What is the cause of bone fusion in joints damaged by rheumatoid arthritis?
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Answer:
Action potentials and chemical neurotransmitters.
Explanation:
Neurons communicate with each other via electrical events called ‘action potentials’ and chemical neurotransmitters. At the junction between two neurons (synapse), an action potential causes neuron A to release a chemical neurotransmitter. The neurotransmitter can either help (excite) or hinder (inhibit) neuron B from firing its own action potential.
In an intact brain, the balance of hundreds of excitatory and inhibitory inputs to a neuron determines whether an action potential will result. Neurons are essentially electrical devices. There are many channels sitting in the cell membrane (the boundary between a cell’s inside and outside) that allow positive or negative ions to flow into and out of the cell. Normally, the inside of the cell is more negative than the outside; neuroscientists say that the inside is around -70 mV with respect to the outside, or that the cell’s resting membrane potential is -70 mV.
This membrane potential isn’t static. It’s constantly going up and down, depending mostly on the inputs coming from the axons of other neurons. Some inputs make the neuron’s membrane potential become more positive (or less negative, e.g. from -70 mV to -65 mV), and others do the opposite.
These are respectively termed excitatory and inhibitory inputs, as they promote or inhibit the generation of action potentials (the reason some inputs are excitatory and others inhibitory is that different types of neuron release different neurotransmitters; the neurotransmitter used by a neuron determines its effect).
Action potentials are the fundamental units of communication between neurons and occur when the sum total of all of the excitatory and inhibitory inputs makes the neuron’s membrane potential reach around -50 mV (see diagram), a value called the action potential threshold. Neuroscientists often refer to action potentials as ‘spikes’, or say a neuron has ‘fired a spike’ or ‘spiked’. The term is a reference to the shape of an action potential as recorded using sensitive electrical equipment.
Neurons talk to each other across synapses. When an action potential reaches the presynaptic terminal, it causes neurotransmitter to be released from the neuron into the synaptic cleft, a 20–40nm gap between the presynaptic axon terminal and the postsynaptic dendrite (often a spine).
After travelling across the synaptic cleft, the transmitter will attach to neurotransmitter receptors on the postsynaptic side, and depending on the neurotransmitter released (which is dependent on the type of neuron releasing it), particular positive (e.g. Na+, K+, Ca+) or negative ions (e.g. Cl-) will travel through channels that span the membrane.
Synapses can be thought of as converting an electrical signal (the action potential) into a chemical signal in the form of neurotransmitter release, and then, upon binding of the transmitter to the postsynaptic receptor, switching the signal back again into an electrical form, as charged ions flow into or out of the postsynaptic neuron.
