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  • 1
    In: The Journal of Neuroscience, Society for Neuroscience
    Abstract: During rest, intrinsic neural dynamics manifest at multiple timescales, which progressively increase along visual and somatosensory hierarchies. Theoretically, intrinsic timescales are thought to facilitate processing of external stimuli at multiple stages. However, direct links between timescales at rest and sensory processing, as well as translation to the auditory system are lacking. Here, we measured intracranial electroencephalography in 11 human patients with epilepsy (4 women), while listening to pure tones. We show that in the auditory network, intrinsic neural timescales progressively increase, while the spectral exponent flattens, from temporal to entorhinal cortex, hippocampus, and amygdala. Within the neocortex, intrinsic timescales exhibit spatial gradients that follow the temporal lobe anatomy. Crucially, intrinsic timescales at baseline can explain the latency of auditory responses: as intrinsic timescales increase, so do the single-electrode response onset and peak latencies. Our results suggest that the human auditory network exhibits a repertoire of intrinsic neural dynamics, which manifest in cortical gradients with millimeter resolution and may provide a variety of temporal windows to support auditory processing. SIGNIFICANCE STATEMENT: Endogenous neural dynamics are often characterized by their intrinsic timescales. These are thought to facilitate processing of external stimuli. However, a direct link between intrinsic timing at rest and sensory processing is missing. Here, with intracranial electroencephalography (iEEG), we show that intrinsic timescales progressively increase from temporal to entorhinal cortex, hippocampus, and amygdala. Intrinsic timescales at baseline can explain the variability in the timing of iEEG responses to sounds: cortical electrodes with fast timescales also show fast and short-lasting responses to auditory stimuli, which progressively increase in the hippocampus and amygdala. Our results suggest that a hierarchy of neural dynamics in the temporal lobe manifests across cortical and limbic structures and can explain the temporal richness of auditory responses.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2023
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2020
    In:  European Journal of Neuroscience Vol. 52, No. 5 ( 2020-09), p. 3353-3374
    In: European Journal of Neuroscience, Wiley, Vol. 52, No. 5 ( 2020-09), p. 3353-3374
    Abstract: Lack of dopamine (DA) in the striatum and the consequential dysregulation of thalamocortical circuits are major causes of motor impairments in Parkinson's disease. The striatum receives multiple cortical and subcortical afferents. Its role in movement control and motor skills learning is regulated by DA from the nigrostriatal pathway. In Parkinson's disease, DA loss affects striatal network activity and induces a functional imbalance of its output pathways, impairing thalamocortical function. Striatal projection neurons are GABAergic and form two functionally antagonistic pathways: the direct pathway, originating from DA receptor type 1‐expressing medium spiny neurons (D 1 R‐MSN), and the indirect pathway, from D 2 R‐MSN. Here, we investigated whether DA depletion in mouse striatum also affects GABAergic function. We recorded GABAergic miniature IPSCs (mIPSC) and tonic inhibition from D 1 R‐ and D 2 R‐MSN and used immunohistochemical labeling to study GABA A R function and subcellular distribution in DA‐depleted and control mice. We observed slower decay kinetics and increased tonic inhibition in D 1 R‐MSN, while D 2 R‐MSN had increased mIPSC frequency after DA depletion. Perisomatic synapses containing the GABA A R subunits α 1 or α 2 were not affected, but there was a strong decrease in non‐synaptic GABA A Rs containing these subunits, suggesting altered receptor trafficking. To broaden these findings, we also investigated GABA A Rs in GABAergic and cholinergic interneurons and found cell type‐specific alterations in receptor distribution, likely reflecting changes in connectivity. Our results reveal that chronic DA depletion alters striatal GABAergic transmission, thereby affecting cellular and circuit activity. These alterations either result from pathological changes or represent a compensatory mechanism to counteract imbalance of output pathways.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Wiley ; 2019
    In:  Journal of Comparative Neurology Vol. 527, No. 12 ( 2019-08-15), p. 2030-2046
    In: Journal of Comparative Neurology, Wiley, Vol. 527, No. 12 ( 2019-08-15), p. 2030-2046
    Abstract: The striatum is the main input nucleus of the basal ganglia, mediating motor and cognitive functions. Striatal projection neurons are GABAergic medium spiny neurons (MSN), expressing either the dopamine receptor type 1 (D 1 ‐R MSN) and forming the direct, movement‐promoting pathway, or dopamine receptor type 2 (D 2 ‐R MSN), forming the indirect movement‐suppressing pathway. Locally, activity and synchronization of MSN are modulated by several subtypes of GABAergic and cholinergic interneurons. Overall, GABAergic circuits in the striatum remain poorly characterized, and little is known about the intrastriatal connectivity of interneurons and the distribution of GABA A receptor (GABA A R) subtypes, distinguished by their subunit composition, in striatal synapses. Here, by using immunofluorescence in mouse tissue, we investigated the distribution of GABA A Rs containing the α 1 , α 2 , or α 3 subunit in perisomatic synapses of striatal MSN and interneurons, as well as the innervation pattern of D 1 R‐ and D 2 R‐MSN soma and axonal initial segment (AIS) by GABAergic and cholinergic interneurons. Our results show that perisomatic GABAergic synapses of D 1 R‐ and D 2 R‐MSN contain the GABA A R α 1 and/or α 2 subunits, but not the α 3 subunit; D 2 R‐MSN have significantly more α 1 ‐GABA A Rs on their soma than D 1 R‐MSN. Further, interneurons have few perisomatic synapses containing α 2 ‐GABA A Rs, whereas α 3 ‐GABA A Rs (along with the α 1 ‐GABA A Rs) are abundant in perisomatic synapses of CCK + , NPY + /SOM + , and vAChT + interneurons. Each MSN and interneuron population analyzed received a distinct pattern of GABAergic and cholinergic innervation, complementing this postsynaptic heterogeneity. In conclusion, intra‐striatal GABAergic circuits are distinguished by cell‐type specific innervation patterns, differential expression and postsynaptic targeting of GABA A R subtypes.
    Type of Medium: Online Resource
    ISSN: 0021-9967 , 1096-9861
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1474879-4
    SSG: 12
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  • 4
    In: Cell Reports, Elsevier BV, Vol. 43, No. 7 ( 2024-07), p. 114500-
    Type of Medium: Online Resource
    ISSN: 2211-1247
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2024
    detail.hit.zdb_id: 2649101-1
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