Repeated applications of high potassium elicit long-term changes in a motor circuit from the crab, Cancer borealis

Rue, Mara C.P.; Alonso, Leandro M.; Marder, Eve

doi:10.1016/j.isci.2022.104919

Cited by 4 publications

(1 citation statement)

References 65 publications

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“…Our data highlight the impact of [K + ] e homeostasis on neural activity in vivo and suggest [K + ] e as a potent regulator of local NE level and brain state. Interestingly, fluctuations in [K + ] e have recently been shown to facilitate rapid and long-term circuit activity adaptation ( 50 ), which is known to involve neuromodulator signaling ( 51 ).…”

Section: Discussionmentioning

confidence: 99%

Local extracellular K ⁺ in cortex regulates norepinephrine levels, network state, and behavioral output

Dietz,

Weikop,

Hauglund

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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Extracellular potassium concentration ([K + ] e ) is known to increase as a function of arousal. [K + ] e is also a potent modulator of transmitter release. Yet, it is not known whether [K + ] e is involved in the neuromodulator release associated with behavioral transitions. We here show that manipulating [K + ] e controls the local release of monoaminergic neuromodulators, including norepinephrine (NE), serotonin, and dopamine. Imposing a [K + ] e increase is adequate to boost local NE levels, and conversely, lowering [K + ] e can attenuate local NE. Electroencephalography analysis and behavioral assays revealed that manipulation of cortical [K + ] e was sufficient to alter the sleep–wake cycle and behavior of mice. These observations point to the concept that NE levels in the cortex are not solely determined by subcortical release, but that local [K + ] e dynamics have a strong impact on cortical NE. Thus, cortical [K + ] e is an underappreciated regulator of behavioral transitions.

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Section: Discussionmentioning

confidence: 99%

Local extracellular K ⁺ in cortex regulates norepinephrine levels, network state, and behavioral output

Dietz,

Weikop,

Hauglund

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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Gating of homeostatic regulation of intrinsic excitability produces cryptic long-term storage of prior perturbations

Alonso

Rue

Marder

2023

Proc. Natl. Acad. Sci. U.S.A.

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Neurons and neuronal circuits must maintain their function throughout the life of the organism despite changing environments. Previous theoretical and experimental work suggests that neurons monitor their activity using intracellular calcium concentrations to regulate their intrinsic excitability. Models with multiple sensors can distinguish among different patterns of activity, but previous work using models with multiple sensors produced instabilities that lead the models’ conductances to oscillate and then to grow without bound and diverge. We now introduce a nonlinear degradation term that explicitly prevents the maximal conductances to grow beyond a bound. We combine the sensors’ signals into a master feedback signal that can be used to modulate the timescale of conductance evolution. Effectively, this means that the negative feedback can be gated on and off according to how far the neuron is from its target. The modified model recovers from multiple perturbations. Interestingly, depolarizing the models to the same membrane potential with current injection or with simulated high extracellular K + produces different changes in conductances, arguing that caution must be used in interpreting manipulations that serve as a proxy for increased neuronal activity. Finally, these models accrue traces of prior perturbations that are not visible in their control activity after perturbation but that shape their responses to subsequent perturbations. These cryptic or hidden changes may provide insight into disorders such as posttraumatic stress disorder that only become visible in response to specific perturbations.

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Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

McIlvried,

Del Rosario,

Pullen

et al. 2023

Preprint

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In response to changes in activity induced by environmental cues, neurons in the central nervous system undergo homeostatic plasticity to sustain overall network function during abrupt changes in synaptic strengths. Homeostatic plasticity involves changes in synaptic scaling and regulation of intrinsic excitability. Increases in spontaneous firing and excitability of sensory neurons are evident in some forms of chronic pain in animal models and human patients. However, whether mechanisms of homeostatic plasticity are engaged in sensory neurons under normal conditions or altered after chronic pain is unknown. Here, we showed that sustained depolarization induced by 30mM KCl induces a compensatory decrease in the excitability in mouse and human sensory neurons. Moreover, voltage–gated sodium currents are robustly reduced in mouse sensory neurons contributing to the overall decrease in neuronal excitability. Decreased efficacy of these homeostatic mechanisms could potentially contribute to the development of the pathophysiology of chronic pain.

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Repeated applications of high potassium elicit long-term changes in a motor circuit from the crab, Cancer borealis

Cited by 4 publications

References 65 publications

Local extracellular K ⁺ in cortex regulates norepinephrine levels, network state, and behavioral output

Local extracellular K ⁺ in cortex regulates norepinephrine levels, network state, and behavioral output

Gating of homeostatic regulation of intrinsic excitability produces cryptic long-term storage of prior perturbations

Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

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Repeated applications of high potassium elicit long-term changes in a motor circuit from the crab, Cancer borealis

Cited by 4 publications

References 65 publications

Local extracellular K + in cortex regulates norepinephrine levels, network state, and behavioral output

Local extracellular K + in cortex regulates norepinephrine levels, network state, and behavioral output

Gating of homeostatic regulation of intrinsic excitability produces cryptic long-term storage of prior perturbations

Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

Contact Info

Product

Resources

About

Local extracellular K ⁺ in cortex regulates norepinephrine levels, network state, and behavioral output

Local extracellular K ⁺ in cortex regulates norepinephrine levels, network state, and behavioral output