scholarly journals Temporal evolution of beta bursts in the parkinsonian cortical and basal ganglia network

2019 ◽  
Vol 116 (32) ◽  
pp. 16095-16104 ◽  
Author(s):  
Hayriye Cagnan ◽  
Nicolas Mallet ◽  
Christian K. E. Moll ◽  
Alessandro Gulberti ◽  
Abbey B. Holt ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Temporal Evolution ◽  
Phase Locking ◽  
Stable Phase ◽  
Striatal Neurons ◽  
Action Potential Firing ◽  
Beta Oscillations ◽  
Oscillation Phase ◽  
Potential Firing ◽  
Basal Ganglia Structures

Beta frequency oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in Parkinson’s disease (PD). How excessive beta oscillations emerge in these circuits is unclear. We addressed this issue by defining the firing properties of basal ganglia neurons around the emergence of cortical beta bursts (β bursts), transient (50 to 350 ms) increases in the beta amplitude of cortical signals. In PD patients, the phase locking of background spiking activity in the subthalamic nucleus (STN) to frontal electroencephalograms preceded the onset and followed the temporal profile of cortical β bursts, with conditions of synchronization consistent within and across bursts. Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed that these dynamics were recapitulated in STN, but also in external globus pallidus and striatum. The onset of consistent phase-locking conditions was preceded by abrupt phase slips between cortical and basal ganglia ensemble signals. Single-unit recordings demonstrated that ensemble-level properties of synchronization were not underlain by changes in firing rate but, rather, by the timing of action potentials in relation to cortical oscillation phase. Notably, the preferred angle of phase-locked action potential firing in each basal ganglia structure was shifted during burst initiation, then maintained stable phase relations during the burst. Subthalamic, pallidal, and striatal neurons engaged and disengaged with cortical β bursts to different extents and timings. The temporal evolution of cortical and basal ganglia synchronization is cell type-selective, which could be key for the generation/ maintenance of excessive beta oscillations in parkinsonism.

scholarly journals Frequency matters: Up- and Down-Regulation of Dopamine Tone Induces Similar Frequency Shifts in Cortico-Basal Ganglia Beta Oscillations

2020 ◽  
Author(s):  
L. Iskhakova ◽  
P. Rappel ◽  
G. Fonar ◽  
O. Marmor ◽  
R. Paz ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Phase Locking ◽  
Oscillatory Activity ◽  
Dopamine Depletion ◽  
Beta Oscillations ◽  
Similar Frequency ◽  
Strongly Coupled ◽  
Beta Power ◽  
Oscillatory Power ◽  
Network Studies

AbstractBeta oscillatory activity (13-30Hz) is pervasive within the cortico-basal ganglia (CBG) network. Studies in Parkinson’s disease (PD) patients and animal models suggested that beta-power increases with dopamine depletion. However, the exact relationship between oscillatory power, frequency and dopamine-tone remains unclear. We recorded neural activity in the CBG network of non-human-primates (NHP) while acutely up- and down-modulating dopamine levels. Further, we assessed changes in beta oscillations of PD patients following acute and chronic changes in dopamine-tone. Beta oscillation frequency was strongly coupled with dopamine-tone in both NHPs and human patients. In contrast, power, coherence between single-units and LFP, and spike-LFP phase-locking were not systematically regulated by dopamine levels. These results demonstrate via causal manipulations that frequency, rather than other properties, is the key property of pathological oscillations in the CBG networks. These insights can lead to improvements in understanding of CBG physiology, PD progression tracking and patient care.

scholarly journals Modulation of dopamine tone induces frequency shifts in cortico-basal ganglia beta oscillations

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
L. Iskhakova ◽  
P. Rappel ◽  
M. Deffains ◽  
G. Fonar ◽  
O. Marmor ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Phase Locking ◽  
Oscillatory Activity ◽  
Dopamine Depletion ◽  
Beta Oscillations ◽  
Strongly Coupled ◽  
Beta Power ◽  
Oscillatory Power ◽  
Phase Amplitude ◽  
Beta Frequency

AbstractΒeta oscillatory activity (human: 13–35 Hz; primate: 8–24 Hz) is pervasive within the cortex and basal ganglia. Studies in Parkinson’s disease patients and animal models suggest that beta-power increases with dopamine depletion. However, the exact relationship between oscillatory power, frequency and dopamine tone remains unclear. We recorded neural activity in the cortex and basal ganglia of healthy non-human primates while acutely and chronically up- and down-modulating dopamine levels. We assessed changes in beta oscillations in patients with Parkinson’s following acute and chronic changes in dopamine tone. Here we show beta oscillation frequency is strongly coupled with dopamine tone in both monkeys and humans. Power, coherence between single-units and local field potentials (LFP), spike-LFP phase-locking, and phase-amplitude coupling are not systematically regulated by dopamine levels. These results demonstrate that beta frequency is a key property of pathological oscillations in cortical and basal ganglia networks.

