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Journal articles on the topic 'Striatum Dynamics'

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Author: Grafiati
Published: 10 March 2023

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1

Bakhurin, Konstantin I., Victor Mac, Peyman Golshani, and Sotiris C. Masmanidis. "Temporal correlations among functionally specialized striatal neural ensembles in reward-conditioned mice." Journal of Neurophysiology 115, no. 3 (March 1, 2016): 1521–32. http://dx.doi.org/10.1152/jn.01037.2015.

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As the major input to the basal ganglia, the striatum is innervated by a wide range of other areas. Overlapping input from these regions is speculated to influence temporal correlations among striatal ensembles. However, the network dynamics among behaviorally related neural populations in the striatum has not been extensively studied. We used large-scale neural recordings to monitor activity from striatal ensembles in mice undergoing Pavlovian reward conditioning. A subpopulation of putative medium spiny projection neurons (MSNs) was found to discriminate between cues that predicted the delivery of a reward and cues that predicted no specific outcome. These cells were preferentially located in lateral subregions of the striatum. Discriminating MSNs were more spontaneously active and more correlated than their nondiscriminating counterparts. Furthermore, discriminating fast spiking interneurons (FSIs) represented a highly prevalent group in the recordings, which formed a strongly correlated network with discriminating MSNs. Spike time cross-correlation analysis showed the existence of synchronized activity among FSIs and feedforward inhibitory modulation of MSN spiking by FSIs. These findings suggest that populations of functionally specialized (cue-discriminating) striatal neurons have distinct network dynamics that sets them apart from nondiscriminating cells, potentially to facilitate accurate behavioral responding during associative reward learning.
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2

Evans, R. C., G. A. Herin, S. L. Hawes, and K. T. Blackwell. "Calcium-dependent inactivation of calcium channels in the medial striatum increases at eye opening." Journal of Neurophysiology 113, no. 7 (April 2015): 2979–86. http://dx.doi.org/10.1152/jn.00818.2014.

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Influx of calcium through voltage-gated calcium channels (VGCCs) is essential for striatal function and plasticity. VGCCs expressed in striatal neurons have varying kinetics, voltage dependences, and densities resulting in heterogeneous subcellular calcium dynamics. One factor that determines the calcium dynamics in striatal medium spiny neurons is inactivation of VGCCs. Aside from voltage-dependent inactivation, VGCCs undergo calcium-dependent inactivation (CDI): inactivating in response to an influx of calcium. CDI is a negative feedback control mechanism; however, its contribution to striatal neuron function is unknown. Furthermore, although the density of VGCC expression changes with development, it is unclear whether CDI changes with development. Because calcium influx through L-type calcium channels is required for striatal synaptic depression, a change in CDI could contribute to age-dependent changes in striatal synaptic plasticity. Here we use whole cell voltage clamp to characterize CDI over developmental stages and across striatal regions. We find that CDI increases at the age of eye opening in the medial striatum but not the lateral striatum. The developmental increase in CDI mostly involves L-type channels, although calcium influx through non-L-type channels contributes to the CDI in both age groups. Agents that enhance protein kinase A (PKA) phosphorylation of calcium channels reduce the magnitude of CDI after eye opening, suggesting that the developmental increase in CDI may be related to a reduction in the phosphorylation state of the L-type calcium channel. These results are the first to show that modifications in striatal neuron properties correlate with changes to sensory input.
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3

Kondabolu, Krishnakanth, Erik A. Roberts, Mark Bucklin, Michelle M. McCarthy, Nancy Kopell, and Xue Han. "Striatal cholinergic interneurons generate beta and gamma oscillations in the corticostriatal circuit and produce motor deficits." Proceedings of the National Academy of Sciences 113, no. 22 (May 16, 2016): E3159—E3168. http://dx.doi.org/10.1073/pnas.1605658113.

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Cortico-basal ganglia-thalamic (CBT) neural circuits are critical modulators of cognitive and motor function. When compromised, these circuits contribute to neurological and psychiatric disorders, such as Parkinson’s disease (PD). In PD, motor deficits correlate with the emergence of exaggerated beta frequency (15–30 Hz) oscillations throughout the CBT network. However, little is known about how specific cell types within individual CBT brain regions support the generation, propagation, and interaction of oscillatory dynamics throughout the CBT circuit or how specific oscillatory dynamics are related to motor function. Here, we investigated the role of striatal cholinergic interneurons (SChIs) in generating beta and gamma oscillations in cortical-striatal circuits and in influencing movement behavior. We found that selective stimulation of SChIs via optogenetics in normal mice robustly and reversibly amplified beta and gamma oscillations that are supported by distinct mechanisms within striatal-cortical circuits. Whereas beta oscillations are supported robustly in the striatum and all layers of primary motor cortex (M1) through a muscarinic-receptor mediated mechanism, gamma oscillations are largely restricted to the striatum and the deeper layers of M1. Finally, SChI activation led to parkinsonian-like motor deficits in otherwise normal mice. These results highlight the important role of striatal cholinergic interneurons in supporting oscillations in the CBT network that are closely related to movement and parkinsonian motor symptoms.
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4

Carrillo-Reid, Luis, Fatuel Tecuapetla, Nicolas Vautrelle, Adán Hernández, Ramiro Vergara, Elvira Galarraga, and José Bargas. "Muscarinic Enhancement of Persistent Sodium Current Synchronizes Striatal Medium Spiny Neurons." Journal of Neurophysiology 102, no. 2 (August 2009): 682–90. http://dx.doi.org/10.1152/jn.00134.2009.

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Network dynamics denoted by synchronous firing of neuronal pools rely on synaptic interactions and intrinsic properties. In striatal medium spiny neurons, N-methyl-d-aspartate (NMDA) receptor activation endows neurons with nonlinear capabilities by inducing a negative-slope conductance region (NSCR) in the current–voltage relationship. Nonlinearities underlie associative learning, procedural memory, and the sequential organization of behavior in basal ganglia nuclei. The cholinergic system modulates the function of medium spiny projection neurons through the activation of muscarinic receptors, increasing the NMDA-induced NSCR. This enhancement is reflected as a change in the NMDA-induced network dynamics, making it more synchronous. Nevertheless, little is known about the contribution of intrinsic properties that promote this activity. To investigate the mechanisms underlying the cholinergic modulation of bistable behavior in the striatum, we used whole cell and calcium-imaging techniques. A persistent sodium current modulated by muscarinic receptor activation participated in the enhancement of the NSCR and the increased network synchrony. These experiments provide evidence that persistent sodium current generates bistable behavior in striatal neurons and contributes to the regulation of synchronous network activity. The neuromodulation of bistable properties could represent a cellular and network mechanism for cholinergic actions in the striatum.
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5

Ding, Long. "Distinct dynamics of ramping activity in the frontal cortex and caudate nucleus in monkeys." Journal of Neurophysiology 114, no. 3 (September 2015): 1850–61. http://dx.doi.org/10.1152/jn.00395.2015.

