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Numerous research investigations using animal models and functional brain imaging in the human brain, intended at understanding and subsequently defining the underlying mechanisms of drug addiction have been concluded or are underway. While probing the biological basis of drug addiction, what is imperative is the understanding of the pathways in which drugs act, along with the factors that effect alterations in those pathways (Jones & Bonci, 2005). 

The affect of all drugs of abuse occurs in the reward circuit of the brain, which is also referred to as the mesolimbic system and is characterised by the interaction of several areas of the brain, which include the ventral tegmental area, the nucleus accumbens, the prefrontal cortex and the basolateral amygdala (Rang, 2003). The principal connected sections are the ventral tegmental area (VTA) and the nucleus accumbens. These are also linked to the prefrontal cortex in the pathway where they communicate through neurons. The ventral tegmental area of the reward circuit consists of dopaminergic neurons that respond to glutamate. These cells respond in the presence of stimuli indicative of a reward. In addition to supporting learning and sensitisation development, the VTA releases dopamine (DA) not just into the forebrain (Jones & Bonci, 2005) but also into the nucleus accumbens (Eisch & Harburg, 2006), an activity that occurs through the mesolimbic pathway. Interestingly, just about all drugs of abuse that result in addiction, increase the release of dopamine into the nucleus accumbens through the mesolimbic pathway (Rang, 2003).

The hippocampus, a scrolled structure located in the medial temporal lobe is crucial in laying down declarative memory, although it isn't essential for working memory, procedural memory, or memory storage. Damage to the hippocampus will only affect the formation of new declarative memories. Research on non-human primates reveals that cortical regions neighbouring the hippocampal formation, consisting of entorhinal, perirhinal, and parahippocampal cortices, are key elements of the medial temporal lobe (MTL) memory system. In addition, studies on human subjects reveals that bilateral damage to the hippocampal formation is enough to generate severe anterograde amnesia together with severe, temporally graded retrograde amnesia (Squire & Zola, 1996).  (Bayley & Squire, 2003) reported that damage limited for the most part to the hippocampal region weakens the learning of new facts (semantic memory), even as such damage impairs the learning of new events (episodic memory). However, remote memory for factual knowledge is spared and in addition, damage to the medial temporal lobe spares remote memory for autobiographical events (episodic memory).

Perhaps the most significant case of hippocampus damage in humans is the patient named H.M (Corkin, 1997). During an epilepsy surgery, doctors removed nearly all of his medial temporal lobes. Since that surgery, in 1953, H.M. had formed no new memories. He could remember his childhood and facts and events before the surgery, able to use his working memory and had the capacity to form procedural memories but had entirely lost the capability to dictate declarative memory.

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