Improvement of spatial learning by facilitating large-conductance calcium-activated potassium channel with transcranial magnetic stimulation in Alzheimer's disease model mice

Wang, Furong; Zhang, Yu; Wang, Li; Sun, Peng; Luo, Xue‐Gang; Ishigaki, Yasuhito; Sugai, Tokio; Yamamoto, Ryo; Kato, Nobuo

doi:10.1016/j.neuropharm.2015.05.027

Cited by 67 publications

(54 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistent with these findings, both ventricular injection of isopimaric acid, a BK channel opener, and the use of transcranial magnetic stimulation ameliorate cognitive deficits and cortical hyperexcitability in 3xTg mice (Wang, Kang et al, 2015; Wang, Zhang, et al, 2015). Interestingly, these treatments not only restore BK channel activity but also reduce brain Aβ content, which reveals a two-way relationship between BK currents and Aβ accumulation (Wang, Kang, et al, 2015; Wang, Zhang, et al, 2015).…”

Section: Role Of Bk Channels In Cns Function and Pathologiessupporting

confidence: 58%

See 1 more Smart Citation

BK Channels in the Central Nervous System

Contet

Goulding

Kuljis

et al. 2016

International Review of Neurobiology

136

170

View full text Add to dashboard Cite

Large conductance Ca2+- and voltage-activated K+ (BK) channels are widely distributed in the postnatal central nervous system (CNS). BK channels play a pleiotropic role in regulating the activity of brain and spinal cord neural circuits by providing a negative feedback mechanism for local increases in intracellular Ca2+ concentrations. In neurons, they regulate the timing and duration of K+ influx such that they can either increase or decrease firing depending on the cellular context, and they can suppress neurotransmitter release from presynaptic terminals. In addition, BK channels located in astrocytes and arterial myocytes modulate cerebral blood flow. Not surprisingly, both loss and gain of BK channel function have been associated with CNS disorders such as epilepsy, ataxia, mental retardation, and chronic pain. On the other hand, the neuroprotective role played by BK channels in a number of pathological situations could potentially be leveraged to correct neurological dysfunction.

show abstract

Section: Role Of Bk Channels In Cns Function and Pathologiessupporting

confidence: 58%

“…Interestingly, these treatments not only restore BK channel activity but also reduce brain Aβ content, which reveals a two-way relationship between BK currents and Aβ accumulation (Wang, Kang, et al, 2015; Wang, Zhang, et al, 2015). …”

Section: Role Of Bk Channels In Cns Function and Pathologiesmentioning

confidence: 94%

BK Channels in the Central Nervous System

Contet

Goulding

Kuljis

et al. 2016

International Review of Neurobiology

136

170

View full text Add to dashboard Cite

show abstract

“…Here, we conducted several behavioral tests to systematically determine the effect of DMS on cognitive deficits in AD mice. Consistent with the previous finding of improved spatial cognitive ability in the aging mice by TMS [34] , [35] , hippocampus-dependent cognitive performance of 5XFAD mice measured by MWM was ameliorated after DMS application in the present study. Furthermore, we tested novelty recognition behavior.…”

Section: Discussionsupporting

confidence: 93%

Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease

Zhen

Qian

Weng

et al. 2017

A&D Transl Res & Clin Interv

View full text Add to dashboard Cite

IntroductionThe abnormal amyloid β (Aβ) accumulation and Aβ-related neural network dysfunction are considered central to the pathogenesis of Alzheimer's disease (AD) at the early stage. Deep-brain reachable low field magnetic stimulation (DMS), a novel noninvasive approach that was designed to intervene the network activity in brains, has been found to alleviate stress-related cognitive impairments.MethodsAmyloid precursor protein/presenilin-1 transgenic mice (5XFAD) were treated with DMS, and cognitive behavior and AD-like pathologic changes in the neurochemical and electrophysiological properties in 5XFAD mice were assessed.ResultsWe demonstrate that DMS treatment enhances cognitive performances, attenuates Aβ load, upregulates postsynaptic density protein 95 level, and promotes hippocampal long-term potentiation in 5XFAD mouse brain. Intriguingly, the gamma burst magnetic stimulation reverses the aberrant gamma oscillations in the transgenic hippocampal network.DiscussionThis work establishes a solid foundation for the effectiveness of DMS in treating AD and proposes a future study of gamma rhythm stimulation on reorganizing rhythmic neural activity in AD brain.