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The prefronto-striatal network is involved in many cognitive functions, including perceptual decision making and reward-modulated behaviors. For well-trained subjects, neural responses frequently show similar patterns in the prefrontal cortex and striatum, making it difficult to tease apart distinct regional contributions. Here I show that, despite similar mean firing rate patterns, prefrontal and striatal responses differ in other temporal dynamics for both perceptual and reward-based tasks. Compared with simulation results, the temporal dynamics of prefrontal activity are consistent with an accumulation of sensory evidence used to solve a perceptual task but not with an accumulation of reward context-related information used for the development of a reward bias. In contrast, the dynamics of striatal activity is consistent with an accumulation of reward context-related information and with an accumulation of sensory evidence during early stimulus viewing. These results suggest that prefrontal and striatal neurons may have specialized functions for different tasks even with similar average activity.
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6

Kudryavtseva, V. A., A. V. Moiseeva, S. G. Mukhamedova, G. A. Piavchenko, and S. L. Kuznetsov. "Age- and sex-related dynamics of structural and functional motor behavior interactions in striatum neurons in rats." Sechenov Medical Journal 13, no. 2 (December 7, 2022): 20–29. http://dx.doi.org/10.47093/2218-7332.2022.13.2.20-29.

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Aim. To study the age-related dynamics of structural and functional interactions of striatal neurons in the implementation of acts of motor behaviour in rats of both sexes.Materials and methods. The study was carried out on 36 Wistar rats of both sexes aged 2, 7 and 16 months (n = 6 per group). In animals of all groups, locomotor activity was determined using a Laboras device (Metris, the Netherlands) for15 minutes, after which the brain was sampled to determine the number and size of neurons in the striatum. The median and interquartile range of the index of motor activity and the number of neurons were determined, and to study the relationship between these indicators, a correlation and regression analysis was performed with the construction of linear and polynomial trends, and the coefficient of determination R2 was calculated.Results. The size of neurons did not change significantly with age in the rats of both sexes. The number of neurons differed statistically in the rats of different sexes in all age groups. In male rats, the maximum number of neurons was noted at the age of 7 months with a decrease to 16 months. In female rats, the maximum number of neurons was recorded at the age of 2 months with a further decrease to 7 and 16 months. According to the regression analysis, a linear strong relationship (R2 =0.80 for males, R2 = 0.79 for females) was established between the number of neurons in the striatum and motor activity in 2-month-old animals. At the age of 7 and 16 months the relationship is non-linear.Conclusion. The number of neurons in the striatum is subject to sex and age dynamics, while their size remains unchanged from 2 to 16 months. For animals of both sexes, a decrease in the role of the striatum in providing motor activity in the process of growing up was noted. This relationship reaches its maximum in 2-month-old rats and then decreases.
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7

Zhang, Rui L., Michael Chopp, Sara R. Gregg, Yier Toh, Cindi Roberts, Yvonne LeTourneau, Benjamin Buller, Longfei Jia, Siamak P. Nejad Davarani, and Zheng G. Zhang. "Patterns and Dynamics of Subventricular Zone Neuroblast Migration in the Ischemic Striatum of the Adult Mouse." Journal of Cerebral Blood Flow & Metabolism 29, no. 7 (May 13, 2009): 1240–50. http://dx.doi.org/10.1038/jcbfm.2009.55.

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The migratory behavior of neuroblasts after a stroke is poorly understood. Using time-lapse microscopy, we imaged migration of neuroblasts and cerebral vessels in living brain slices of adult doublecortin (DCX, a marker of neuroblasts) enhanced green fluorescent protein (eGFP) transgenic mice that were subjected to 7 days of stroke. Our results show that neuroblasts originating in the subventricular zone (SVZ) of adult mouse brain laterally migrated in chains or individually to reach the ischemic striatum. The chains were initially formed at the border between the SVZ and the striatum by neuroblasts in the SVZ and then extended to the striatum. The average speed of DCX-eGFP-expressing cells within chains was 28.67 ± 1.04 μm/h, which was significantly faster ( P < 0.01) than the speed of the cells in the SVZ (17.98 ± 0.57 μm/h). Within the ischemic striatum, individual neuroblasts actively extended or retracted their processes, suggestive of probing the immediate microenvironment. The neuroblasts close to cerebral blood vessels exhibited multiple processes. Our data suggest that neuroblasts actively interact with the microenvironment to reach the ischemic striatum by multiple migratory routes.
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8

Chepkova, Aisa N., Susanne Schönfeld, and Olga A. Sergeeva. "Age-Related Alterations in the Expression of Genes and Synaptic Plasticity Associated with Nitric Oxide Signaling in the Mouse Dorsal Striatum." Neural Plasticity 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/458123.

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Age-related alterations in the expression of genes and corticostriatal synaptic plasticity were studied in the dorsal striatum of mice of four age groups from young (2-3 months old) to old (18–24 months of age) animals. A significant decrease in transcripts encoding neuronal nitric oxide (NO) synthase and receptors involved in its activation (NR1 subunit of the glutamate NMDA receptor and D1 dopamine receptor) was found in the striatum of old mice using gene array and real-time RT-PCR analysis. The old striatum showed also a significantly higher number of GFAP-expressing astrocytes and an increased expression of astroglial, inflammatory, and oxidative stress markers. Field potential recordings from striatal slices revealed age-related alterations in the magnitude and dynamics of electrically induced long-term depression (LTD) and significant enhancement of electrically induced long-term potentiation in the middle-aged striatum (6-7 and 12-13 months of age). Corticostriatal NO-dependent LTD induced by pharmacological activation of group I metabotropic glutamate receptors underwent significant reduction with aging and could be restored by inhibition of cGMP hydrolysis indicating that its age-related deficit is caused by an altered NO-cGMP signaling cascade. It is suggested that age-related alterations in corticostriatal synaptic plasticity may result from functional alterations in receptor-activated signaling cascades associated with increasing neuroinflammation and a prooxidant state.
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9

Gangarossa, Giuseppe, Sylvie Perez, Yulia Dembitskaya, Ilya Prokin, Hugues Berry, and Laurent Venance. "BDNF Controls Bidirectional Endocannabinoid Plasticity at Corticostriatal Synapses." Cerebral Cortex 30, no. 1 (April 25, 2019): 197–214. http://dx.doi.org/10.1093/cercor/bhz081.

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AbstractThe dorsal striatum exhibits bidirectional corticostriatal synaptic plasticity, NMDAR and endocannabinoids (eCB) mediated, necessary for the encoding of procedural learning. Therefore, characterizing factors controlling corticostriatal plasticity is of crucial importance. Brain-derived neurotrophic factor (BDNF) and its receptor, the tropomyosine receptor kinase-B (TrkB), shape striatal functions, and their dysfunction deeply affects basal ganglia. BDNF/TrkB signaling controls NMDAR plasticity in various brain structures including the striatum. However, despite cross-talk between BDNF and eCBs, the role of BDNF in eCB plasticity remains unknown. Here, we show that BDNF/TrkB signaling promotes eCB-plasticity (LTD and LTP) induced by rate-based (low-frequency stimulation) or spike-timing–based (spike-timing–dependent plasticity, STDP) paradigm in striatum. We show that TrkB activation is required for the expression and the scaling of both eCB-LTD and eCB-LTP. Using 2-photon imaging of dendritic spines combined with patch-clamp recordings, we show that TrkB activation prolongs intracellular calcium transients, thus increasing eCB synthesis and release. We provide a mathematical model for the dynamics of the signaling pathways involved in corticostriatal plasticity. Finally, we show that TrkB activation enlarges the domain of expression of eCB-STDP. Our results reveal a novel role for BDNF/TrkB signaling in governing eCB-plasticity expression in striatum and thus the engram of procedural learning.
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10

Bigan, Erwan, Satish Sasidharan Nair, François-Xavier Lejeune, Hélissande Fragnaud, Frédéric Parmentier, Lucile Mégret, Marc Verny, Jeff Aaronson, Jim Rosinski, and Christian Neri. "Genetic cooperativity in multi-layer networks implicates cell survival and senescence in the striatum of Huntington’s disease mice synchronous to symptoms." Bioinformatics 36, no. 1 (June 22, 2019): 186–96. http://dx.doi.org/10.1093/bioinformatics/btz514.

