The danger is found in drugs’ effect on GABA receptors.
Drugs like alcohol, barbiturates, and benzodiazepines all seems to affect the same target – the major inhibitory neurotransmitter GABA. Neurons containing GABA 
receptors are very common in the nervous system and their function is to inhibit other neurons. One such receptor that is affected by GABA is the GABAa receptor that contains chloride channels. When the receptor is excited, an influx of Cl ions takes place, increasing the negative charge on the inside – hyperpolarization – making initiation, or propagation of an action potential much more difficult. However, this GABAa receptor has not only a binding site for GABA, but two other binding sites as well. One is the sedative-hypnotic site, the other is the anxiety site. That’s why it is possible that both sedative-hypnotic drugs (alcohol and barbiturates) and antianxiety drugs (benzodiazepines) can bind to the same receptor, amplifying their effects. Sedative-hypnotic drugs (alcohol or barbiturates) have precisely this effect -making it hard for action potential to take place and, therefore, sedating the body and affecting bodily functions. Antianxiety drugs (benzodiazepines) enhance binding effects of GABA and so alcohol, or barbiturates will have an even stronger sedative effect, possibly leading to coma, or even death.
The threat of mixing drugs and alcohol is not just a myth, it is a deadly cocktail that you don’t want to be experimenting with.
Does Cl- stand for Cl electrons? And if yes, are these electrons unstable?
Cl- stands for chlorine ions (how silly of me to put it this way indeed).
I wouldn’t say they are unstable. This is merely the flow of ions in response to a stimulus.
Each and every neuron is covered by a membrane. This membrane maintains an electrical gradient – a slight difference in electrical charge between the inside and outside of the cell. However this membrane is flexible and has gates/channels that allow the flow of certain chemicals inside/outside, so that the electrical gradient is maintained.
In the absence of any outside disturbance, the inside of the neuron is slightly polarized (difference in electrical charge). More specifically, the inside of the neuron has a negative electrical potential, compared to the outside. This undisturbed state is called resting potential. This resting potential is much needed, because it allows the neuron to respond rapidly to a stimulus. Any sort of excitation causes the neuron to open its channels.
GABAa receptors, in particular, contain Chloride channels, that allow the passage of Chloride ions in and out of the cell. When excited, the cell opens these Cl channels and allows the inflow of Chloride ions, increasing the negative charge inside the cell – hyperpolarization.
When a neuron initiates reaction to a stimulus it is through a propagation of an action potential. An action potential occurs when the neuron is depolarized (the slight negative charge inside the neuron is depolarized towards zero, until a threshold of excitation is reached, at which point the neuron fires rapidly to a positive charge). Again, we need depolarization in order to have action potential. If the cell is hyperpolarized (which is cause by antianxiety drugs like Valium, for example) the cell will not react. That is why overdose can lead to coma, or death.
I hope that was helpful, instead of confusing.
That was really helpful. Thank you!