Simplified pictorial representation | Synaptic cleft

Simplified pictorial representation

For better understanding the following illustration: A group of hikers (=action potentials) wants to cross a river (=synaptic cleft) with boats (=synaptic vesicles), but there is only one docking and undocking point per side (=pre- & postsynaptic membrane). If they have successfully crossed the flow, they can continue their migration on the other side of the flow (=redirection to the target cell). Of course, the landing stage on the other side of the river may already be occupied, or the current is too strong, in which case the hikers would capsize or not arrive at all. This would be, so to speak, the effect of drugs or medication, because they interfere with the signal transmission process in the synaptic cleft by blocking the pre- or postsynaptic membrane.

Modulation by drugs and medications

The synaptic cleft offers many possibilities of manipulation by drugs or medication. A well-known group of antidepressants, the so-called Selective Serotonin Reuptake Inhibitors (SSRI), for example, inhibit the reuptake of the messenger substance serotonin at the presynaptic membrane. As a result, serotonin remains permanently in the synaptic cleft and continuously excites the postsynaptic membrane – i.e. continuously sends signals to the following cell.

Only when the effect of the drug wears off can the serotonin disappear from the synaptic cleft again. It thus has a similar effect to cocaine – except that cocaine is not limited to the messenger substance serotonin, but also blocks the reuptake of dopamine and noradrenaline. Thus it is not selective, and above all it is also very difficult to control.

After all, two of the three catecholamines in the body are affected. (In addition, cocaine is not subject to pharmacological control and can have a very different intensity of action…) The three catecholamines adrenaline, noradrenaline and dopamine are messenger substances that are released during escape and stress situations. This also explains the effect of cocaine: Sweating, excitement, nervousness, but also euphoria and increased performance.

Overdoses are accompanied by aggressiveness, paranoia, hallucinations and cardiac arrhythmia up to cardiac arrest. After the consumption there is usually a so-called crash phase, in which depression-like states occur. The synaptic cleft is therefore a popular starting point for pharmaceuticals, especially in neurology, anesthesia and psychiatry.

The duration of the effect depends on the drug group and the chemical properties of the drug. Long-acting benzodiazepines work for up to 3 days, others for only a few hours. Nicotine, which is the drug of tobacco, is also a transmitter that can occupy receptors in the human body and thus excite nerve cells, e.g. the nicotinic acetylcholine receptor, which, as the name suggests, can be activated by nicotine and acetylcholine.

In the central nervous system, nicotine leads to activation of the reward system – the consumer feels happy and comfortable. This is one of the addictive components of the drug. In the nervous system of the gastrointestinal tract it can also have an activating effect.