current injection. However, the oscillations are only prevalent in the subthreshold range and therefore require enough membrane potential depolarization[5]. In response to synaptic input, our model neuron only enters the subthreshold oscillatory regime with AMPA and NMDA synapses located at distal dendrites. Proximal synaptic input leads to more random fluctuations of the membrane potential, reflecting a smaller extent of dendritic filtering of the Poisson-distributed postsynaptic potentials. We furthermore investigate the effect of GABAergic (i.e. inhibitory) input to the model of the fast-spiking neuron and predict that inhibitory input is able to induce a stuttering episode in these cells. We finally discuss our results in the context of the feedforward inhibitory network, which is likely to play an important role in striatal and basal ganglia function.
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| 3. |
- Lindahl, Mikael, et al.
(författare)
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Short term plasticity within the basal ganglia - a systems level computational investigation
- 2011
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Ingår i: BMC Neuroscience. - 1471-2202. ; 12:Suppl 1, s. P145-
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Tidskriftsartikel (refereegranskat)abstract
- Striatal direct pathway medium spiny neurons (MSNs) converge, with inhibitory synapses onto output nuclei substantia nigra reticulata (SNr), which keep neurons in the thalamus, superior colliculus and pendunculopontine nuclei under tonic inhibition[1]. Recent experimental findings[2] have found short term facilitation in MSN synapses onto SNr neurons. We investigate the functional consequences of these findings using a basal ganglia system level model, with spiking MSNs modeled according to Izhikevich’s simple model[3] and with facilitating synapses[4] fitted to data in[2]. The model is implemented in the NEST[5] simulator. We quantify how striatal populations of MSNs can control activity in SNr neurons, and to what extent this depends on having weak static, strong static and facilitating synapses between MSNs and SNr neurons. Our simulation experiments predict that facilitating synapses allow baseline firing of presynaptic MSNs without suppressing target SNr neurons, while burst activation of only a few of these presynaptic striatal neurons can suppress the activity of one SNr neuron. This is in accordance with extracellular recordings in awake animals[6], where task dependent activity is transferred from a broad striatal population to a smaller subpopulation, responding increasingly stronger during learning of a task dependent behavior.
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| 4. |
- Belic, Jovana, et al.
(författare)
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The role of striatal feedforward inhibition in propagation of cortical oscillations
- 2017
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Ingår i: BMC Neuroscience. - Antwerpen. - 1471-2202. ; 18, s. 91-91
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Tidskriftsartikel (refereegranskat)abstract
- Fast spiking interneurons (FSIs) and feedforward (FF) inhibition are a common property of neuronal networks throughout the brain and play crucial role in neural computations. For instance, in the cortex FF inhibition sets the window of temporal integration and spiking and thereby contributes to the control of firing rate and correlations [1]. In the striatum (the main input structure of the basal ganglia) despite their high firing rates and strong synapses, FSIs (comprise 1–2% of striatal neurons) do not seem to play a major role in controlling the firing of medium spiny neurons (MSNs; comprise 95% of striatal neurons) [2] and so far, it has not been possible to attribute a functional role to FSIs in the striatum. Here we use a spiking neuron network model in order to investigate how externally induced oscillations propagate through striatal circuitry. Recordings in the striatum have shown robust oscillatory activity that might be in fact cortical oscillations transmitted by the corticostriatal projections [3–5]. We propose that FSIs can perform an important role in transferring cortical oscillations to the striatum especially to those MSNs that are not directly driven by the cortical oscillations. Strong and divergent connectivity of FSIs implies that even weak oscillations in FSI population activity can be spread to the whole MSN population [6]. Further, we have identified multiple factors that influence the transfer of oscillations to MSNs. The variables such as the number of activated neurons, ongoing activity, connectivity, and synchronicity of inputs influence the transfer of oscillations by modifying the levels of feedforward and feedback inhibitions suggesting that the striatum can exploit different parameters to impact the transfer of oscillatory signals.References1. Isaacson, J. S., & Scanziani, M. (2011). How inhibition shapes cortical activity. Neuron, 72(2), 231–243. 2. Berke, J. D. (2011). Functional properties of striatal fast-spiking interneurons. Frontiers in systems neuroscience, 5.3. Belić, J. J., Halje, P., Richter, U., Petersson, P., & Kotaleski, J. H. (2016). Untangling cortico-striatal connectivity and cross-frequency coupling in L-DOPA-induced dyskinesia. Frontiers in systems neuroscience, 10.4. Berke, J. D. (2009). Fast oscillations in cortical‐striatal networks switch frequency following rewarding events and stimulant drugs. European Journal of Neuroscience, 30(5), 848–859.5. Boraud, T., Brown, P., Goldberg, J. A., Graybiel, A. M., & Magill, P. J. (2005). Oscillations in the basal ganglia: the good, the bad, and the unexpected. In The basal ganglia VIII (pp. 1–24). Springer US.6. Belić, J. J., Kumar, A., & Kotaleski, J. H. (2017). Interplay between periodic stimulation and GABAergic inhibition in striatal network oscillations. PloS one, 12(4), e0175135.
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