Echogenicity of basal ganglia structures in different phenotypes of Huntington's disease

2014 ◽  
Vol 45 (01) ◽  
Author(s):  
C Krogias ◽  
R Hoffmann ◽  
K Straßburger-Krogias ◽  
P Klotz ◽  
G Ellrichmann ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Basal Ganglia Structures

scholarly journals Thalamic Volume Mediates Associations Between Cardiorespiratory Fitness and Memory in People With Parkinson’s

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 501-502
Author(s):  
Andrew Petkus ◽  
Megan Gomez ◽  
Dawn Schiehser ◽  
Vincent Filoteo ◽  
Jennifer Hui ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Executive Functioning ◽  
Episodic Memory ◽  
Cognitive Performance ◽  
Cardiorespiratory Fitness ◽  
Indirect Effect ◽  
Structural Equation Models ◽  
Intracranial Volume ◽  
Vo2 Max ◽  
Basal Ganglia Structures

Abstract Cognitive deficits occur in patients with Parkinson’s disease (PD), and cardiorespiratory fitness (CRF) is associated with both current and future cognitive decline in this disease. The underlying neurobiological factors explaining this relationship, however, are not well known. In this cross-sectional study we examined the associations between CRF and cognitive performance and whether such associations were mediated by grey matter volumes of basal ganglia structures. A total of 33 individuals with PD underwent structural magnetic resonance imaging (sMRI), CRF evaluation (VO2max), and neuropsychological assessment. Composite scores of episodic memory, executive functioning, attention, language, and visuospatial functioning were generated. Brain MRI morphological measurements was performed with the Freesurfer image analysis suite. Structural equation models were constructed to examine whether sMRI volume estimates of basal ganglia structures, specifically the thalamus and pallidum, mediated associations between VO2 max and cognitive performance while adjusting for age, education, PD disease duration, sex, and intracranial volume. Higher VO2max was associated with better episodic memory (Standardized β=0.390; p=0.009), executive functioning (Standardized β=0.263; p=0.021), and visuospatial performance (β=0.408; p=0.004). Higher VO2max was associated with larger thalamic (Standardized β=0.602; p<0.001) and pallidum (Standardized β=0.539; p<0.001) volumes. Thalamic volume significantly mediated the association between higher VO2max and better episodic memory (indirect effect=0.209) and visuospatial ability (indirect effect=0.178) performance (p<.05). The pallidum did not significantly mediate associations between VO2 max and cognitive outcomes. These results suggest the thalamus plays an important role in the association between CRF episodic memory and visuospatial functioning in individuals with PD.

scholarly journals Zinc Enhances the Inhibitory Effects of Strychnine-Sensitive Glycine Receptors in Mouse Hippocampal Neurons

2007 ◽  
Vol 98 (6) ◽  
pp. 3666-3676 ◽  
Author(s):  
Hai Xia Zhang ◽  
Liu Lin Thio
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Neuronal Excitability ◽  
Hippocampal Slices ◽  
Glycine Receptors ◽  
Inhibitory Effects ◽  
Action Potential Firing ◽  
Embryonic Mouse ◽  
Potential Firing

