T-type calcium channels contribute to calcium disturbances in brain during hyponatremia

Odackal, John; Sherpa, Ang D.; Patel, Nisha; Colbourn, Robert; Hrabětová, Sabina

doi:10.1016/j.expneurol.2015.08.003

Cited by 4 publications

(3 citation statements)

References 19 publications

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“…Animal studies have shown that hyponatremia causes hippocampal neurotransmitter changes, and thus cortically spreading depression and epilepsy (4,5). To our knowledge, our case is the first to be associated with hyponatremia.…”

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confidence: 82%

Hyponatremia Mimicking Transient Global Amnesia

Kehaya¹,

Güldiken²,

Doğru³

2017

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Dear Editor, Transient global amnesia (TGA) is a clinical syndrome characterized by temporary loss of anterograde memory, followed by retrograde amnesia, with preserved consciousness, attention and awareness. It usually lasts 1-8 hours and recovers without need for treatment. TGA usually occurs as a single attack and does not recur. The annual recurrence rate is reported to be 6-10%. Time and place orientation may be impaired and patients may repeat the same questions, leading to anxiety and agitation. However, consciousness is not affected and higher cortical activities such as driving and talking are preserved. TGA is often seen in patients aged over 50 years and is equally common in both sexes.Although TGA was first described in 1956, no definite pathogenesis has been revealed. Ischemic, epileptic, metabolic, migrainous, and psychological factors are thought to be responsible. The affected brain regions are memory-related structures such as the thalamus, hippocampus (especially CA1 domain), splenium of the corpus callosum, fornix, and cingulate gyrus (1,2). In contrast, there are usually no etiologic factors in patients. Ischemia (vasospasm, venous congestion) or changes in neurotransmitter concentrations are usually listed among the causes of TGA. To the best of our knowledge, TGA accompanied by hyponatremia has never been identified in the literature.A man aged 56 years was admitted to our neurology clinic with memory loss lasting 5-6 hours. He did not remember where he lived and how he had been brought to the hospital during this time. He was asking the same questions again and again. The patient was fully conscious, he could recognize his relatives and could fulfill instructions given by the physician. It was observed that he could solve mathematical problems and count backwards from 100 by 7 (93, 86…) in serial 7 examination. It was learned that there had had no such previous attacks, and that he only had arterial hypertension in his medical history; he was not on any antihypertensive drugs. The patient's wife said that the patient was on salt restriction and he drank about 6 liters of water that day. His blood pressure was normal and the neurologic examination was normal except for the amnestic situation. The other blood tests were within normal limits except that the serum sodium level, which was 120 mEq/L. No lesions were detected in computed tomography and diffusion-weighted magnetic resonance imaging (MRI) scans. Electroencephalography (EEG) of the patient was reported as normal. After sodium replacement, the patient returned to normal, recalling events that occurred before the attack, but he could not remember the 8-hour symptomatic period. The patient was diagnosed as having sodium electrolyte imbalance mimicking TGA.Ad dress for Cor res pon den ce/Ya z›fl ma Ad re si: Babürhan Güldiken MD,

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confidence: 82%

Hyponatremia Mimicking Transient Global Amnesia

Kehaya¹,

Güldiken²,

Doğru³

2017

tnd

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“…[75] Moreover, changes in CSF Ca 2+ concentrations can also severely disrupt neurotransmission. [76] Therapeutically, ventricular infusion with osmotic sugar alcohols (e.g., mannitol) can temporarily correct for CSF over-secretion. However, CSF secretory machinery senses and quickly responds to abnormal osmolality after these treatments.…”

Section: Classic Functions Of the Csf: Osmolarity Buoyancy Waste CLmentioning

confidence: 99%

Brain Ventricular System and Cerebrospinal Fluid Development and Function: Light at the End of the Tube

2020

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The brain ventricular system is a series of connected cavities, filled with cerebrospinal fluid (CSF), that forms within the vertebrate central nervous system (CNS). The hollow neural tube is a hallmark of the chordate CNS, and a closed neural tube is essential for normal development. Development and function of the ventricular system is examined, emphasizing three interdigitating components that form a functional system: ventricle walls, CSF fluid properties, and activity of CSF constituent factors. The cellular lining of the ventricle both can produce and is responsive to CSF. Fluid properties and conserved CSF components contribute to normal CNS development. Anomalies of the CSF/ventricular system serve as diagnostics and may cause CNS disorders, further highlighting their importance. This review focuses on the evolution and development of the brain ventricular system, associated function, and connected pathologies. It is geared as an introduction for scholars with little background in the field.

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“…In mammals, hypercalcemia as well as hypocalcemia is life threatening [4] because of the effects on function of the cardiovascular system, neurons as well as synaptic transmission. To address the effects of Ca 2+ on intact neural circuitry, brain slices of rodents [5,6] has been used where most of the attention is focused on the impact on synaptic transmission [2,7,8] and ionic currents in single cells [9]. It still remains to understand how the [Ca 2+ ] impacts conduction along central neurons.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Calcium Ions on Mechanosensation and Neuronal Activity in Proprioceptive Neurons

et al. 2021

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Proprioception of all animals is important in being able to have coordinated locomotion. Stretch activated ion channels (SACs) transduce the mechanical force into electrical signals in the proprioceptive sensory endings. The types of SACs vary among sensory neurons in animals as defined by pharmacological, physiological and molecular identification. The chordotonal organs within insects and crustaceans offer a unique ability to investigate proprioceptive function. The effects of the extracellular environment on neuronal activity, as well as the function of associated SACs are easily accessible and viable in minimal saline for ease in experimentation. The effect of extracellular [Ca2+] on membrane properties which affect voltage-sensitivity of ion channels, threshold of action potentials and SACs can be readily addressed in the chordotonal organ in crab limbs. It is of interest to understand how low extracellular [Ca2+] enhances neural activity considering the SACs in the sensory endings could possibly be Ca2+ channels and that all neural activity is blocked with Mn2+. It is suggested that axonal excitability might be affected independent from the SAC activity due to potential presence of calcium activated potassium channels (K(Ca)) and the ability of Ca2+ to block voltage gated Na+ channels in the axons. Separating the role of Ca2+ on the function of the SACs and the excitability of the axons in the nerves associated with chordotonal organs is addressed. These experiments may aid in understanding the mechanisms of neuronal hyperexcitability during hypocalcemia within mammals.

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T-type calcium channels contribute to calcium disturbances in brain during hyponatremia

Cited by 4 publications

References 19 publications

Hyponatremia Mimicking Transient Global Amnesia

Hyponatremia Mimicking Transient Global Amnesia

Brain Ventricular System and Cerebrospinal Fluid Development and Function: Light at the End of the Tube

The Effect of Calcium Ions on Mechanosensation and Neuronal Activity in Proprioceptive Neurons

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