What happens when a neurotransmitter binds to a receptor on the post-synaptic cell? We will study two examples. The first is the simplest: binding of the neurotransmitter acetylcholine, released by a motor neuron, to its receptor on muscle. This region is called the neuromuscular junction. Binding of acetylcholine will lead to a transient depolarization of the muscle cell. Next we will discuss the interaction of a neurotransmitter with a post-synaptic neuron in the central nervous system. This is a much more complex system. Their differences are described below:
In neurons interacting with muscles:
- Most muscle fibers are innervated by only one neuron - a motor neuron
- Neurotransmitter release at the neuromuscular junction leads only to muscle excitation, not inhibition.
- All fibers are excited by the same neurotransmitter - acetylcholine.
In the central nervous system, life is more complicated:
- Stimuli are received from hundreds to thousands of different neurons.
- Nerves receive both excitatory and inhibitory stimuli from neurotransmitters
- Different kinds of receptors are present to receive stimuli, which control the activity of different kinds of channels.
- The ion channels in neurons are gated by a variety of mechanisms in addition to changes in membrane potential, including gating by heat, cold, stretch, or covalent modification.
- Most nerve cells have a resting potential of about -65 mV compared to a -90 mV for a muscle cell.
What happens when a neurotransmitter binds to the receptor on the post-synaptic cell? A depolarization occurs (mediated by conformational changes in the transmitter-receptor complex), raising the membrane potential from the resting equilibrium level. What happens next depends on the identity of the post synaptic cell. In the muscle cell, the rising potential caused by binding of acetylcholine ultimately leads to muscle contraction by opening intracellular organelle membrane calcium channels. In a neuron, the rising potential triggers an action potential by opening voltage-gated sodium channels. The potential rises to about + 35 mV, but does not reach the Na ion equilibrium potential, because the high positive potential opens a voltage-gated potassium channel. The potential then falls until it reaches the K ion equilibrium potential where the cells is hyperpolarized. It slowly then relaxes back to the resting potential of -60 mV. This wave of changes in potential sweeps down the post-synaptic cell membrane and is the basis for the "firing" of the neuron.
Figure: DEPOLARIZATION OF TRANSMEMBRANE POTENTIAL
Figure: NA AND K PERMEABILITIES DURING DEPOLARIZATION
- Animation: The Synapse
- Animation: Nerve Impulse
- Animation: Voltage-Gated Channels and Action Potentials
- Animation: Sodium Potassium ATPase
- Animation: Channel Gating During An Action Potential
- Animation: Propagation of An Action Potential