Although extracellular Zn2+ is an endogenous biphasic modulator of strychnine-sensitive glycine receptors (GlyRs), the physiological significance of this modulation remains poorly understood. Zn2+ modulation of GlyR may be especially important in the hippocampus where presynaptic Zn2+ is abundant. Using cultured embryonic mouse hippocampal neurons, we examined whether 1 μM Zn2+, a potentiating concentration, enhances the inhibitory effects of GlyRs activated by sustained glycine applications. Sustained 20 μM glycine (EC25) applications alone did not decrease the number of action potentials evoked by depolarizing steps, but they did in 1 μM Zn2+. At least part of this effect resulted from Zn2+ enhancing the GlyR-induced decrease in input resistance. Sustained 20 μM glycine applications alone did not alter neuronal bursting, a form of hyperexcitability induced by omitting extracellular Mg2+. However, sustained 20 μM glycine applications depressed neuronal bursting in 1 μM Zn2+. Zn2+ did not enhance the inhibitory effects of sustained 60 μM glycine (EC70) applications in these paradigms. These results suggest that tonic GlyR activation could decrease neuronal excitability. To test this possibility, we examined the effect of the GlyR antagonist strychnine and the Zn2+ chelator tricine on action potential firing by CA1 pyramidal neurons in mouse hippocampal slices. Co-applying strychnine and tricine slightly but significantly increased the number of action potentials fired during a depolarizing current step and decreased the rheobase for action potential firing. Thus Zn2+ may modulate neuronal excitability normally and in pathological conditions such as seizures by potentiating GlyRs tonically activated by low agonist concentrations.

scholarly journals Corticostriatal Plastic Changes in Experimental L-DOPA-Induced Dyskinesia

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Veronica Ghiglieri ◽  
Vincenza Bagetta ◽  
Valentina Pendolino ◽  
Barbara Picconi ◽  
Paolo Calabresi
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Experimental Models ◽  
Striatal Neurons ◽  
Da Receptors ◽  
Electrophysiological Studies ◽  
Plastic Changes ◽  
Stimulation Of

In Parkinson’s disease (PD), alteration of dopamine- (DA-) dependent striatal functions and pulsatile stimulation of DA receptors caused by the discontinuous administration of levodopa (L-DOPA) lead to a complex cascade of events affecting the postsynaptic striatal neurons that might account for the appearance of L-DOPA-induced dyskinesia (LID). Experimental models of LID have been widely used and extensively characterized in rodents and electrophysiological studies provided remarkable insights into the inner mechanisms underlying L-DOPA-induced corticostriatal plastic changes. Here we provide an overview of recent findings that represent a further step into the comprehension of mechanisms underlying maladaptive changes of basal ganglia functions in response to L-DOPA and associated to development of LID.

scholarly journals The thalamic low-threshold Ca 2+ potential: a key determinant of the local and global dynamics of the slow (<1 Hz) sleep oscillation in thalamocortical networks

2011 ◽  
Vol 369 (1952) ◽  
pp. 3820-3839 ◽  
Author(s):  
Vincenzo Crunelli ◽  
Adam C. Errington ◽  
Stuart W. Hughes ◽  
Tibor I. Tóth
Keyword(s):  
Action Potential ◽  
Slow Oscillation ◽  
Global Dynamics ◽  
Action Potential Firing ◽  
Local And Global Dynamics ◽  
Up States ◽  
Potential Firing ◽  
Low Threshold

During non-rapid eye movement sleep and certain types of anaesthesia, neurons in the neocortex and thalamus exhibit a distinctive slow (<1 Hz) oscillation that consists of alternating UP and DOWN membrane potential states and which correlates with a pronounced slow (<1 Hz) rhythm in the electroencephalogram. While several studies have claimed that the slow oscillation is generated exclusively in neocortical networks and then transmitted to other brain areas, substantial evidence exists to suggest that the full expression of the slow oscillation in an intact thalamocortical (TC) network requires the balanced interaction of oscillator systems in both the neocortex and thalamus. Within such a scenario, we have previously argued that the powerful low-threshold Ca 2+ potential (LTCP)-mediated burst of action potentials that initiates the UP states in individual TC neurons may be a vital signal for instigating UP states in related cortical areas. To investigate these issues we constructed a computational model of the TC network which encompasses the important known aspects of the slow oscillation that have been garnered from earlier in vivo and in vitro experiments. Using this model we confirm that the overall expression of the slow oscillation is intricately reliant on intact connections between the thalamus and the cortex. In particular, we demonstrate that UP state-related LTCP-mediated bursts in TC neurons are proficient in triggering synchronous UP states in cortical networks, thereby bringing about a synchronous slow oscillation in the whole network. The importance of LTCP-mediated action potential bursts in the slow oscillation is also underlined by the observation that their associated dendritic Ca 2+ signals are the only ones that inform corticothalamic synapses of the TC neuron output, since they, but not those elicited by tonic action potential firing, reach the distal dendritic sites where these synapses are located.

