Low-sodium Acsf Perfusion
Low-sodium Acsf Perfusion - Related Videos
08:53
Whole Animal Perfusion Fixation for Rodents
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Cited by 531 •
2012
Here we describe a low-cost, rapid, controlled and uniform fixation procedure using 4% paraformaldehyde perfused via the vascular system: through the heart of the rat to obtain the best possible preservation of the brain.
04:31
Testing Monosynaptic Connections Using Tetrodotoxin and Tetrodotoxin-Resistant Sodium Channels
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2025
This video demonstrates testing monosynaptic connections using a transgenic fly. The fly has tetrodotoxin-resistant sodium channels and red light-activated channels in its presynaptic neurons, which are optogenetically excited to transmit signals to postsynaptic neurons.
04:44
Antegrade Perfusion Model: An Ex Vivo Technique to Perfuse Isolated Mouse Heart
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2025
This video describes an antegrade perfusion technique of an isolated mouse heart during which a perfusate is injected through the left ventricle, and eventually, it perfuses the entire myocardium. This method can be used to isolate cardiomyocytes from murine models and generate decellularized hearts for further downstream applications.
08:19
The Mouse Isolated Perfused Kidney Technique
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Cited by 24 •
2016
The mouse isolated perfused kidney (MIPK) is a technique for keeping a mouse kidney under ex vivo conditions perfused and functional for 1 hr. The buffers and surgical technique are described in detail.
01:26
Regulation of Sodium and Potassium
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2024
The regulation of sodium and potassium ion concentrations in the human body is a complex process governed primarily by hormones such as aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP). Sodium Regulation Sodium ions make up approximately 90% of extracellular cations, with a normal blood plasma concentration of 136–148 mEq/L. A decrease in blood volume and pressure triggers the release of renin from granular cells in the juxtaglomerular complex (JGC), primarily in...
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Lower extracellular sodium weakens the transmembrane sodium gradient, reducing the driving force available for voltage-gated sodium currents. Because these currents support rapid electrical signaling, changing the gradient can modify how readily neurons generate and propagate activity. This makes sodium reduction useful for testing whether an observed change in excitability depends specifically on sodium-mediated mechanisms rather than on neural activity in general.
The approach can separate sodium-dependent contributions to action-potential propagation from broader effects of altered ionic conditions. It also helps examine how sodium availability influences synaptic communication, where changes in neuronal signaling may reflect altered excitability or transmission. Comparing responses under different sodium conditions therefore supports more precise interpretation of electrophysiological mechanisms in neural tissue.
Pathological hyperexcitability reflects abnormal increases in neural activity, and sodium-dependent currents contribute to the electrical signaling that sustains neuronal responses. Reducing extracellular sodium provides a controlled way to test how strongly that activity depends on the sodium gradient. The resulting observations can refine models of excessive excitability and identify mechanisms that may be obscured under physiological ionic conditions.
A typical experiment places neural tissue in artificial cerebrospinal fluid formulated with reduced sodium and maintains that exposure while neural responses are examined. Investigators then assess how the altered ionic environment affects signaling or circuit activity, often in relation to another experimental condition. The controlled bath composition allows sodium availability to serve as a defined variable in the study.
Brain slices are a principal preparation for low-sodium ACSF perfusion, and related neural tissue preparations may also be examined. These models allow researchers to investigate ionic effects while preserving organized neuronal circuits or local tissue interactions. The method is therefore useful when the goal is to connect sodium-dependent cellular signaling with changes in circuit-level function.
Measurements obtained under reduced sodium conditions can reveal changes in neuronal excitability, action-potential propagation, synaptic communication, and overall circuit activity. Interpreting these responses helps determine which features of neural signaling rely on sodium-dependent mechanisms. The findings can contribute to electrophysiological models and support comparisons between normal circuit behavior and activity associated with pathological hyperexcitability.