Basal ganglia and cortical control of thalamic rebound spikes

Nejad, Mohammadreza Mohagheghi; Rotter, Stefan; Schmidt, Robert

doi:10.1111/ejn.15258

Cited by 5 publications

(3 citation statements)

References 64 publications

(135 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These processes can occur through feedforward or feedback recurrent circuits between the cortex and thalamus and can be the underlying mechanisms of attention and goal-directed behavior (55,56). In addition, neuronal hyperpolarization in the VPL region is known to trigger activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and the occurrence of rebound spike-burst firing of thalamocortical neurons in the thalamus-cortex recurrent loop (57)(58)(59).…”

Section: Forelimb Sensory Pathways Revealed By Diana Fmrimentioning

confidence: 99%

Direct imaging of neural activity reveals neural circuits via spatiotemporal activation mapping

Keum,

Toi,

Park

et al. 2024

Preprint

View full text Add to dashboard Cite

Two years ago, our group reported direct imaging of neuronal activity (DIANA), a functional magnetic resonance imaging (fMRI) technique that directly detects neuronal activity at high spatiotemporal resolution. In this study, we successfully reproduced the DIANA response in medetomidine-anesthetized mice using forelimb electrical stimulation at 11.7 T. More importantly, we showed that multiple neural circuits can be effectively revealed by DIANA fMRI through spatiotemporal activation mapping. The spatiotemporal activation mapping proposed here utilizes the temporal information of the DIANA response, that is, the time when the DIANA response reaches its peak, which is a unique feature that distinguishes it from the activation mapping method used in existing fMRI. Based on DIANA activation areas, we identified several neural circuits involved in forelimb sensory processing in the somatosensory network, which includes multiple brain regions: ventral posterolateral nucleus of the thalamus (VPL), posteromedial thalamic nucleus (POm), forelimb primary somatosensory cortex (S1FL), secondary somatosensory cortex (S2), primary motor cortex (M1), and secondary motor cortex (M2). Additionally, we also identified a pain-related neural circuit involving brain regions of the anterior cingulate cortex (ACC) and mediodorsal nucleus (MD). Interestingly, the spatiotemporal activation mapping also allowed us to identify subregions with different DIANA response times within the same functional region (e.g., VPL, POm, S1FL, and S2). Our study highlights the potential of DIANA fMRI to advance our understanding of sensory information processing throughout the brain and to provide insight into the spatiotemporal dynamics of brain networks at the level of neural circuits.

show abstract

Section: Forelimb Sensory Pathways Revealed By Diana Fmrimentioning

confidence: 99%

Direct imaging of neural activity reveals neural circuits via spatiotemporal activation mapping

Keum,

Toi,

Park

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…These bursts are enhanced and linked to motor dysfunction in SPR-knockout mice, which are dopamine-deficient due to defects in tetrahydrobiopterin synthesis (Kim et al, 2017). Furthermore, models suggest that synchronous BG output is especially effective at generating rebound bursting (Nejad et al, 2021).…”

Section: Bg-thalamic Interactions In Health and Parkinsonismmentioning

confidence: 99%

Revisiting the “Paradox of Stereotaxic Surgery”: Insights Into Basal Ganglia-Thalamic Interactions

Magnússon

Leventhal

2021

Front. Syst. Neurosci.

View full text Add to dashboard Cite

Basal ganglia dysfunction is implicated in movement disorders including Parkinson Disease, dystonia, and choreiform disorders. Contradicting standard “rate models” of basal ganglia-thalamic interactions, internal pallidotomy improves both hypo- and hyper-kinetic movement disorders. This “paradox of stereotaxic surgery” was recognized shortly after rate models were developed, and is underscored by the outcomes of deep brain stimulation (DBS) for movement disorders. Despite strong evidence that DBS activates local axons, the clinical effects of lesions and DBS are nearly identical. These observations argue against standard models in which GABAergic basal ganglia output gates thalamic activity, and raise the question of how lesions and stimulation can have similar effects. These paradoxes may be resolved by considering thalamocortical loops as primary drivers of motor output. Rather than suppressing or releasing cortex via motor thalamus, the basal ganglia may modulate the timing of thalamic perturbations to cortical activity. Motor cortex exhibits rotational dynamics during movement, allowing the same thalamocortical perturbation to affect motor output differently depending on its timing with respect to the rotational cycle. We review classic and recent studies of basal ganglia, thalamic, and cortical physiology to propose a revised model of basal ganglia-thalamocortical function with implications for basic physiology and neuromodulation.

show abstract

“…In the central nervous system, the inhibitory synapse transmission may induce excitatory signals via RF. 10,[14][15][16]30,31 Although RF was elicited in vitro 14,30,31 or in vivo from isoflurane-anaesthetized adult mice, 32 however, Alviña et al found that intact mouse or rat deep cerebellar nuclei neurons rarely show RF under physiological conditions in vivo, 33 implying RF may not be observed in awake behaving intact animals but is most likely to contribute to neural hyperexcitability under pathophysiological condition. In PNS, different from central neuron, DRG neurons do not receive synapse transmission, but there are a variety of receptors on DRG neurons.…”

mentioning

confidence: 99%

Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons

Zhu¹,

Wei²,

Wang³

2022

JPR

View full text Add to dashboard Cite

Background: In the central nervous system, post-inhibitory rebound firing (RF) may mediate overactivity of neurons under pathophysiological condition. RF is also observed in dorsal root ganglion (IRA) neurons. However, the functional significance of RF in primary sensory neurons has remained unknown. After peripheral sensory nerve/neuron injury, DRG neurons exhibit hyperexcitability. Therefore, RF may play a role in neuropathic pain. Methods: Chronic compression of DRG (CCD) is used as a neuropathic pain model. Rats were divided into 2 groups: Sham and CCD groups. Patch clamp was performed on the whole DRG and cultured DRG neurons to record RF and T-type Ca 2+ currents. The blocker of T-type Ca 2+ channels, NiCl 2 , was applied to DRG neurons. Results: Rebound neurons were more excitable than non-rebound neurons. And they discharged RF with prominent after depolarizing potentials, which were blocked by NiCl 2 . After DRG injury, the proportion of rebound neurons augmented, and rebound neurons' excitability increased. Meanwhile, the steady-state activation curve of T-type Ca 2+ channels was shifted toward the left. Conclusion: RF may be related to highly excitable neurons and sensitive to both depolarization and hyperpolarization. T-type Ca 2+ channels were critical to RF, potentially enhancing the spontaneous firing of rebound neurons in response to resting membrane potential fluctuations.

show abstract

Basal ganglia and cortical control of thalamic rebound spikes

Abstract: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Cited by 5 publications

References 64 publications

Direct imaging of neural activity reveals neural circuits via spatiotemporal activation mapping

Direct imaging of neural activity reveals neural circuits via spatiotemporal activation mapping

Revisiting the “Paradox of Stereotaxic Surgery”: Insights Into Basal Ganglia-Thalamic Interactions

Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons

Contact Info

Product

Resources

About