At the NMJ, the enzyme — sitting on the basal lamina — rapidly cleaves ACh into acetate and choline. Choline is taken back up into the LMN via the choline transporter (CHT1) , then reused.
At the synapse onto the LMN, in the cleft take up excess glutamate via EAAT2 transporters , converting it to glutamine (via glutamine synthetase), sending it back to you to recycle.
You are about to initiate movement. The EPSP travels down your dendrites, summing at the axon hillock — your decision zone. Here, voltage-gated sodium channels wait. The membrane potential crosses threshold (-55 mV from resting -70 mV). Bang.
Your biceps contracts. The cup lifts. But movement must be smooth and precise. You can't just blast away. brain bee study guide
On the other side is your target: a in the ventral horn of the spinal cord, at the level of C5-C6 (imagine reaching for a cup). This LMN has ionotropic glutamate receptors — specifically, AMPA receptors (fast, Na+/K+) and NMDA receptors (slower, Ca2+ permeable, blocked by Mg2+ at rest).
A volley of signals races up through the of the thalamus. And then — you feel it. A massive excitatory postsynaptic potential (EPSP) arrives at your basal dendrites.
Your action potential speeds down your (courtesy of oligodendrocytes in the CNS). The myelin sheaths are interrupted by Nodes of Ranvier , where saltatory conduction leaps the signal from node to node — much faster than unmyelinated axons. Step 2: The Synapse You arrive at the presynaptic terminal . Depolarization opens voltage-gated calcium channels (VGCCs) . Calcium rushes in. This triggers synaptic vesicles — loaded with glutamate — to dock at the active zone via SNARE proteins (synaptobrevin on vesicle, syntaxin and SNAP-25 on membrane). At the NMJ, the enzyme — sitting on
This is a — a narrative-style, memorable walkthrough of key Brain Bee concepts, designed to help you retain neuroscience competition material by embedding facts into a vivid scenario. The Synaptic Symphony: A Brain Bee Deep Story You are a neuron. Specifically, you are a pyramidal cell in Layer 5 of the primary motor cortex (Brodmann Area 4). Your name is Pyra.
Calcium binds to . Tropomyosin shifts away. Myosin heads — already loaded with ADP and Pi — bind to actin. Power stroke. Pi released. New ATP binds, myosin releases actin, then hydrolyzes ATP to recock the head.
Sodium floods in (phase 0: depolarization). Then, open, repolarizing you (phase 3). But a special class of calcium-dependent potassium channels ensures you have an afterhyperpolarization — a refractory period so you don't fire chaotically. You are about to initiate movement
The LMN fires. Its axon travels via the into the brachial plexus , then the radial nerve , finally reaching the neuromuscular junction (NMJ) of your biceps brachii . Step 3: The Neuromuscular Junction At the NMJ, the LMN releases acetylcholine (ACh) . ACh binds to nicotinic acetylcholine receptors (nAChRs) on the muscle fiber's motor end plate. These are ligand-gated ion channels — they let Na+ in, K+ out, creating an end-plate potential (EPP) .
One day, you receive an urgent message from the . A structure called the subthalamic nucleus has fired a burst of glutamate (excitatory) at your rival, an inhibitory neuron in the globus pallidus internus (GPi) . That GPi neuron normally clamps down on the thalamus like a hand squeezing a hose. But now, GPi is silenced.
The hose is open.