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Abstract Motivation Huntington’s disease (HD) may evolve through gene deregulation. However, the impact of gene deregulation on the dynamics of genetic cooperativity in HD remains poorly understood. Here, we built a multi-layer network model of temporal dynamics of genetic cooperativity in the brain of HD knock-in mice (allelic series of Hdh mice). To enhance biological precision and gene prioritization, we integrated three complementary families of source networks, all inferred from the same RNA-seq time series data in Hdh mice, into weighted-edge networks where an edge recapitulates path-length variation across source-networks and age-points. Results Weighted edge networks identify two consecutive waves of tight genetic cooperativity enriched in deregulated genes (critical phases), pre-symptomatically in the cortex, implicating neurotransmission, and symptomatically in the striatum, implicating cell survival (e.g. Hipk4) intertwined with cell proliferation (e.g. Scn4b) and cellular senescence (e.g. Cdkn2a products) responses. Top striatal weighted edges are enriched in modulators of defective behavior in invertebrate models of HD pathogenesis, validating their relevance to neuronal dysfunction in vivo. Collectively, these findings reveal highly dynamic temporal features of genetic cooperativity in the brain of Hdh mice where a 2-step logic highlights the importance of cellular maintenance and senescence in the striatum of symptomatic mice, providing highly prioritized targets. Availability and implementation Weighted edge network analysis (WENA) data and source codes for performing spectral decomposition of the signal (SDS) and WENA analysis, both written using Python, are available at http://www.broca.inserm.fr/HD-WENA/. Supplementary information Supplementary data are available at Bioinformatics online.
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11

Orpella, Joan, Ernest Mas-Herrero, Pablo Ripollés, Josep Marco-Pallarés, and Ruth de Diego-Balaguer. "Language statistical learning responds to reinforcement learning principles rooted in the striatum." PLOS Biology 19, no. 9 (September 7, 2021): e3001119. http://dx.doi.org/10.1371/journal.pbio.3001119.

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Statistical learning (SL) is the ability to extract regularities from the environment. In the domain of language, this ability is fundamental in the learning of words and structural rules. In lack of reliable online measures, statistical word and rule learning have been primarily investigated using offline (post-familiarization) tests, which gives limited insights into the dynamics of SL and its neural basis. Here, we capitalize on a novel task that tracks the online SL of simple syntactic structures combined with computational modeling to show that online SL responds to reinforcement learning principles rooted in striatal function. Specifically, we demonstrate—on 2 different cohorts—that a temporal difference model, which relies on prediction errors, accounts for participants’ online learning behavior. We then show that the trial-by-trial development of predictions through learning strongly correlates with activity in both ventral and dorsal striatum. Our results thus provide a detailed mechanistic account of language-related SL and an explanation for the oft-cited implication of the striatum in SL tasks. This work, therefore, bridges the long-standing gap between language learning and reinforcement learning phenomena.
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12

Bello-Medina, Paola C., Gonzalo Flores, Gina L. Quirarte, James L. McGaugh, and Roberto A. Prado Alcalá. "Mushroom spine dynamics in medium spiny neurons of dorsal striatum associated with memory of moderate and intense training." Proceedings of the National Academy of Sciences 113, no. 42 (October 3, 2016): E6516—E6525. http://dx.doi.org/10.1073/pnas.1613680113.

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A growing body of evidence indicates that treatments that typically impair memory consolidation become ineffective when animals are given intense training. This effect has been obtained by treatments interfering with the neural activity of several brain structures, including the dorsal striatum. The mechanisms that mediate this phenomenon are unknown. One possibility is that intense training promotes the transfer of information derived from the enhanced training to a wider neuronal network. We now report that inhibitory avoidance (IA) induces mushroom spinogenesis in the medium spiny neurons (MSNs) of the dorsal striatum in rats, which is dependent upon the intensity of the foot-shock used for training; that is, the effect is seen only when high-intensity foot-shock is used in training. We also found that the relative density of thin spines was reduced. These changes were evident at 6 h after training and persisted for at least 24 h afterward. Importantly, foot-shock alone did not increase spinogenesis. Spine density in MSNs in the accumbens was also increased, but the increase did not correlate with the associative process involved in IA; rather, it resulted from the administration of the aversive stimulation alone. These findings suggest that mushroom spines of MSNs of the dorsal striatum receive afferent information that is involved in the integrative activity necessary for memory consolidation, and that intense training facilitates transfer of information from the dorsal striatum to other brain regions through augmented spinogenesis.
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13

Rebec, George V., Steven R. Witowski, Michael I. Sandstrom, Rebecca D. Rostand, and Robert T. Kennedy. "Extracellular ascorbate modulates cortically evoked glutamate dynamics in rat striatum." Neuroscience Letters 378, no. 3 (April 2005): 166–70. http://dx.doi.org/10.1016/j.neulet.2004.12.027.

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14

Carrillo-Reid, Luis, Fatuel Tecuapetla, Osvaldo Ibáñez-Sandoval, Arturo Hernández-Cruz, Elvira Galarraga, and José Bargas. "Activation of the Cholinergic System Endows Compositional Properties to Striatal Cell Assemblies." Journal of Neurophysiology 101, no. 2 (February 2009): 737–49. http://dx.doi.org/10.1152/jn.90975.2008.

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Striatal cell assemblies are thought to encode network states related to associative learning, procedural memory, and the sequential organization of behavior. Cholinergic neurotransmission modulates memory processes in the striatum and other brain structures. This work asks if the activity of striatal microcircuits observed in living nervous tissue, with attributes similar to cell assemblies, exhibit some of the properties proposed to be necessary to compose memory traces. Accordingly, we used whole cell and calcium-imaging techniques to investigate the cholinergic modulation of striatal neuron pools that have been reported to exhibit several properties expected from cell assemblies such as synchronous states of activity and the alternation of this activity among different neuron pools. We analyzed the cholinergic modulation of the activity of neuron pools with multidimensional reduction techniques and vectorization of network dynamics. It was found that the activation of the cholinergic system enables striatal cell assemblies with properties that have been posited for recurrent neural artificial networks with memory storage capabilities. Graph theory techniques applied to striatal network states revealed sequences of vectors with a recursive dynamics similar to closed reverberating cycles. The cycles exhibited a modular architecture and a hierarchical organization. It is then concluded that, under certain conditions, the cholinergic system enables the striatal microcircuit with the ability to compose complex sequences of activity. Neuronal recurrent networks with the characteristics encountered in the present experiments are proposed to allow repeated sequences of activity to become memories and repeated memories to compose learned motor procedures.
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15

Castagnola, Elisa, Elaine M. Robbins, Bingchen Wu, May Yoon Pwint, Raghav Garg, Tzahi Cohen-Karni, and Xinyan Tracy Cui. "Flexible Glassy Carbon Multielectrode Array for In Vivo Multisite Detection of Tonic and Phasic Dopamine Concentrations." Biosensors 12, no. 7 (July 20, 2022): 540. http://dx.doi.org/10.3390/bios12070540.

