The role of intracellular calcium stores in synaptic plasticity and memory consolidation

Baker, Kathryn; Edwards, Thomas M.; Rickard, Nikki

doi:10.1016/j.neubiorev.2013.04.011

Cited by 87 publications

(64 citation statements)

References 492 publications

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“…Intracellular calcium stores in neurons regulate synaptic plasticity and signaling cascades that are important for longterm potentiation in memory (Baker et al, 2013). Intracellular ryanodine receptor activation leads to calcium-induced Fig.…”

Section: Discussionmentioning

confidence: 99%

Intrathecal Intermittent Orexin-A Causes Sympathetic Long-Term Facilitation and Sensitizes the Peripheral Chemoreceptor Response to Hypoxia in Rats

Kim

Pilowsky

Farnham

2016

Journal of Pharmacology and Experimental Therapeutics

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Intermittent hypoxia causes a persistent increase in sympathetic nerve activity (SNA), which progresses to hypertension in conditions such as obstructive sleep apnea. Orexins (A and B) are hypothalamic neurotransmitters with arousal-promoting and sympathoexcitatory effects. We investigated whether the sustained elevation of SNA, termed sympathetic long-term facilitation, after acute intermittent hypoxia (AIH) is caused by endogenous orexin acting on spinal sympathetic preganglionic neurons. The role of orexin in the increased SNA response to AIH was investigated in urethane-anesthetized, vagotomized, and artificially ventilated Sprague-Dawley rats (n 5 58). A spinally infused subthreshold dose of orexin-A (intermittent; 10 pmol Â 10) produced long-term enhancement in SNA (41.4% 6 6.9%) from baseline. This phenomenon was not produced by the same dose of orexin-A administered as a bolus intrathecal infusion (100 pmol; 7.3% 6 2.3%). The dual orexin receptor blocker, Almorexant, attenuated the effect of sympathetic long-term facilitation generated by intermittent orexin-A (20.7% 6 4.5% for Almorexant at 30 mg•kg 21 and 18.5% 6 1.2% for 75 mg•kg 21), but not in AIH. The peripheral chemoreflex sympathoexcitatory response to hypoxia was greatly enhanced by intermittent orexin-A and AIH. In both cases, the sympathetic chemoreflex sensitization was reduced by Almorexant. Taken together, spinally acting orexin-A is mechanistically sufficient to evoke sympathetic long-term facilitation. However, AIH-induced sympathetic long-term facilitation appears to rely on mechanisms that are independent of orexin neurotransmission. Our findings further reveal that the activation of spinal orexin receptors is critical to enhance peripheral chemoreceptor responses to hypoxia after AIH.

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Section: Discussionmentioning

confidence: 99%

Intrathecal Intermittent Orexin-A Causes Sympathetic Long-Term Facilitation and Sensitizes the Peripheral Chemoreceptor Response to Hypoxia in Rats

Kim

Pilowsky

Farnham

2016

Journal of Pharmacology and Experimental Therapeutics

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“…Yukarida bahsedilen her üç reseptör alt tipi de memeli beyninde eksprese edilmiştir ve beynin birçok bölgesinde lokalizasyon gösterirler [8,9]. 3 H-ryanodin bağlama ve otoradyografik yöntemler kullanilarak serebellum, korteks, serebrum ve spinal kord'da RyR'nin varliği bulunmuştur.…”

Section: Santral Sinir Sistemindeki Ryanodin Reseptörleriunclassified

“…RyR3, beyinde özellikle hipokampus ve striatumda eksprese edilir [11]. Nöronlar, astrositler ve serebral vasküler düz kas hücrelerinde de RyR vardir ve astrositlerde büyük çoğunlukla RyR3 bulunur [8]. Ayrica RyR soma ve dendritlerde, aksonlarda, pre-ve post-sinaptik terminallerde yer almaktadir [8,9].…”

