The Effects of Cocaine on Neurotransmission

When cocaine is administered, it is absorbed into the bloodstream and then into the brain. Cocaine molecules then appear throughout the brain, but particularly affect the nucleus accumbens region of the brain. The nucleus accumbens is located in the basal forebrain, just in front of the hypothalamus. This is a small yet critically important part of the brain that is central to several different brain functions. The most relevant of these in this case include aversion, reward, pleasure and motive salience (Wenzel et al., 2015.)

Cocaine makes people feel euphoric and is considered to be so addictive because it intensifies the effect of dopamine, a neurotransmitter that is very important in developing motive salience i.e., how a person weighs up what is desirable and what is not desirable to do, especially in the future (insert wiki reference.) This means that cocaine is a stimulant, because it causes a temporary increase in the functional activity of the brain.

The transmitting neuron will transmit dopamine just as normal, but the cocaine molecules block the dopamine transporters on the surface of the transmitting neuron from reabsorbing any excess dopamine that it secretes. Without cocaine, the dopamine transporters would absorb any excess dopamine, lowering the intensity of the effect and likely causing a euthymic state. However, because the cocaine is blocking the dopamine transporters, it is inhibiting the reuptake of dopamine. This means that the cocaine molecules are acting as a reuptake inhibitor, and that it causes what neuroscientists call an inhibitory effect. It is worth noting that this completely excludes the other neurotransmitters that cocaine interferes with, including norepinephrine and serotonin.

Because the dopamine transporters into the transmitting neuron are blocked by the cocaine, there is an excess of dopamine that resides in the synapse between the transmitting neuron that has just transmitted the dopamine and the receiving neuron that is trying to receive it. The receiving neuron has dopamine receptors, little gateways specifically shaped to absorb dopamine molecules whilst blocking non-dopamine molecules from entering. There are a limited number of dopamine receptors on any receiving neuron, so they can only absorb so much dopamine at any one time. When the cocaine blocks the transmitting neurons transporters from reabsorbing excess dopamine, the receiving neurons receptors cannot absorb all the dopamine in a ‘normal’ period of time. With every receptor absorbing dopamine, this increases the intensity of the effect. Because there is still excess dopamine for the receptors to absorb despite being overloaded, this increases the length of the effect over time.

Because the receiving neuron is completely flooded with dopamine to absorb, this means the cocaine user’s nervous system is flooded with dopamine neurotransmitters. Whilst the effects of dopamine on the nervous system are complex, varied and too long to articulate here, one pertinent way it can affect a cocaine user is by greatly strengthening a dopamine pathway that relates to reward-motivated behaviour. This means that even anticipating cocaine increases dopamine secretion in the brain, meaning that even wanting cocaine can be addictive and pleasurable, never mind taking it. (Berridge, 2007)

References

Wenzel J.M., Rauscher N.A., Cheer J.F., and Oleson E.B. (2015) A Role for Phasic Dopamine Release within the Nucleus Accumbens in Encoding Aversion: A Review of the Neurochemical Literature. ACS Chemical Neuroscience 6(1), 16–26. doi: 10.1021/cn500255p

Puglisi-Allegra, S. and Ventura, R. (2012) Prefrontal/accumbal catecholamine system processes high motivational salience. Frontiers of Behavioural Neuroscience 6(31). doi: 10.3389/fnbeh.2012.00031

Berridge, K.C. (2007) The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191, 391–431. doi: 10.1007/s00213–006–0578-x