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Dopamine (DA) plays a central role in the modulation of various physiological brain functions, including learning, motivation, reward, and movement control. The DA dynamic occurs over multiple timescales, including fast phasic release, as a result of neuronal firing and slow tonic release, which regulates the phasic firing. Real-time measurements of tonic and phasic DA concentrations in the living brain can shed light on the mechanism of DA dynamics underlying behavioral and psychiatric disorders and on the action of pharmacological treatments targeting DA. Current state-of-the-art in vivo DA detection technologies are limited in either spatial or temporal resolution, channel count, longitudinal stability, and ability to measure both phasic and tonic dynamics. We present here an implantable glassy carbon (GC) multielectrode array on a SU-8 flexible substrate for integrated multichannel phasic and tonic measurements of DA concentrations. The GC MEA demonstrated in vivo multichannel fast-scan cyclic voltammetry (FSCV) detection of electrically stimulated phasic DA release simultaneously at different locations of the mouse dorsal striatum. Tonic DA measurement was enabled by coating GC electrodes with poly(3,4-ethylenedioxythiophene)/carbon nanotube (PEDOT/CNT) and using optimized square-wave voltammetry (SWV). Implanted PEDOT/CNT-coated MEAs achieved stable detection of tonic DA concentrations for up to 3 weeks in the mouse dorsal striatum. This is the first demonstration of implantable flexible MEA capable of multisite electrochemical sensing of both tonic and phasic DA dynamics in vivo with chronic stability.
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Stott, Jeffrey J., and A. David Redish. "A functional difference in information processing between orbitofrontal cortex and ventral striatum during decision-making behaviour." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1655 (November 5, 2014): 20130472. http://dx.doi.org/10.1098/rstb.2013.0472.

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Both orbitofrontal cortex (OFC) and ventral striatum (vStr) have been identified as key structures that represent information about value in decision-making tasks. However, the dynamics of how this information is processed are not yet understood. We recorded ensembles of cells from OFC and vStr in rats engaged in the spatial adjusting delay-discounting task , a decision-making task that involves a trade-off between delay to and magnitude of reward. Ventral striatal neural activity signalled information about reward before the rat's decision, whereas such reward-related signals were absent in OFC until after the animal had committed to its decision. These data support models in which vStr is directly involved in action selection, but OFC processes decision-related information afterwards that can be used to compare the predicted and actual consequences of behaviour.
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Damianich, Ana, Carolina Lucia Facal, Javier Andrés Muñiz, Camilo Mininni, Mariano Soiza-Reilly, Magdalena Ponce De León, Leandro Urrutia, German Falasco, Juan Esteban Ferrario, and María Elena Avale. "Tau mis-splicing correlates with motor impairments and striatal dysfunction in a model of tauopathy." Brain 144, no. 8 (June 1, 2021): 2302–9. http://dx.doi.org/10.1093/brain/awab130.

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Abstract Tauopathies are neurodegenerative diseases caused by the abnormal metabolism of the microtubule associated protein tau (MAPT), which is highly expressed in neurons and critically involved in microtubule dynamics. In the adult human brain, the alternative splicing of exon 10 in MAPT pre-mRNA produces equal amounts of protein isoforms with either three (3R) or four (4R) microtubule binding domains. Imbalance in the 3R:4R tau ratio is associated with primary tauopathies that develop atypical parkinsonism, such as progressive supranuclear palsy and corticobasal degeneration. Yet, the development of effective therapies for those pathologies is an unmet goal. Here we report motor coordination impairments in the htau mouse model of tauopathy which harbour abnormal 3R:4R tau isoforms content, and in contrast to TauKO mice, are unresponsive to l-DOPA. Preclinical-PET imaging, array tomography and electrophysiological analyses indicated the dorsal striatum as the candidate structure mediating such phenotypes. Indeed, local modulation of tau isoforms by RNA trans-splicing in the striata of adult htau mice, prevented motor coordination deficits and restored basal neuronal firing. Together, these results suggest that abnormal striatal tau isoform content might lead to parkinsonian-like phenotypes and demonstrate a proof of concept that modulation of tau mis-splicing is a plausible disease-modifying therapy for some primary tauopathies.
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18

Tan, Can Ozan, and Daniel Bullock. "A Dopamine–Acetylcholine Cascade: Simulating Learned and Lesion-Induced Behavior of Striatal Cholinergic Interneurons." Journal of Neurophysiology 100, no. 4 (October 2008): 2409–21. http://dx.doi.org/10.1152/jn.90486.2008.

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The giant cholinergic interneurons of the striatum are tonically active neurons (TANs) that respond with pauses to appetitive and aversive cues and to novel events. Whereas tonic activity emerges from intrinsic properties of these neurons, glutamatergic inputs from intralaminar thalamic nuclei and dopaminergic inputs from midbrain are required for genesis of pause responses. No prior computational models encompass both intrinsic and synaptically gated dynamics. We present a mathematical model that robustly accounts for behavior-related electrophysiological properties of TANs in terms of their intrinsic physiological properties and known afferents. In the model, balanced intrinsic hyperpolarizing and depolarizing currents engender tonic firing and glutamatergic inputs from thalamus (and cortex) both directly excite and indirectly inhibit TANs. If this inhibition, probably mediated by GABAergic nitric oxide synthase interneurons, exceeds a threshold, a persistent K+ conductance current amplifies its effect to generate a prolonged pause. Dopamine (DA) signals modulate both the intrinsic mechanisms and the external inputs of TANs. Simulations revealed that many learning-dependent behaviors of TANs, including acquired pauses to task-relevant cues, are explicable without recourse to learning-dependent changes in synapses onto TANs, due to a tight coupling between DA bursts and TAN pauses. These interactions imply that reward-predicting cues often cause striatal projection neurons to receive a cascade of signals: an adaptively scaled DA burst, a brief acetylcholine (ACh) burst, and an ACh pause. A sensitivity analysis revealed a unique TAN response surface, which shows that DA inputs robustly cooperate with thalamic inputs to control cue-dependent pauses of ACh release, which strongly affects performance- and learning-related dynamics in the striatum.
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Bass, Caroline E., Valentina P. Grinevich, Alexandra D. Kulikova, Keith D. Bonin, and Evgeny A. Budygin. "Terminal effects of optogenetic stimulation on dopamine dynamics in rat striatum." Journal of Neuroscience Methods 214, no. 2 (April 2013): 149–55. http://dx.doi.org/10.1016/j.jneumeth.2013.01.024.

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Zhao, Fanpeng, Quillan Austria, Wenzhang Wang, and Xiongwei Zhu. "Mfn2 Overexpression Attenuates MPTP Neurotoxicity In Vivo." International Journal of Molecular Sciences 22, no. 2 (January 9, 2021): 601. http://dx.doi.org/10.3390/ijms22020601.