Section: Santral Sinir Sistemindeki Ryanodin Reseptörleriunclassified

“…Nöronlar, astrositler ve serebral vasküler düz kas hücrelerinde de RyR vardir ve astrositlerde büyük çoğunlukla RyR3 bulunur [8]. Ayrica RyR soma ve dendritlerde, aksonlarda, pre-ve post-sinaptik terminallerde yer almaktadir [8,9]. Purkinje hücrelerinin dendritlerinde de çok miktarda RyR1 eksprese edilir [12].…”

Section: Santral Sinir Sistemindeki Ryanodin Reseptörleriunclassified

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Roles of ryanodine receptors in the central nervous system

Karabacak-Taşdemir¹,

İnan²,

Şahin³

2017

Pau Med J

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ÖzetRyanodin reseptörleri (RyR) endoplazmik retikulumdan kalsiyum iyonu saliverilmesine neden olan iyon kanallaridir. Kaslarin uyarilmasindan ve kasilmasindan sorumludurlar. Bununla beraber, son yillarda RyR'nin kas-iskelet hastaliklarindan, kardiyak aritmilerden, çeşitli kalitsal hastaliklardan ve santral sinir sistemi ile ilgili nörodejeneratif bozukluklardan sorumlu olduğu gösterilmiştir. Bu derlemede RyR'nin santral sinir sistemi üzerindeki etkilerini inceledik. Pam Tıp Derg 2017;10(1):115-119Anahtar Sözcüker: Ryanodin reseptörleri, santral sinir sistemi, kalsiyum, nörodejenerasyon. AbstractRyanodine receptors (RyR) are important for calcium release from endoplasmic reticulum and they are also responsible for muscle excitability and contraction. Besides, it has recently been shown that, alteration in RyR can cause musculoskeletal diseases, cardiac arrhythmias, various hereditary diseases and neurodegenerative disorders in the central nervous system. In the present review, we aimed to investigate the effects of RyR in the central nervous system.

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“…Intracellular calcium concentration maintenance is very important for proper functioning of the cell. Calcium plays an important role in nerve physiology, impulse transmission and memory formation [5]. Changes in the cytosolic free calcium concentration are key regulators of almost any cellular function in eukaryotes.…”

mentioning

confidence: 99%

Untitled

2018

RJLBPCS

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Nanomaterial stimulated alteration in the neuron is a great concern as the nanoparticles are widely used in the diagnosis of some neural disorders. Among the different nanoparticles, gold nanoparticles have a wide scope of applicability in the living system due to less toxicity. Gold nanoparticles can be used for cancer therapy especially for the killing of malignant cells in the brain. These particles can cross the bloodbrain barrier and can change the physiological functions of the brain. Gold nanoparticles may cause the change of different membrane proteins that might be responsible for defective transport of chemical through the membrane and finally leads to cellular loss. The experiment has been designed to study the changes of membrane polarity and intracellular calcium level in gold nanoparticles exposed cultured neuron. Citratestabilized gold nanoparticles are prepared from chloro-auric acid using sodium citrate as a stabilizing agent.Gold nanoparticles are characterized by UV Vis-spectrophotometer. Intracellular calcium level is monitored using fluorescence dye fluo 3. Membrane depolarization is studied using voltage-sensitive dye DiBAC(4)3. A higher level of intracellular calcium is observed in AuNP treated neurons. Elevation of intracellular calcium level might be due to the release of calcium from the intracellular storage or transport from extracellular media.Membrane depolarization and hyperpolarization study reveals that AuNP treated neurons membrane is present in depolarized state in comparison with the control neurons. A higher level of intracellular calcium and prolong depolarization in AuNP treated neuron may trigger some signaling mechanism leading to neuronal death

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The role of intracellular calcium stores in synaptic plasticity and memory consolidation

Cited by 87 publications

References 492 publications

Intrathecal Intermittent Orexin-A Causes Sympathetic Long-Term Facilitation and Sensitizes the Peripheral Chemoreceptor Response to Hypoxia in Rats

Intrathecal Intermittent Orexin-A Causes Sympathetic Long-Term Facilitation and Sensitizes the Peripheral Chemoreceptor Response to Hypoxia in Rats

Roles of ryanodine receptors in the central nervous system

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