This document is discussed the concept of production of new neurons in adults and the effect of cocaine in memory and neurogenesis.
The complete relevance of functional significance of grown-up neurogenesis is yet uncertain. The careful ablation of the proliferative populations in neurogenic regions by irradiation or genetic management is established to produce severe cognitive deficits.
It is hypothesized that neurogenesis in the OB are concerned in the functions, the consolidation of olfactory memory and the distinction of odors.
However, the majority of research work has focused on adult neurogenesis in the DG. The function of DG is incorporated in the neocortical-hippocampus memory system, which is implicated in the establishment of temporal lobe dependent memories, such as episodic memories. Some authors have proposed that DG function is related to the formation of working memory, complex spatial learning and associative context memories, and that new cells may play an important role in these processes. The results suggest that the key to a deeper knowledge of mature neurogenesis function is better understanding of DG and OB functions.
Fig 1 New adult neurons
Drugs of abuse, such as nicotine, ethanol and cocaine have also recently been considered as negative factors that influence grown-up neurogenesis, mainly in the hippocampus. Chronic or acute use of these drugs can provoke alterations in the proliferation rate, survival and differentiation of new cells in neurogenic regions. In addition, some hippocampus-dependent memories are affected by psychomotor drugs in humans and preclinical studies, and these memories are influenced by adult hippocampus neurogenesis.
Cocaine is one of the most widely consumed illegal drugs in developing countries and is associated with several health problems. This drug acts as an indirect agonist of several neurotransmitters, including dopamine (DA), norepinephrine (NE), and serotonin (5-HT). Chronic cocaine treatments produce toxicity and an increase in oxidative stress and pro-inflammatory mediators.
Fig 2 Leaf of coca (Erytroxilon coca)
In the DG, some cognitive functions such as working and recognition memory are affected by cocaine treatments. The drug alters neurotransmission at structural and functional levels.
On the other hand, in the adult brain, the implication of new hippocampal neurons in some memory processes is firmly documented. The effects of drugs on the hippocampal neurogenesis seem to induce alterations on memory performance.
One report shows that adult neurogenesis is associated with drug-taking or drug-seeking behaviors. Also, that adult neurogenesis plays a function in addiction and relapse. The authors proposed that the suppression of new neurons may induce a hippocampal dishinbition, conduct to an enlarged activation of the neural circuit accountable for cocaine-taking.
However, repeated cocaine administration reduces the threshold of long term potentiation (LTP), required for the long term memory, and may induce stronger context-emotional memories.
Other types of memory without a high emotional association are not easy to link with adult neurogenesis. It has been described that working memory is damaged by high doses of cocaine. The involvement of new cells to the generation of hippocampus LTP and the improvement in encoding of new information are possible mechanisms that assist working memory.
Some results indicate that adult neurogenesis is essential in certain situations with increased memory demands or high emotional interference, such as context conditioning memories and consolidation of drug-seeking behaviors.
The modulation of adult neurogenesis by pharmacologic treatments or natural processes may contribute to an increase in the activity of the DG and positively influence anxiety behaviors.
The participation of the cocaine as a recreational product, in the deterioration of the work and long term memory is very likely. In addition, it is necessary to determine its precise effect on the production of new adult neurons.
Journal Reference
Vivian Capilla-Gonzalez and Vicente Hernandez-Rabaza (2011)