Drugs reduce the capacity to learn
Substantial work (NasifFJetal2005a, NasifFJetal2005b , DongYetal2005 , HuXT2004, Marinellietal2006) has shown that repeated cocaine administration changes the intrinsic excitability of prefrontal cortical (PFC) neurons (in rats), by altering the expression of ion channels. It downregulates voltage-gated K+ channels, and increases membrane excitability in principal (excitatory) prefrontal cortex (PFC) neurons.
An important consequence of this result is the following: by restricting expression levels of major ion channels, the capacity of the neuron to undergo plasticity is limited, and therefore its learning or storage capacity is reduced. The range of parameters available for K+ channel expression is smaller.
Cocaine dependency leads to reduced neural plasticity, and, as a consequence reduced synaptic (associative) plasticity, at a principal neuron’s site. If the neuron is reduced in its ability to learn, i.e. to adjust its voltage-gated K+ channels, such that it always operates with heightened membrane excitability, then its dendritic synapses are also restricted in their capacity to learn (for instance to undergo synaptic weight adjustment).
Drugs like cocaine hijack the brain’s learning capacity and reduce it. Of course this is most evident in what we experience as “emotional learning”, i.e. striatal-PFC interactions, but the principle of reduced parameter ranges underlying reduced plasticity is a universal one.