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Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson’s disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP+ induces mitochondrial fragmentation in vitro. In this study, we aimed to assess whether blocking MPTP-induced mitochondrial fragmentation by overexpressing Mfn2 affords neuroprotection in vivo. We found that the significant loss of dopaminergic neurons in the substantia nigra (SN) induced by MPTP treatment, as seen in wild-type littermate control mice, was almost completely blocked in mice overexpressing Mfn2 (hMfn2 mice). The dramatic reduction in dopamine neuronal fibers and dopamine levels in the striatum caused by MPTP administration was also partially inhibited in hMfn2 mice. MPTP-induced oxidative stress and inflammatory response in the SN and striatum were significantly alleviated in hMfn2 mice. The impairment of motor function caused by MPTP was also blocked in hMfn2 mice. Overall, our work demonstrates that restoration of mitochondrial dynamics by Mfn2 overexpression protects against neuronal toxicity in an MPTP-based PD mouse model, which supports the modulation of mitochondrial dynamics as a potential therapeutic target for PD treatment.
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Zhao, Fanpeng, Quillan Austria, Wenzhang Wang, and Xiongwei Zhu. "Mfn2 Overexpression Attenuates MPTP Neurotoxicity In Vivo." International Journal of Molecular Sciences 22, no. 2 (January 9, 2021): 601. http://dx.doi.org/10.3390/ijms22020601.

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Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson’s disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP+ induces mitochondrial fragmentation in vitro. In this study, we aimed to assess whether blocking MPTP-induced mitochondrial fragmentation by overexpressing Mfn2 affords neuroprotection in vivo. We found that the significant loss of dopaminergic neurons in the substantia nigra (SN) induced by MPTP treatment, as seen in wild-type littermate control mice, was almost completely blocked in mice overexpressing Mfn2 (hMfn2 mice). The dramatic reduction in dopamine neuronal fibers and dopamine levels in the striatum caused by MPTP administration was also partially inhibited in hMfn2 mice. MPTP-induced oxidative stress and inflammatory response in the SN and striatum were significantly alleviated in hMfn2 mice. The impairment of motor function caused by MPTP was also blocked in hMfn2 mice. Overall, our work demonstrates that restoration of mitochondrial dynamics by Mfn2 overexpression protects against neuronal toxicity in an MPTP-based PD mouse model, which supports the modulation of mitochondrial dynamics as a potential therapeutic target for PD treatment.
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Yang, Long, and Sotiris C. Masmanidis. "Differential encoding of action selection by orbitofrontal and striatal population dynamics." Journal of Neurophysiology 124, no. 2 (August 1, 2020): 634–44. http://dx.doi.org/10.1152/jn.00316.2020.

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While previous literature shows that both orbitofrontal cortex (OFC) and dorsomedial striatum (DMS) represent information relevant to selecting specific actions, few studies have directly compared neural signals between these areas. Here we compared OFC and DMS dynamics in mice performing a two-alternative choice task. We found that the animal’s choice could be decoded more accurately from DMS population activity. This work provides among the first evidence that OFC and DMS differentially represent information about an animal’s selected action.
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Kolacheva, Anna A., and M. V. Ugrumov. "A Mouse Model of Nigrostriatal Dopaminergic Axonal Degeneration As a Tool for Testing Neuroprotectors." Acta Naturae 13, no. 3 (November 15, 2021): 110–13. http://dx.doi.org/10.32607/actanaturae.11433.

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Degeneration of nigrostriatal dopaminergic neurons in Parkinsons disease begins from the axonal terminals in the striatum and, then, in retrograde fashion, progresses to the cell bodies in the substantia nigra. Investigation of the dynamics of axonal terminal degeneration may help in the identification of new targets for neuroprotective treatment and be used as a tool for testing potential drugs. We have shown that the degeneration rate of dopaminergic axonal terminals changes over time, and that the striatal dopamine concentration is the most sensitive parameter to the action of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). This model was validated using neuroprotectors with well-known mechanisms of action: the dopamine transporter inhibitor nomifensine and SEMAX peptide that stimulates the secretion of endogenous neurotrophic factors or acts as an antioxidant. Nomifensine was shown to almost completely protect dopaminergic fibers from the toxic effect of MPTP and maintain the striatal dopamine concentration at the control level. However, SEMAX, slightly but reliably, increased striatal dopamine when administered before MPTP treatment, which indicates that it is more effective as an inductor of endogenous neurotrophic factor secretion rather than as an antioxidant.
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Schechtman, Eitan, Maria Imelda Noblejas, Aviv D. Mizrahi, Omer Dauber, and Hagai Bergman. "Pallidal spiking activity reflects learning dynamics and predicts performance." Proceedings of the National Academy of Sciences 113, no. 41 (September 26, 2016): E6281—E6289. http://dx.doi.org/10.1073/pnas.1612392113.

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The basal ganglia (BG) network has been divided into interacting actor and critic components, modulating the probabilities of different state–action combinations through learning. Most models of learning and decision making in the BG focus on the roles of the striatum and its dopaminergic inputs, commonly overlooking the complexities and interactions of BG downstream nuclei. In this study, we aimed to reveal the learning-related activity of the external segment of the globus pallidus (GPe), a downstream structure whose computational role has remained relatively unexplored. Recording from monkeys engaged in a deterministic three-choice reversal learning task, we found that changes in GPe discharge rates predicted subsequent behavioral shifts on a trial-by-trial basis. Furthermore, the activity following the shift encoded whether it resulted in reward or not. The frequent changes in stimulus–outcome contingencies (i.e., reversals) allowed us to examine the learning-related neural activity and show that GPe discharge rates closely matched across-trial learning dynamics. Additionally, firing rates exhibited a linear decrease in sequences of correct responses, possibly reflecting a gradual shift from goal-directed execution to automaticity. Thus, modulations in GPe spiking activity are highest for attention-demanding aspects of behavior (i.e., switching choices) and decrease as attentional demands decline (i.e., as performance becomes automatic). These findings are contrasted with results from striatal tonically active neurons, which show none of these task-related modulations. Our results demonstrate that GPe, commonly studied in motor contexts, takes part in cognitive functions, in which movement plays a marginal role.
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Salvatore, M. F., O. Hudspeth, L. E. Arnold, P. E. Wilson, J. A. Stanford, C. F. MacTutus, R. M. Booze, and G. A. Gerhardt. "Prenatal cocaine exposure alters potassium-evoked dopamine release dynamics in rat striatum." Neuroscience 123, no. 2 (January 2004): 481–90. http://dx.doi.org/10.1016/j.neuroscience.2003.10.002.

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Parikh, Vinay, Sean X. Naughton, Xiangdang Shi, Leslie K. Kelley, Brittney Yegla, Christopher S. Tallarida, Scott M. Rawls, and Ellen M. Unterwald. "Cocaine-induced neuroadaptations in the dorsal striatum: Glutamate dynamics and behavioral sensitization." Neurochemistry International 75 (September 2014): 54–65. http://dx.doi.org/10.1016/j.neuint.2014.05.016.

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Estrada-Sánchez, Ana María, Courtney L. Blake, Scott J. Barton, Andrew G. Howe, and George V. Rebec. "Lack of mutant huntingtin in cortical efferents improves behavioral inflexibility and corticostriatal dynamics in Huntington’s disease mice." Journal of Neurophysiology 122, no. 6 (December 1, 2019): 2621–29. http://dx.doi.org/10.1152/jn.00777.2018.

