How we change what others think, feel, believe and do
Neurons communicate with one another where the terminal button from what is called the pre-synaptic neuron connects with the dendrite or soma (and sometimes axon) of the post-synaptic neuron. These three connection points are called axodendritic, axosomatic and axoaxonic.
Neurons do not quite touch. The synapse (or synaptic cleft) is the small gap (about 20nm) between the pre-synaptic terminal button and the post-synaptic neuron (and, more closely, the pre-synaptic membrane and the post-synaptic membrane).
Synapses at muscles are called neuromuscular (or myoneural) junctions.
The terminal button contains synaptic vesicules suspended in cytoplasm, along with some mitochondria. These vesicules are little balls (literally 'bladders') with lipid membranes containing some special proteins.
Vesicules are produced in the Golgi apparatus and transmitted down the axon by axoplasmic transport. contain from few dozen to a few hundred neurotransmitter. Their membrane contains about 10,000 lipid molecules and about 200 protein molecules. Transport proteins (or vesicular transporters) located in the vesicule membrane 'pump' neurotransmitters from the outside to the inside of the vesicule. Trafficking proteins help release the neurotransmitters and recycle the vesicule.
Vesicules approach the terminal button end wall and special protein clusters in their membrane 'dock' against corresponding protein clusters in the terminal button membrane.
An action potential opens calcium channels in the button membrane, allowing calcium (Ca2+) ions in from the extracellular fluid, where they abound. When Ca2+ ions reach the docked vesicules, they make the docking proteins pull apart, literally ripping open the vesicule to create a fusion pore and emptying the neurotransmitters into the synapse (this takes about 0.1ms). The vesicule membrane is often then absorbed into the terminal membrane, although they may also close up again and even detach from the membrane.
The membrane material is recycled when little buds of membrane pinch off into the cyctoplasm and form pools of membrane material called endosomes. These may then be recycled in synaptic vesicules.
Once binding is complete, the receptors open neurotransmitter-dependent ion channels. This can be done by direct and indirect method.
Direct ion channel opening
Ionotropic receptors are neurotransmitter-dependent and contain their own sodium ion channels which are opened by acetylcholine.
When sodium ions enter the postsynaptic neuron they depolarize the membrane and hence trigger or inhibit an action potential.
Indirect channel opening
Metabotropic receptors do not contain ion channels, but set off a chemical chain that opens channels elsewhere.
There are two types of metabotropic receptor. In the first type, When a neurotransmitter molecule binds with the receptor, the receptor activates a G-protein, which sits inside the membrane near the receptor. The G-protein then releases alpha subunits which moves to a nearby ion channels to open them.
In the second type, the alpha subunits activates an enzyme that stimulates the creation of a second-messenger units within the neuron, which travel to nearby ion channels to open them.
Second-messenger chemicals can also travel around the neuron performing other tasks such as going to the nucleus to trigger further biochemical changes or turning genes on and off.
Cyclic adenosine monophosphate (cAMP) is common second messenger.
Postsynaptic potentials triggered by metabotropic receptors take longer and last longer than those from ionotropic receptors.
Many neurons contain autoreceptors: receptors that they themselves respond to neurotransmitters and may be on the terminal button. They regulate internal processes including the synthesis and release of neurotransmitters. They are metabotropic, using G-proteins to carry out their purpose.
Autoreceptors act as regulators, managing quantities of neurotransmitters by sending a signal to the presynaptic neuron when there are sufficient neurotransmitters in the synapse.
Postsynaptic can be either depolarizing/excitatory or hyperpolarizing/inhibitory. Which happens depends on the ion channel. Postsynaptic ion channels include sodium (Na+), potassium (K+), chloride (Cl-) and calcium (Ca2+). Any of these can be opened with G-proteins.
Different ion channel effects
Opening sodium channels results in a depolarization as the Na+ ions enter the cell, known as an excitatory postsynaptic potential (EPSP).
Opening potassium channels results in a hyperpolarization as the K+ ions leave the cell, known as an inhibitory postsynaptic potential (IPSP).
Opening chorine channels when the membrane potential is at rest has no effect as Cl- ions are already in balance. If the membrane potential is depolarized (due to an action potential being fired) then the chorine ions will enter to bring the cell back to rest.
Opening calcium channels not only causes depolarization (like sodium), the calcium ions also triggers the migration of synaptic vesicules and the release of the neurotransmitter. Calcium binds with and activates enzymes in postsynaptic dendrites that have various effects that can change the structure of the neuron.
Postsynaptic potentials are terminated by reuptake of neurotransmitters that are not used and are still floating in the synapse. The neurotransmitters are not re-used but are forced into the terminal button cytoplasm by special membrane transporter molecules.
In this way the neurotransmitters are made available to the postsynaptic neuron for only a short period.
The post synaptic membrane may also help termination in enzymatic deactivation, for example where ACh neurotransmitters that bound with the postsynaptic membrane are destroyed by the acetylcholinesterase (AChE) by breaking it into constituents choline and acetate.
Some narcotics work by preventing re-update, thus prolonging the transmission effect.
Excitation occurs through depolarization in a excitatory postsynaptic potential (EPSP). It's aim is to create an action potential. Inhibition seeks to block any excitation through hyperpolarization and IPSP.
One neuron can have multiple input presynaptic neurons, any of which may seek to excite or inhibit the postsynaptic neuron from firing. One IPSP might thus prevent a EPSP, provided it arrives at the right time.
For stronger effects, inputs are repeated many times. With no inhibition, the number of postsynaptic action potentials matches the presynaptic exitatory action potentials. However when there is repeated EPSP and IPSP firing, fewer of the exitatory triggers get through, with an effective attentuation of the effect (for example 20 EPSPs could result in only 5 action potentials being propagated.
There are some other communication aspects of note:
Neuromodulators are chemicals released by neurons that travel further than neurotransmitters and have modulating effects on particular parts of the brain, affecting behavioral states such as attention and anxiety.
Many neuromodulators are chains of amino acids known as peptides.
Hormones are created in the endocrine gland and other organs. They travel by the bloodstream and affect a number of types of target cell. Neurons may have hormone receptors.
Hormones can affect behavior significantly, for example testostorone increasing aggression.
When one axon terminal button connects with that of another neuron, the first neuron may act to stimulate or prevent neurotransmitter release in the second.
the second terminal button contains presynaptic heteroreceptors which are sensitive to release of neurotransmitters from the first one. This arrangement may result in the activation or inhibition of neurotransmitters from the second neuron.
Some dendrites have autoreceptors. When these neurons are activated, the dendrite as well as the terminal button releases neurotransmitters. These activate receptors on the same dendrite and regulate firing by causing hyperpolarization.
And the big