7.1
La unión neuromuscular y el bloqueo
El sitio de comunicación química entre una neurona motora y una fibra muscular se llama la unión neuromuscular (NMJ, por sus siglas en inglés). El ext…
La unión neuromuscular, o NMJ, es un sitio de comunicación química entre una neurona motora y la fibra muscular para facilitar la contracción del músculo esquelético. Los medicamentos llamados bloqueadores neuromusculares se dirigen a la NMJ y ayudan a inducir la parálisis muscular.
La NMJ consiste en la terminal nerviosa motora y la placa terminal motora de una fibra muscular separadas por una pequeña hendidura sináptica. La acetilcolina, un neurotransmisor liberado desde la terminal nerviosa, actúa como un mensajero químico entre las dos células.
Cuando un potencial de acción alcanza el extremo neuronal, desencadena la liberación de acetilcolina en la hendidura sináptica. La acetilcolina se une a los receptores nicotínicos en la placa terminal del motor y abre los canales iónicos para permitir que los iones de sodio ingresen a la célula.
La afluencia de iones de sodio despolariza la membrana muscular, propagando el potencial de acción y provocando la contracción muscular.
Debido a su similitud estructural con la acetilcolina, los bloqueadores neuromusculares pueden unirse a los receptores nicotínicos y bloquear la transmisión de impulsos.
Por ejemplo, la succinilcolina compite con la acetilcolina para unirse a los receptores e inhibir su acción. Este bloqueo neuromuscular hace que los músculos se relajen en los pacientes sedados durante la cirugía.
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Q1: What is the neuromuscular junction and what role does it play in muscle contraction?
The neuromuscular junction (NMJ) is a site of chemical communication between a motor neuron and muscle fiber that facilitates skeletal muscle contraction. It consists of the motor nerve terminal, synaptic cleft, and motor end plate. When an action potential reaches the nerve terminal, it triggers acetylcholine release into the synaptic cleft, enabling impulse transmission across the NMJ and initiating muscle contraction.
Q2: How does acetylcholine trigger muscle contraction at the neuromuscular junction?
Acetylcholine, released from synaptic vesicles, binds to nicotinic receptors on the motor end plate. Two acetylcholine molecules open sodium ion channels, allowing Na+ influx that depolarizes the muscle membrane. This depolarization propagates an action potential along the muscle fiber, triggering muscle contraction. Acetylcholinesterase then breaks down acetylcholine to terminate the signal.
Q3: What is the mechanism by which neuromuscular blockers induce muscle paralysis?
Neuromuscular blockers bind to nicotinic receptors on the motor end plate, blocking acetylcholine from attaching and preventing impulse transmission across the NMJ. Because of their structural similarity with acetylcholine, drugs like succinylcholine compete for receptor binding sites. This blockade prevents sodium influx and action potential propagation, resulting in muscle relaxation and temporary paralysis during surgery.
Q4: How do botulinum toxin and tubocurarine differ in blocking neuromuscular transmission?
Botulinum toxin prevents acetylcholine release by blocking exocytosis of synaptic vesicles at the nerve terminal. Tubocurarine and similar nondepolarizing blockers bind to acetylcholine receptors on the motor end plate, preventing acetylcholine attachment. Both agents block impulse transmission but act at different sites within the NMJ to prevent muscle contraction.
Q5: What role does calcium play in acetylcholine release at the neuromuscular junction?
When a nerve impulse arrives at the synaptic bulb, it opens calcium channels, allowing Ca2+ influx into the nerve terminal. This calcium influx stimulates exocytosis of synaptic vesicles, releasing acetylcholine into the synaptic cleft. Without calcium entry, acetylcholine cannot be released, preventing neuromuscular transmission and muscle contraction.
Q6: Why are neuromuscular blockers used during surgical procedures?
Neuromuscular blockers induce muscle relaxation and temporary paralysis by blocking impulse transmission at the NMJ, making them valuable during surgery. They prevent involuntary muscle movement, allowing surgeons better access and control during procedures. This pharmacological paralysis is reversible and essential for anesthesia management in operating rooms.
Q7: What structural features allow neuromuscular blockers to interfere with acetylcholine function?
Neuromuscular blockers possess structural similarity to acetylcholine, enabling them to bind to nicotinic receptors on the motor end plate. This structural mimicry allows them to compete with acetylcholine for receptor binding sites. By occupying these receptors, blockers prevent acetylcholine attachment and subsequent ion channel opening, effectively halting neuromuscular transmission.