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Abnormal communication between cerebral cortex and striatum plays a major role in the motor symptoms of Huntington’s disease (HD), a neurodegenerative disorder caused by a mutation of the huntingtin gene ( mHTT). Because cortex is the main driver of striatal processing, we recorded local field potential (LFP) activity simultaneously in primary motor cortex (M1) and dorsal striatum (DS) in BACHD mice, a full-length HD gene model, and in a conditional BACHD/Emx-1 Cre (BE) model in which mHTT is suppressed in cortical efferents, while mice freely explored a plus-shaped maze beginning at 20 wk of age. Relative to wild-type (WT) controls, BACHD mice were just as active across >40 wk of testing but became progressively less likely to turn into a perpendicular arm as they approached the choice point of the maze, a sign of HD motor inflexibility. BE mice, in contrast, turned as freely as WT throughout testing. Although BE mice did not exactly match WT in LFP activity, the reduction in alpha (8–13 Hz), beta (13–30 Hz), and low-gamma (30–50 Hz) power that occurred in M1 of turning-impaired BACHD mice was reversed. No reversal occurred in DS. In fact, BE mice showed further reductions in DS theta (4–8 Hz), beta, and low-gamma power relative to the BACHD model. Coherence analysis indicated a dysregulation of corticostriatal information flow in both BACHD and BE mice. Collectively, our results suggest that mHTT in cortical outputs drives the dysregulation of select cortical frequencies that accompany the loss of behavioral flexibility in HD. NEW & NOTEWORTHY BACHD mice, a full-length genetic model of Huntington’s disease (HD), express aberrant local field potential (LFP) activity in primary motor cortex (M1) along with decreased probability of turning into a perpendicular arm of a plus-shaped maze, a motor inflexibility phenotype. Suppression of the mutant huntingtin gene in cortical output neurons prevents decline in turning and improves alpha, beta, and low-gamma activity in M1. Our results implicate cortical networks in the search for therapeutic strategies to alleviate HD motor signs.
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Verstynen, Timothy D. "The organization and dynamics of corticostriatal pathways link the medial orbitofrontal cortex to future behavioral responses." Journal of Neurophysiology 112, no. 10 (November 15, 2014): 2457–69. http://dx.doi.org/10.1152/jn.00221.2014.

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Accurately making a decision in the face of incongruent options increases the efficiency of making similar congruency decisions in the future. Contextual factors like reward can modulate this adaptive process, suggesting that networks associated with monitoring previous success and failure outcomes might contribute to this form of behavioral updating. To evaluate this possibility, a group of healthy adults ( n = 30) were tested with functional MRI (fMRI) while they performed a color-word Stroop task. In a conflict-related region of the medial orbitofrontal cortex (mOFC), stronger BOLD responses predicted faster response times (RTs) on the next trial. More importantly, the degree of behavioral adaptation of RTs was correlated with the magnitude of mOFC-RT associations on the previous trial, but only after accounting for network-level interactions with prefrontal and striatal regions. This suggests that congruency sequencing effects may rely on interactions between distributed corticostriatal circuits. This possibility was evaluated by measuring the convergence of white matter projections from frontal areas into the striatum with diffusion-weighted imaging. In these pathways, greater convergence of corticostriatal projections correlated with stronger functional mOFC-RT associations that, in turn, provided an indirect pathway linking anatomical structure to behavior. Thus distributed corticostriatal processing may mediate the orbitofrontal cortex's influence on behavioral updating, even in the absence of explicit rewards.
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Smigielski, Lukasz, Diana Wotruba, Valerie Treyer, Julian Rössler, Sergi Papiol, Peter Falkai, Edna Grünblatt, Susanne Walitza, and Wulf Rössler. "The Interplay Between Postsynaptic Striatal D2/3 Receptor Availability, Adversity Exposure and Odd Beliefs: A [11C]-Raclopride PET Study." Schizophrenia Bulletin 47, no. 5 (April 20, 2021): 1495–508. http://dx.doi.org/10.1093/schbul/sbab034.

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Abstract Background Between unaffected mental health and diagnosable psychiatric disorders, there is a vast continuum of functioning. The hypothesized link between striatal dopamine signaling and psychosis has guided a prolific body of research. However, it has been understudied in the context of multiple interacting factors, subclinical phenotypes, and pre-postsynaptic dynamics. Method This work investigated psychotic-like experiences and D2/3 dopamine postsynaptic receptor availability in the dorsal striatum, quantified by in vivo [11C]-raclopride positron emission tomography, in a sample of 24 healthy male individuals. Additional mediation and moderation effects with childhood trauma and key dopamine-regulating genes were examined. Results An inverse relationship between nondisplaceable binding potential and subclinical symptoms was identified. D2/3 receptor availability in the left putamen fully mediated the association between traumatic childhood experiences and odd beliefs, that is, inclinations to see meaning in randomness and unfounded interpretations. Moreover, the effect of early adversity was moderated by a DRD2 functional variant (rs1076560). The results link environmental and neurobiological influences in the striatum to the origination of psychosis spectrum symptomology, consistent with the social defeat and diathesis–stress models. Conclusions Adversity exposure may affect the dopamine system as in association with biases in probabilistic reasoning, attributional style, and salience processing. The inverse relationship between D2/3 availability and symptomology may be explained by endogenous dopamine occupying the receptor, postsynaptic compensatory mechanisms, and/or altered receptor sensitivity. This may also reflect a cognitively stabilizing mechanism in non-help-seeking individuals. Future research should comprehensively characterize molecular parameters of dopamine neurotransmission along the psychosis spectrum and according to subtype profiling.
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Cadotte, M. W., S. Jantz, and D. V. Mai. "Photo-dependent population dynamics of Stentor coeruleus and its consumption of Colpidium striatum." Canadian Journal of Zoology 85, no. 5 (May 2007): 674–77. http://dx.doi.org/10.1139/z07-044.

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The predatory protozoan Stentor coeruleus Ehrenberg, 1830 is known to show photosensitivity and photodispersion, avoiding regions of high light intensity as an antipredation strategy. This physiological and behavioral response to light likely has demographic consequences. We manipulated light intensity to determine population responses of S. coeruleus and the resulting effects on its prey Colpidium striatum Stokes, 1886. We show that S. coeruleus maintained the highest population density under ambient light levels and low densities under both high and no light treatments. The results from the no light treatment were surprising because little work has been done on possible important behavioral and physiological processes cued by light. These results add power to the use of S. coeruleus as a model predator system to test ecological dynamics and processes associated with predation.
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Phillips, Paul E. M., Lauren M. Burgeno, Ryan D. Farero, Nicole L. Murray, Jennifer S. Steger, Marta E. Soden, Ingo Willuhn, and Larry S. Zweifel. "Dynamics of dopamine release in the striatum and its alterations with psychiatric pathology." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): SY72–1. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_sy72-1.

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Liu, Fu-Chin, and Ann M. Graybiel. "Spatiotemporal Dynamics of CREB Phosphorylation: Transient versus Sustained Phosphorylation in the Developing Striatum." Neuron 17, no. 6 (December 1996): 1133–44. http://dx.doi.org/10.1016/s0896-6273(00)80245-7.

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Plenz, D., and A. Aertsen. "Neural dynamics in cortex-striatum co-cultures—II. Spatiotemporal characteristics of neuronal activity." Neuroscience 70, no. 4 (February 1996): 893–924. http://dx.doi.org/10.1016/0306-4522(95)00405-x.

