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Old 10-27-11, 01:53 PM
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Dopaminergic Structures Related to Reward, Motivation, and Addiction

The article is not weighed down too heavily by "substance abuse" though. I really don't know if I'm organizing this information properly, but I've given it significant time and would like to share the information as completely as possible . If there's an even bigger picture regarding this topic you would like to illustrate or some additions to point out, go ahead.

How does experimental use of substances of abuse lead to drug addiction in some individuals? How do these drugs cause intoxication? Part of the answer lies in a common reinforcement pathway in the human brain which drugs of abuse stimulate, potentially leading to addiction (1,2,3,4,7). This reinforcement pathway, which is composed of both central nervous system structures and endogenous neurotransmitters communicating between these structures, has been termed the “reward pathway”(1). The reward pathway evolved to promote activities that are essential to the survival of the human race as well as other mammals.
Cocaine acts to increase dopamine levels by inhibiting monoamine (dopamine, serotonin, and norepinephrine) re-uptake from the synaptic cleft (1,2,3,4,6,7). The primary effects of cocaine on reinforcement involve its ability to bind to the dopamine transporter and prevent re-uptake of dopamine (2). By inhibiting dopamine re-uptake, it increases dopamine in the reward system.

Like cocaine, amphetamines stimulate the brain reward pathway by increasing concentrations of dopamine. Amphetamines both decrease the re-uptake of dopamine and directly increase the neuronal release of dopamine (1,2,3,4)

Nicotine is thought to affect the brain reward system by increasing dopamine concentrations through interacting with nicotinic acetylcholine receptors. It has been shown to mimic endogenous (or the body’s natural) acetylcholine neurotransmitter. Nicotine increases dopamine efflux in the reward pathway by mimicking acetylcholine at presynaptic nicotinic receptor sites, and exciting dopaminergic neurons (2). Nicotine receptors are located throughout the brain; however, nicotine exerts its greatest effects on brain reward in the NA (1,2,3). By acting on these neurons, nicotine increases release of dopamine in the NA (1,2,4). Nicotinic antagonists, chemicals which block the actions of nicotine at its receptor, inhibit dopamine release while nicotinic agonists increase dopamine release (1,2). Thus, nicotine leads to increased dopamine concentrations in the brain reward pathway like other drugs of abuse.

Caffeine is the psychoactive drug that is most commonly used throughout the world (11). Caffeine blocks the actions of adenosine, an inhibitory neurotransmitter, by binding to its receptor and preventing post binding changes from taking place (2). Caffeine is a “competitive antagonist” of adenosine. Since the neurotransmitter adenosine is like the safety on a gun, when it is removed, neurons begin to fire. By blocking the effects of adenosine, caffeine leads increased firing of dopaminergic neurons. This is especially evident in the NA (4,5).
Nucleus Accumbens (NA)

The nucleus accumbens (NAcc), also known as the accumbens nucleus or as the nucleus accumbens septi (Latin for nucleus leaning against the septum), is a collection of neurons and forms the main part of the ventral striatum. It is thought to play an important role in reward, pleasure, laughter, addiction, aggression, fear, and the placebo effect.

Amygdala volume correlates positively with both the size (the number of contacts a person has) and the complexity (the number of different groups to which a person belongs) of social networks.[38][39] Individuals with larger amygdalae had larger and more complex social networks. They were also better able to make accurate social judgments about other persons' faces.[40] It is hypothesized that larger amygdalae allow for greater emotional intelligence, enabling greater societal integration and cooperation with others.[41]
The amygdala sends impulses to the hypothalamus for activation of the sympathetic nervous system, to the thalamic reticular nucleus for increased reflexes, to the nuclei of the trigeminal nerve and the facial nerve, and to the ventral tegmental area, locus coeruleus, and laterodorsal tegmental nucleus for activation of dopamine, norepinephrine and epinephrine.[4]
Ventral Tegmental Area (VTA)

The dopaminergic neurons of the substantia nigra and the ventral tegmental area of the midbrain project to the dorsolateral caudate/putamen and to the ventromedially located nucleus accumbens, respectively, establishing the mesostriatal and the mesolimbic pathways. The close proximity of these two pathways causes them to be grouped together under dopaminergic projections. Several disorders result from the disruption of these two pathways: schizophrenia, Parkinson's disease, and attention deficit hyperactivity disorder (ADHD). Current research is examining the subtle difference between the neurons that are involved in these diseases and trying to find a way to selectively treat a specific dopamine projection.
((( these things have something in common apparently )))

Mesolimbic Pathway

The following structures are considered to be a part of the mesolimbic pathway:

Ventral Tegmental Area
The ventral tegmental area (VTA) is a part of the midbrain. It consists of dopaminergic, GABAergic, and glutamatergic neurons.[2] The VTA communicates with the nucleus accumbens via the unmyelinated medial forebrain bundle.
Nucleus Accumbens
The nucleus accumbens is found in the ventral striatum and is composed of medium spiny neurons.[3][4] It is subdivided into limbic and motor subregions known as the shell and core.[2] The medium spiny neurons receive input from both the dopaminergic neurons of the VTA and the glutamatergic neurons of the hippocampus, amygdala, and medial prefrontal cortex. When they are activated by these inputs, the medium spiny neurons' projections release GABA onto the ventral pallidum.[2] The release of dopamine in this structure drives the mesolimbic system.
The amygdala is a large nuclear mass in the temporal lobe anterior to the hippocampus. It has been associated with the assignment of emotions, especially fear and anxiety. There are two, one in each temporal lobe, and their functions may be lateralized.
The hippocampus is located in the medial portion of the temporal lobe. It is known for its association with double memory[clarification needed].
Bed Nucleus of the Stria Terminalis
Anyway that was a trip. I hope that was followable.

Last edited by qinkin; 10-27-11 at 02:08 PM..
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