Drug addictionis a tremendously complex condition that is triggered by an intricate combination of physiological , psychological , and societal factors , all of which makes it extremely unmanageable to plow . As such , neuroscientists tend to start by looking for ways to reverse the concrete biological change that leave from long - condition drug ill-usage , and a field published this calendar month in theJournal of Neurosciencesuggests a major breakthrough could be on the horizon .
Like many drug , cocaine leads to an increment indopaminesignaling in the brain ’s reinforcement circuit , create an intense belief of pleasure . However , recur utilisation can cause animbalancein some of the brain region involve in this circle , such as thenucleus accumbens .
old research has demo that these changes occur because cocaine use causes an increment in levels of a protein calledbrain - come neurotrophic factor(BDNF ) , which helps to control the growth , maturation , and connectivity of nerve cell . Because BDNF works by activating a eccentric of genius sensory receptor known as the TrkB receptor , scientists have in the yesteryear undertake to treat cocaine addiction by blocking these receptor .
Several sketch have exhibit that inhibiting TrkB activation in the nucleus accumbens of cocaine - addicted dirty dog does indeed alleviate their drug dependance , causing them to stop choose cocaine - fortify water over regular water .
However , there is a sting in the tail , as further inquiry has shown that cocaine dependency has the accurate opposite effect in another brain region called the prefrontal pallium , where it causes a decrement in TrkB activation . Only when scientist injected BDNF into this part of the brain did scab show a reduction in cocaine - seeking conduct .
Dopamine indicate in the reward circuit plays a major role in cocain addiction . Blamb / Shutterstock
Given the contradictory effects of BDNF on cocaine addiction in different brain part , the authors of the latest field of study question what would happen if they blocked it across the entire brain . To enquire , they developed a TrkB antagonist that could cross the blood - brain barrier when inject into the blood stream .
Results showed that suppress these receptor did indeed cause cocain - addicted rats to significantly reduce their drug dependency behaviour , showing a rock-bottom preference for cocain over a sugar solution and less interestingness in ego - administering the drug by press a lever tumbler .
When analyzing TrkB signaling in unlike brain area , the study authors found that this was massively reduced in the karyon accumbens , bring back to normal levels see in non - addicted rats , which they trust explains the “ reversal ” of the rats ’ addiction . Interestingly , TrkB signaling also returned to normal in the prefrontal cortex , increase despite the comportment of an inhibitor .
In astatement , study co - author Candice Contet explain that “ the antagonist has its elemental activity in the nucleus accumbens , where it ’s logical that it would forbid the activating that is trip by cocaine . ”