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Patriarchi, Tommaso, Jounhong Ryan Cho, Katharina Merten, Mark W. Howe, Aaron Marley, Wei-Hong Xiong, Robert W. Folk, et al. "Ultrafast neuronal imaging of dopamine dynamics with designed genetically encoded sensors." Science 360, no. 6396 (May 31, 2018): eaat4422. http://dx.doi.org/10.1126/science.aat4422.

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Neuromodulatory systems exert profound influences on brain function. Understanding how these systems modify the operating mode of target circuits requires spatiotemporally precise measurement of neuromodulator release. We developed dLight1, an intensity-based genetically encoded dopamine indicator, to enable optical recording of dopamine dynamics with high spatiotemporal resolution in behaving mice. We demonstrated the utility of dLight1 by imaging dopamine dynamics simultaneously with pharmacological manipulation, electrophysiological or optogenetic stimulation, and calcium imaging of local neuronal activity. dLight1 enabled chronic tracking of learning-induced changes in millisecond dopamine transients in mouse striatum. Further, we used dLight1 to image spatially distinct, functionally heterogeneous dopamine transients relevant to learning and motor control in mouse cortex. We also validated our sensor design platform for developing norepinephrine, serotonin, melatonin, and opioid neuropeptide indicators.
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Kopaeva, Marina Yu, Anton B. Cherepov, Mikhail V. Nesterenko, and Irina Yu Zarayskaya. "Pretreatment with Human Lactoferrin Had a Positive Effect on the Dynamics of Mouse Nigrostriatal System Recovery after Acute MPTP Exposure." Biology 10, no. 1 (January 1, 2021): 24. http://dx.doi.org/10.3390/biology10010024.

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We studied the effect of human lactoferrin (hLf) on degenerative changes in the nigrostriatal system and associated behavioral deficits in the animal model of Parkinson disease. Nigrostriatal dopaminergic injury was induced by single administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 40 mg/kg) to five-month-old C57Bl/6 mice. Behavioral disturbances were assessed in the open field and rotarod tests and by the stride length analysis. Structural deficits were assessed by the counts of tyrosine hydroxylase (TH)-immunoreactive neurons in the substantia nigra and optical density (OD) of TH-immunolabeled fibers in the striatum. Acute MPTP treatment induced long-term behavioral deficit and degenerative changes in the nigrostriatal system. Pretreatment with hLf prevented body weight loss and promoted recovery of motor functions and exploratory behavior. Importantly, OD of TH-positive fibers in the striatum of mice treated with hLf almost returned to normal, and the number of TH-positive cells in the substantia nigra significantly increased on day 28. These results indicate that hLf produces a neuroprotective effect and probably stimulates neuroregeneration under conditions of MPTP toxicity in our model. A relationship between behavioral deficits and nigrostriatal system disturbances at delayed terms after MPTP administration was found.
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D'Amore, Drew E., Brittany A. Tracy, and Vinay Parikh. "Exogenous BDNF facilitates strategy set-shifting by modulating glutamate dynamics in the dorsal striatum." Neuropharmacology 75 (December 2013): 312–23. http://dx.doi.org/10.1016/j.neuropharm.2013.07.033.

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Salinas, Armando G., Margaret I. Davis, David M. Lovinger, and Yolanda Mateo. "Dopamine dynamics and cocaine sensitivity differ between striosome and matrix compartments of the striatum." Neuropharmacology 108 (September 2016): 275–83. http://dx.doi.org/10.1016/j.neuropharm.2016.03.049.

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Holloway, Zade R., Timothy G. Freels, Josiah F. Comstock, Hunter G. Nolen, Helen J. Sable, and Deranda B. Lester. "Comparing phasic dopamine dynamics in the striatum, nucleus accumbens, amygdala, and medial prefrontal cortex." Synapse 73, no. 2 (October 30, 2018): e22074. http://dx.doi.org/10.1002/syn.22074.

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Hernandez, Ledia F. "Firing dynamics and LFP oscillatory patterns in the dopamine-depleted striatum during maze learning." Basal Ganglia 3, no. 4 (April 2014): 213–19. http://dx.doi.org/10.1016/j.baga.2013.11.004.

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Barroso-Flores, Janet, Marco A. Herrera-Valdez, Violeta Gisselle Lopez-Huerta, Elvira Galarraga, and José Bargas. "Diverse Short-Term Dynamics of Inhibitory Synapses Converging on Striatal Projection Neurons: Differential Changes in a Rodent Model of Parkinson’s Disease." Neural Plasticity 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/573543.

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Most neurons in the striatum are projection neurons (SPNs) which make synapses with each other within distances of approximately 100 µm. About 5% of striatal neurons are GABAergic interneurons whose axons expand hundreds of microns. Short-term synaptic plasticity (STSP) between fast-spiking (FS) interneurons and SPNs and between SPNs has been described with electrophysiological and optogenetic techniques. It is difficult to obtain pair recordings from some classes of interneurons and due to limitations of actual techniques, no other types of STSP have been described on SPNs. Diverse STSPs may reflect differences in presynaptic release machineries. Therefore, we focused the present work on answering two questions: Are there different identifiable classes of STSP between GABAergic synapses on SPNs? And, if so, are synapses exhibiting different classes of STSP differentially affected by dopamine depletion? Whole-cell voltage-clamp recordings on SPNs revealed three classes of STSPs: depressing, facilitating, and biphasic (facilitating-depressing), in response to stimulation trains at 20 Hz, in a constant ionic environment. We then used the 6-hydroxydopamine (6-OHDA) rodent model of Parkinson’s disease to show that synapses with different STSPs are differentially affected by dopamine depletion. We propose a general model of STSP that fits all the dynamics found in our recordings.
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Evans, R. C., Y. M. Maniar, and K. T. Blackwell. "Dynamic modulation of spike timing-dependent calcium influx during corticostriatal upstates." Journal of Neurophysiology 110, no. 7 (October 1, 2013): 1631–45. http://dx.doi.org/10.1152/jn.00232.2013.

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The striatum of the basal ganglia demonstrates distinctive upstate and downstate membrane potential oscillations during slow-wave sleep and under anesthetic. The upstates generate calcium transients in the dendrites, and the amplitude of these calcium transients depends strongly on the timing of the action potential (AP) within the upstate. Calcium is essential for synaptic plasticity in the striatum, and these large calcium transients during the upstates may control which synapses undergo plastic changes. To investigate the mechanisms that underlie the relationship between calcium and AP timing, we have developed a realistic biophysical model of a medium spiny neuron (MSN). We have implemented sophisticated calcium dynamics including calcium diffusion, buffering, and pump extrusion, which accurately replicate published data. Using this model, we found that either the slow inactivation of dendritic sodium channels (NaSI) or the calcium inactivation of voltage-gated calcium channels (CDI) can cause high calcium corresponding to early APs and lower calcium corresponding to later APs. We found that only CDI can account for the experimental observation that sensitivity to AP timing is dependent on NMDA receptors. Additional simulations demonstrated a mechanism by which MSNs can dynamically modulate their sensitivity to AP timing and show that sensitivity to specifically timed pre- and postsynaptic pairings (as in spike timing-dependent plasticity protocols) is altered by the timing of the pairing within the upstate. These findings have implications for synaptic plasticity in vivo during sleep when the upstate-downstate pattern is prominent in the striatum.
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Gabitov, Ella, David Manor, and Avi Karni. "Patterns of Modulation in the Activity and Connectivity of Motor Cortex during the Repeated Generation of Movement Sequences." Journal of Cognitive Neuroscience 27, no. 4 (April 2015): 736–51. http://dx.doi.org/10.1162/jocn_a_00751.

