Parkinson's disease is characterized by the selective death of dopaminergic neurons in the substantia nigra of the midbrain, leading to tremors, rigidity, and loss of motor control.
Acetylcholinesterase (AChE) is the enzyme located in the synaptic cleft that rapidly hydrolyzes ACh into acetate and choline, terminating the synaptic signal to prevent continuous stimulation.
Spatial summation is the additive effect of graded potentials occurring at different physical locations (synapses) on the neuron at the same time. Temporal summation occurs at a single synapse over time.
Opening Cl⁻ channels (allowing Cl⁻ influx) or K⁺ channels (allowing K⁺ efflux) leads to hyperpolarization, moving the membrane potential further away from the threshold and inhibiting the neuron.
An EPSP involves the opening of cation channels (usually Na⁺), leading to a localized, graded depolarization that makes the postsynaptic neuron more likely to fire an action potential.
Neurotransmitters bind to specific ligand-gated receptors on the postsynaptic membrane, which undergo a conformational change to open ion channels and generate graded potentials.
Acetylcholine (ACh) is the primary neurotransmitter of the parasympathetic nervous system (both pre- and postganglionic), while the sympathetic system predominantly relies on norepinephrine for postganglionic signaling.
The arrival of an action potential at the synaptic knob opens voltage-gated Ca²⁺ channels. The resulting Ca²⁺ influx causes synaptic vesicles to fuse with the presynaptic membrane and release their contents.
At rest, sodium leak channels are very rare compared to abundant potassium leak channels, making the resting membrane highly impermeable to Na+ and highly permeable to K+.
Once the threshold voltage is reached, the action potential occurs with a constant, maximum amplitude independent of stimulus strength. Stronger stimuli increase the frequency of impulses, not their amplitude.
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