Analeptics are the non-selective CNS stimulants. They either intensify the excitatory process, facilitating the interneuronal (synaptic) transmission of nerve impulses, or depress the inhibitory mechanisms. Analeptics act almost on all levels of the CNS; though, each of the drugs is characterized by a predominant action on certain parts of the CNS. Thus, some drugs have a predominant effect on the centers of the medulla oblongata (pentylenetetrazol, bemegride, nikethamide), others - on the spinal cord (strychnine1). Caffeine is a member of the analeptics group that possesses a psychostimulating effect associated with its effect on the cerebral cortex.
Increasing the dose of analeptic drugs results in a generalization of the excitatory processes accompanied by an increase in reflex excitability. In toxic doses analeptics induce convulsiones and this is why they are sometimes called convulsive poisons. Convulsiones occur with most analeptics as a result of a facilitation of interneuronal transmission of nerve impulses, shortening of the recovery cycle of the action potentials, irradiation of excitation, prolongation of the after-potentials (for example, impulse after-discharges). Other analeptics cause stimulating and convulsive effects by suppressing the inhibitory processes. For example, picrotoxin blocks the chloride channels coupled with GABA-receptors. So the postsynaptic inhibition of GABA is eliminated. Strychnine weakens the postsynaptic inhibition, mediated by glycine (due to blocking glycine receptors). It does not affect the inhibiting effect of GABA.
Convulsiones that occur due to the excitation of the brain are clonic in nature (they are typical of the action of camphor, bemegride and nikethamide), and if they occur due to the excitation of the spinal cord - they are tonic (for example,