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It is not clear how the engagement of motor mnemonic processes is expressed in online brain activity. We scanned participants, using fMRI, during the paced performance of a finger-to-thumb opposition sequence (FOS), intensively trained a day earlier (T-FOS), and a similarly constructed, but novel, untrained FOS (U-FOS). Both movement sequences were performed in pairs of blocks separated by a brief rest interval (30 sec). We have recently shown that in the primary motor cortex (M1) motor memory was not expressed in the average signal intensity but rather in the across-block signal modulations, that is, when comparing the first to the second performance block across the brief rest interval. Here, using an M1 seed, we show that for the T-FOS, the M1–striatum functional connectivity decreased across blocks; however, for the U-FOS, connectivity within the M1 and between M1 and striatum increased. In addition, in M1, the pattern of within-block signal change, but not signal variability per se, reliably differentiated the two sequences. Only for the U-FOS and only within the first blocks in each pair, the signal significantly decreased. No such modulation was found within the second corresponding blocks following the brief rest interval in either FOS. We propose that a network including M1 and striatum underlies online motor working memory. This network may promote a transient integrated representation of a new movement sequence and readily retrieves a previously established movement sequence representation. Averaging over single events or blocks may not capture the dynamics of motor representations that occur over multiple timescales.
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Albouy, Geneviève, Bradley R. King, Pierre Maquet, and Julien Doyon. "Hippocampus and striatum: Dynamics and interaction during acquisition and sleep-related motor sequence memory consolidation." Hippocampus 23, no. 11 (October 25, 2013): 985–1004. http://dx.doi.org/10.1002/hipo.22183.

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Plenz, D., and A. Aertsen. "Neural dynamics in cortex-striatum co-cultures—I. Anatomy and electrophysiology of neuronal cell types." Neuroscience 70, no. 4 (February 1996): 861–91. http://dx.doi.org/10.1016/0306-4522(95)00406-8.

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Raut, Ryan V., Abraham Z. Snyder, and Marcus E. Raichle. "Hierarchical dynamics as a macroscopic organizing principle of the human brain." Proceedings of the National Academy of Sciences 117, no. 34 (August 12, 2020): 20890–97. http://dx.doi.org/10.1073/pnas.2003383117.

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Multimodal evidence suggests that brain regions accumulate information over timescales that vary according to anatomical hierarchy. Thus, these experimentally defined “temporal receptive windows” are longest in cortical regions that are distant from sensory input. Interestingly, spontaneous activity in these regions also plays out over relatively slow timescales (i.e., exhibits slower temporal autocorrelation decay). These findings raise the possibility that hierarchical timescales represent an intrinsic organizing principle of brain function. Here, using resting-state functional MRI, we show that the timescale of ongoing dynamics follows hierarchical spatial gradients throughout human cerebral cortex. These intrinsic timescale gradients give rise to systematic frequency differences among large-scale cortical networks and predict individual-specific features of functional connectivity. Whole-brain coverage permitted us to further investigate the large-scale organization of subcortical dynamics. We show that cortical timescale gradients are topographically mirrored in striatum, thalamus, and cerebellum. Finally, timescales in the hippocampus followed a posterior-to-anterior gradient, corresponding to the longitudinal axis of increasing representational scale. Thus, hierarchical dynamics emerge as a global organizing principle of mammalian brains.
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Yousefzadeh, S. Aryana, Anna E. Youngkin, Nicholas A. Lusk, Shufan Wen, and Warren H. Meck. "Bidirectional role of microtubule dynamics in the acquisition and maintenance of temporal information in dorsolateral striatum." Neurobiology of Learning and Memory 183 (September 2021): 107468. http://dx.doi.org/10.1016/j.nlm.2021.107468.

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Lin, Anya M. Y. "NMDA modulation of dopamine dynamics is diminished in the aged striatum: An in vivo voltametric study." Neurochemistry International 48, no. 2 (January 2006): 151–56. http://dx.doi.org/10.1016/j.neuint.2005.08.005.

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Pezze, M., C. Murphy, J. Feldon, and C. Heidbreder. "Role of dopamine dynamics in subregions of the ventral striatum in the expression of latent inhibition." Schizophrenia Research 41, no. 1 (January 2000): 149. http://dx.doi.org/10.1016/s0920-9964(00)90661-3.

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Tallot, Lucille, Michael Graupner, Lorenzo Diaz-Mataix, and Valérie Doyère. "Beyond Freezing: Temporal Expectancy of an Aversive Event Engages the Amygdalo–Prefronto–Dorsostriatal Network." Cerebral Cortex 30, no. 10 (May 15, 2020): 5257–69. http://dx.doi.org/10.1093/cercor/bhaa100.

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Abstract During Pavlovian aversive conditioning, a neutral conditioned stimulus (CS) becomes predictive of the time of arrival of an aversive unconditioned stimulus (US). Using a paradigm where animals had to discriminate between a CS+ (associated with a footshock) and a CS− (never associated with a footshock), we show that, early in training, dynamics of neuronal oscillations in an amygdalo–prefronto–striatal network are modified during the CS+ in a manner related to the CS–US time interval (30 or 10 s). This is the case despite a generalized high level of freezing to both CS+ and CS−. The local field potential oscillatory power was decreased between 12 and 30 Hz in the dorsomedial striatum (DMS) and increased between 55 and 95 Hz in the prelimbic cortex (PL), while the coherence between DMS, PL, and the basolateral amygdala was increased in the 3–6 Hz frequency range up to the expected time of US arrival only for the CS+ and not for the CS−. Changing the CS–US interval from 30 to 10 s shifted these changes in activity toward the newly learned duration. The results suggest a functional role of the amygdalo–prefronto–dorsostriatal network in encoding temporal information of Pavlovian associations independently of the behavioral output.
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Voelker, Aaron R., and Chris Eliasmith. "Improving Spiking Dynamical Networks: Accurate Delays, Higher-Order Synapses, and Time Cells." Neural Computation 30, no. 3 (March 2018): 569–609. http://dx.doi.org/10.1162/neco_a_01046.

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Researchers building spiking neural networks face the challenge of improving the biological plausibility of their model networks while maintaining the ability to quantitatively characterize network behavior. In this work, we extend the theory behind the neural engineering framework (NEF), a method of building spiking dynamical networks, to permit the use of a broad class of synapse models while maintaining prescribed dynamics up to a given order. This theory improves our understanding of how low-level synaptic properties alter the accuracy of high-level computations in spiking dynamical networks. For completeness, we provide characterizations for both continuous-time (i.e., analog) and discrete-time (i.e., digital) simulations. We demonstrate the utility of these extensions by mapping an optimal delay line onto various spiking dynamical networks using higher-order models of the synapse. We show that these networks nonlinearly encode rolling windows of input history, using a scale invariant representation, with accuracy depending on the frequency content of the input signal. Finally, we reveal that these methods provide a novel explanation of time cell responses during a delay task, which have been observed throughout hippocampus, striatum, and cortex.
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