Effects of cocaine can be reversed by using a novel technique i.e. optogenetics

cocaineResearchers have found the link between cocaine use and physical brain changes through optogenetics. They have also found the means to reverse this link.

This research has been done by Swiss researchers led by Christian Lüscher of the University of Geneva and published online in December 7 issue of the journal Nature.

Researchers used the highly innovative technique, i.e. optogenetics, to prove that after introduction into the brain, cocaine increase the firing potential of the neurons of the nucleus accumbens – a portion of the brain responsible for pleasure and reward – and this leads to the twitchy behavior of the addicts. Optogenetics is a process in which some forms of algae that have certain light sensitive ion channels are used to cause action in a cell in response to the light. However, the team used the technique to decrease the firing potential of certain neurons caused by the introduction of cocaine.

nucleus accumbens in pleasure reward pathwayResearchers expressed channels in cortical neurons that are linked to the neurons in the accumbens in mice, prepared for this experiment by giving many doses of cocaine to cause the change in brain activity. Laser pulses were then fired at them, so that a virtual storm of chatter initiated between the two cell types resulting in overkill – which caused them to decrease their firing on their own – potentially inhibiting the initial impact of the cocaine.

Researchers worked on several mice and found that there must be a link between the two as the same results were obtained. They have reported,

Cocaine potentiates excitatory transmission in D1-receptor-expressing medium-sized spiny neurons (D1R-MSNs) in mice via ERK signalling with a time course that parallels locomotor sensitization. Depotentiation of cortical nucleus accumbens inputs by optogenetic stimulation in vivo efficiently restored normal transmission and abolished cocaine-induced locomotor sensitization. These findings establish synaptic potentiation selectively in D1R-MSNs as a mechanism underlying a core component of addiction, probably by creating an imbalance between distinct populations of MSNs in the nucleus accumbens. Our data also provide proof of principle that reversal of cocaine-evoked synaptic plasticity can treat behavioural alterations caused by addictive drugs and may inspire novel therapeutic approaches involving deep brain stimulation or transcranial magnetic stimulation.

Reference:

Vincent Pascoli, Marc Turiault & Christian Lüscher, (2011). Reversal of cocaine-evoked synaptic potentiation resets drug-induced adaptive behavior. Nature, doi:10.1038/nature10709