show abstract

“…Indeed, studies employing animal models of rTMS (both in vitro and in vivo ) disclose that rTMS is capable of inducing long-lasting changes of glutamatergic neurotransmission onto principal neurons (Levkovitz et al, 1999; Tokay et al, 2009; Gersner et al, 2011; Ghiglieri et al, 2012; Vlachos et al, 2012; Ma et al, 2013; Sykes et al, 2013; Volz et al, 2013; Lenz et al, 2015; Tang et al, 2015). Seemingly consistent with these observations, it was shown for example that rTMS modulates tactile learning performance in healthy animals (Mix et al, 2010), improves spatial learning in experimental vascular dementia (Wang et al, 2015), and promotes motor learning after stroke in humans in some situations (Brodie et al, 2014). However, it remains unclear how rTMS-induced associative plasticity, i.e., LTP or LTD of excitatory synapses, which is induced by trains of external electromagnetic pulses that are not task- or input-specific, can exert positive effects on motor and cognitive function under physiological and pathological conditions (see also Ridding and Rothwell, 2007).…”

Section: Introductionmentioning

confidence: 64%

Releasing the Cortical Brake by Non-Invasive Electromagnetic Stimulation? rTMS Induces LTD of GABAergic Neurotransmission

Lenz

Vlachos

2016

Front. Neural Circuits

View full text Add to dashboard Cite

Repetitive Transcranial Magnetic Stimulation (rTMS) is a non-invasive brain stimulation technique which modulates cortical excitability beyond the stimulation period. However, despite its clinical use rTMS-based therapies which prevent or reduce disabilities in a functionally significant and sustained manner are scarce. It remains unclear how rTMS-mediated changes in cortical excitability, which are not task- or input-specific, exert beneficial effects in some healthy subjects and patients. While experimental evidence exists that repetitive magnetic stimulation (rMS) is linked to the induction of long-term potentiation (LTP) of excitatory neurotransmission, less attention has been dedicated to rTMS-induced structural, functional and molecular adaptations at inhibitory synapses. In this review article we provide a concise overview on basic neuroscience research, which reveals an important role of local disinhibitory networks in promoting associative learning and memory. These studies suggest that a reduction in inhibitory neurotransmission facilitates the expression of associative plasticity in cortical networks under physiological conditions. Hence, it is interesting to speculate that rTMS may act by decreasing GABAergic neurotransmission onto cortical principal neurons. Indeed, evidence has been provided that rTMS is capable of modulating inhibitory networks. Consistent with this suggestion recent basic science work discloses that a 10 Hz rTMS protocol reduces GABAergic synaptic strength on principal neurons. These findings support a model in which rTMS-induced long-term depression (LTD) of GABAergic synaptic strength mediates changes in excitation/inhibition-balance of cortical networks, which may in turn facilitate (or restore) the ability of stimulated networks to express input- and task-specific associative synaptic plasticity.

show abstract

Improvement of spatial learning by facilitating large-conductance calcium-activated potassium channel with transcranial magnetic stimulation in Alzheimer's disease model mice

Cited by 67 publications

References 63 publications

BK Channels in the Central Nervous System

BK Channels in the Central Nervous System

Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease

Releasing the Cortical Brake by Non-Invasive Electromagnetic Stimulation? rTMS Induces LTD of GABAergic Neurotransmission

Contact Info

Product

Resources

About