BICUCULLINE/BACLOFEN-INSENSITIVE GABA RESPONSE IN CRUSTACEAN NEURONES IN CULTURE

1994 ◽  
Vol 191 (1) ◽  
pp. 167-193
Author(s):  
C Jackel ◽  
W Krenz ◽  
F Nagy
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Gamma Aminobutyric Acid ◽  
Action Potential Firing ◽  
Patch Clamp Technique ◽  
Conformationally Restricted ◽  
Whole Cell Patch Clamp ◽  
Gabac Receptor ◽  
Potential Firing ◽  
Sr 95531

Neurones were dissociated from thoracic ganglia of embryonic and adult lobsters and kept in primary culture. When gamma-aminobutyric acid (GABA) was applied by pressure ejection, depolarizing or hyperpolarizing responses were produced, depending on the membrane potential. They were accompanied by an increase in membrane conductance. When they were present, action potential firing was inhibited. The pharmacological profile and ionic mechanism of GABA-evoked current were investigated under voltage-clamp with the whole-cell patch-clamp technique. The reversal potential of GABA-evoked current depended on the intracellular and extracellular Cl- concentration but not on extracellular Na+ and K+. Blockade of Ca2+ channels by Mn2+ was also without effect. The GABA-evoked current was mimicked by application of the GABAA agonists muscimol and isoguvacine with an order of potency muscimol&gt;GABA&gt;isoguvacine. cis-4-aminocrotonic acid (CACA), a folded and conformationally restricted GABA analogue, supposed to be diagnostic for the vertebrate GABAC receptor, also induced a bicuculline-resistant chloride current, although with a potency about 10 times lower than that of GABA. The GABA-evoked current was largely blocked by picrotoxin, but was insensitive to the GABAA antagonists bicuculline, bicuculline methiodide and SR 95531 at concentrations of up to 100 &micro;mol l-1. Diazepam and phenobarbital did not exert modulatory effects. The GABAB antagonist phaclophen did not affect the GABA-induced current, while the GABAB agonists baclophen and 3-aminopropylphosphonic acid (3-APA) never evoked any response. Our results suggest that lobster thoracic neurones in culture express a chloride-conducting GABA-receptor channel which conforms to neither the GABAA nor the GABAB types of vertebrates but shows a pharmacology close to that of the novel GABAC receptor described in the vertebrate retina.

scholarly journals pigkMutation underliesmachobehavior and affects Rohon-Beard cell excitability

2015 ◽  
Vol 114 (2) ◽  
pp. 1146-1157 ◽  
Author(s):  
V. Carmean ◽  
M. A. Yonkers ◽  
M. B. Tellez ◽  
J. R. Willer ◽  
G. B. Willer ◽  
...  
Keyword(s):  
Action Potential ◽  
Sensory Neurons ◽  
Sodium Current ◽  
Genetic Defect ◽  
Sensory Cells ◽  
Loss Of Function ◽  
Wild Type ◽  
Action Potential Firing ◽  
Potential Firing ◽  
Touch Response

The study of touch-evoked behavior allows investigation of both the cells and circuits that generate a response to tactile stimulation. We investigate a touch-insensitive zebrafish mutant, macho (maco), previously shown to have reduced sodium current amplitude and lack of action potential firing in sensory neurons. In the genomes of mutant but not wild-type embryos, we identify a mutation in the pigk gene. The encoded protein, PigK, functions in attachment of glycophosphatidylinositol anchors to precursor proteins. In wild-type embryos, pigk mRNA is present at times when mutant embryos display behavioral phenotypes. Consistent with the predicted loss of function induced by the mutation, knock-down of PigK phenocopies maco touch insensitivity and leads to reduced sodium current (INa) amplitudes in sensory neurons. We further test whether the genetic defect in pigk underlies the maco phenotype by overexpressing wild-type pigk in mutant embryos. We find that ubiquitous expression of wild-type pigk rescues the touch response in maco mutants. In addition, for maco mutants, expression of wild-type pigk restricted to sensory neurons rescues sodium current amplitudes and action potential firing in sensory neurons. However, expression of wild-type pigk limited to sensory cells of mutant embryos does not allow rescue of the behavioral touch response. Our results demonstrate an essential role for pigk in generation of the touch response beyond that required for maintenance of proper INa density and action potential firing in sensory neurons.

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