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Drug action in neurons

 

Explanations > Brains > Brain Chemistry > Drug action in neurons

The system being treated | Binding | Agonism and antagonism | See also

 

Drugs can use a number of different methods in the way they affect neurons and hence our experiences.

The system being treated

Within a neuron, precursor are substances that are converted into neurotransmitters by synthetic enzymes. The neurotransmitters are then packed into vesicules for transport to the synapse and release there. Neurotransmitters are released into the synapse when calcium ions trigger opening of the docked vesicule.

The neurotransmitters then cross the synaptic gap and bind with postsynaptic receptors, which are activated to open ion channels with the result that the post-synaptic neuron is either fired or inhibited.

Further release of neurotransmitters is inhibited by autoreceptors, which tell the presynaptic terminal button to stop releasing neurotransmitters. Reuptake absorbs remaining neurotransmitters in the synapse back into the terminal button. Another termination method is enzymatic deactivation.

Binding

A common method for drugs is to plug into binding sites where other molecules, typically neurotransmitters, normally fit. Competitive binding is where the drug replaces the normal molecule, preventing it from binding. Non-competitive binding is where the drug attaches to alternative sites.

Agonism and antagonism

Drugs can be used to act at any of these stages either as an agonist to amplify the postsynaptic effect, increasing or enhancing neurotransmitter flow, or as an antagonist, decreasing neurotransmitter flow and effect.

Direct antagonists use competitive binding, whilst indirect antagonists use non-competitive binding. A drug that attaches to an alternative site to open an ion channel is called an indirect agonist.

Methods of agonism and antagonism (detailed below) include:

Increasing precursors

Principle (agonist)

Precursors are the substances that are converted into neurotransmitters by synthetic enzymes. By adding more precursors in a drug, more neurotransmitters can be created.

Drug

L-DOPA is used to treat Parkinson's Disease, where dopaminergic neurons in the substantia nigra is reduced. L-DOPA molecules are converted by the enzyme DOPA-decarboxylase, boosting dopamine production in the few remaining dopaminergic neurons.

Deactivating synthetic enzymes

Principle (antagonist)

Synthetic enzymes that convert precursors into neurotransmitters can be inhibited when a drug is attached to it, thus reducing the production of specific neurotransmitters.

Drug

There is little need to prevent neurotransmitter production in treatments. However, in research it can be invaluable. PCPA binds with tryptophan hydroxylase, thus inhibiting the production of seratonin.

Inhibiting filling of vesicules

Principle (antagonist)

Neurotransmitters are pumped into vesicules by transport proteins in the membrane. This filling of the vesicules may be inhibited by certain drugs.

Drug

Reserpine binds with and deactivates the transport proteins for monoamines such as dopamine, seratonin and norepinephrine. It has been used to treat hypertension (though side-effects limits its use).

Stimulating neurotransmitter release

Principle (agonist)

Normally, neurotransmitters are released when calcium ions trigger opening of the docked vesicule. Other substances may be used in place of the calcium ions, thus increasing the number of vesicules full of neurotransmitters which are emptied into the synapse.

Drug

Black widow venom acts to release high levels acetylcholine, thereby severely cramping skeletal muscles and relaxing heart muscles.

Inhibiting release of neurotransmitter

Principle (antagonist)

In reverse of neurotransmitter stimulation, calcium ions can be blocked from opening the docked vesicules by binding with the proteins in the terminal button membrane that normally separate to open the vesicule.

Drug

Botulinum toxin acts in this way, binding with the neuron membrane proteins and inhibiting calcium ion opening of the vesicule. This leads to paralysis as motor neurons are unable to fire.

Stimulating postsynaptic receptors

Principle (agonist)

Normally neurotransmitters cross the synaptic gap and bind with postsynaptic receptors, which are activated to open ion channels with the result that the post-synaptic neuron is either fired or inhibited. Drugs can act to replace neurotransmitters, binding with the postsynaptic receptors to complete the neuron-to-neuron communication.

Normal neurotransmitter activity still happens, resulting in a significantly increased chance of stimulating the post-sypnaptic neuron.

Drug

Nicotine works this way, docking with acetylcholine receptors to increase stimulation.

Inhibiting postsynaptic receptors

Principle (antagonist)

In the reverse of stimulating postsynaptic receptors, some drugs act to block the binding sites in postsynaptic receptors, thus preventing neurotransmitters from docking there.

Stimulating autoreceptors

Principle (antagonist)

Once the target neuron has been activated, further release of neurotransmitters is normally inhibited by autoreceptors, which tell the presynaptic terminal button to stop releasing neurotransmitters. By binding these cells, the release neurotransmitters is inhibited.

Drug

Low doses of apomorphine bind with dopamine autoreceptors. Higher doses also bind with postsynaptic dopamine receptors (thus becoming an agonist).

Blocking autoreceptors

Principle (agonist)

In reverse to stimulation of autoreceptors, some drugs can block them without activating them. Neurotransmitters can thus no longer activate the autoreceptor and the presynaptic neuron continues releasing neurotransmitters.

Blocking reuptake

Principle (agonist)

Normally, reuptake absorbs remaining neurotransmitters in the synapse back into the terminal button. Drugs can be used to block this process.

Drug

Cocaine blocks dopamine transporters, so keeping dopamine longer in the synapse and creating more firing of the dopamine reward system.

Prevent enzymatic deactivation

Principle (agonist)

Some neurotransmitters are taken up via the pre-synaptic membrane and some are destroyed by special enzymes, such as acetylcholinesterase (AChE), which breaks up the common neurotransmitter acetylcholine. Drugs can disrupt this process and hence sustain the effects of the neurotransmitter.

Drug

Physostigmine bonds with acetylcholinesterase, preventing it from breaking down acetylcholine and hence sustaining the reward and arousal effects of the neurotransmitter.

See also

Inter-neuron communication

 

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