Ganglionic Blockers
Ganglionic Blockers - Related Videos
02:08
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2025
This video demonstrates assessing the muscle using cultured motor neurons, Schwann cells, and myotubes, followed by treatment with a neuromuscular blocker to inhibit contraction. Color-coded time-motion graphics show a color-coded time-motion graphic. Red indicates the fastest movement, and blue indicates the slowest.
03:16
Intravenous Delivery of Receptor Blockers to Reduce Brain Edema in a Mouse Model
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2025
Source: Zeynalov, E. et. al., Continuous IV Infusion is the Choice Treatment Route for Arginine-vasopressin Receptor Blocker Conivaptan in Mice to Study Stroke-evoked Brain Edema. J. Vis. Exp. (2016)This video demonstrates the intravenous delivery of an arginine-vasopressin (AVP) receptor antagonist in a mouse model. Transient middle cerebral artery occlusion induces brain edema. An AVP receptor antagonist is administered through a catheter in the left jugular vein, alleviating edema.
04:41
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2025
This video showcases a method for isolating vestibular neurons from a mouse pup's inner ear. It meticulously outlines the steps involved in dissecting the inner ear, harvesting the vestibular ganglion, and subsequently dissociating the ganglion into single cells. These cells are then cultured on glass-bottom dishes to establish a vestibular neuron culture.
01:19
Depolarizing Blockers: Pharmocokinetics
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2023
Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
05:26
Transfection of Mouse Retinal Ganglion Cells by in vivo Electroporation
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Cited by 5 •
2011
We demonstrate an in vivo electroporation protocol for transfecting single or small clusters of retinal ganglion cells (RGCs) and other retinal cell types in postnatal mice over a wide range of ages. The ability to label and genetically manipulate postnatal RGCs in vivo is a powerful tool for developmental studies.
FAQs
At the receptor level, ganglionic blockers antagonize nicotinic acetylcholine receptors located on postganglionic neurons. By preventing acetylcholine-mediated depolarization, they stop the signal from being transmitted through the autonomic ganglion. This receptor action explains why one drug can influence several organ systems rather than producing an effect restricted to a single sympathetic or parasympathetic target.
Autonomic ganglia participate in both sympathetic and parasympathetic pathways, so blocking transmission at this shared relay disrupts signaling in both divisions. Consequently, treatment can change blood pressure and heart rate while also affecting gastrointestinal motility, pupil diameter, and bladder function. The broad physiological profile reflects interruption of autonomic communication rather than selective control of one organ.
Changes in blood pressure, heart rate, gastrointestinal motility, pupil diameter, and bladder function are key observable outcomes. Together, these responses show how strongly autonomic signaling contributes to cardiovascular, digestive, ocular, and urinary regulation. Examining several endpoints is especially informative because the blockade acts at autonomic ganglia and therefore produces a multisystem pharmacological response.
Hexamethonium and mecamylamine are examples used to examine the consequences of nicotinic receptor antagonism in autonomic ganglia. Their effects provide pharmacological evidence that interrupting acetylcholine-mediated depolarization can alter multiple autonomic functions. In pharmacology, these agents therefore help connect receptor-level blockade with measurable changes in cardiovascular and visceral physiology.
Their limited therapeutic value reflects the difficulty of blocking autonomic transmission without disturbing many normal functions at once. The same broad action that can reduce blood pressure may also alter heart rate, gastrointestinal motility, pupil diameter, and bladder function. These widespread effects can produce substantial adverse reactions, making the drugs less practical for routine treatment.
Experimental investigators can use these agents to interrupt autonomic ganglionic transmission and then examine the resulting changes in organ function. Comparing responses such as blood pressure, heart rate, gastrointestinal motility, pupil diameter, and bladder activity helps dissect sympathetic and parasympathetic regulation. This approach makes ganglionic blockers valuable for studying autonomic physiology and pharmacological mechanisms, despite their limited clinical use.