In the late 80’s, my colleagues and I discovered that immature neurons, at an early stage of their development, have a higher concentration of intracellular chloride. The consequence of this is that the gamma-aminobutyric acid (GABA), which is transmitted by the action of chloride fluxes, excites immature neurons, while it inhibits adults ones. But, GABA is the principal transmitter of cerebral inhibition in the adult brain and the target of numerous antiepileptics, anxiolytics and anesthetic molecules, such as benzodiazepines. Thus, these agents consumed by a pregnant woman have opposite effects on the neurons of the mother and the embryo, which can have important clinical implications.
Then, we demonstrated that shortly before delivery, the hormones released by the mother prepare the fetus for birth by reducing intracellular chloride, which causes a decrease in neuronal activity and a kind of anesthesia. This increases the resistance of neurons to childbirth related complications and in particular to anoxic (lack of oxygen) and traumatic events.
We also made the first in utero central neuron recordings on primates and discovered the first “patterns” of neural networks discharge. Thus, we provided a general diagram of the neuronal activity maturation sequence.
These findings, and the conceptual advances that they allow, highlight the importance of the environment in brain development and that alterations of these sequences could have major consequences in terms of public health.