Neurotransmitter system

LTP) in hippocampal slices (89,90). LTP is believed to be a critical step in memory acquisition, and agents that possess the abiUty to augment this process in vivo are expected to be of benefit in memory enhancement. However, this compound has only demonstrated this property in vitro. In addition, because (11) does not appear to affect other neurotransmitter systems, as do other nootropics, the potential of BMY 21502 as a memory-enhancing agent is questionable. 

A medication that causes induction of sleep. The majority of currently available hypnotics (for example benzodiazepine receptor agonists) act via potentiating the brain s inhibitory GABAergic systems, in turn reducing the activity of arousal (i.e. wake promoting) neurotransmitter systems. 

In 1954, experiments by Olds and Milner revealed that the brain has specialized centers for reward functions. In these studies electrical stimulation of certain brain sites was found to be highly rewarding in the sense that rats operantly respond for electrical stimulation of these brain sites, often to the exclusion of any other activity. A neurotransmitter system that is particularly sensitive to electrical self-stimulation is the mesolimbic dopamine projection that originates in the ventral tegmental area and projects to structures closely... 

Lthanol (or alcohol) is a two-carbon molecule that, in contrast to many other drugs of abuse, such as opioids, cocaine, and nicotine, does not bind to specific brain receptors. Nonetheless, alcohol affects a variety of neurotransmitter systems, including virtually all of the major systems that have been associated with psychiatric symptoms (Kranzier 1995). Alcohol affects these neurotransmitter systems indirectly by modifying the composition and functioning of... 

The two major approaches to the use of medications in the secondary prevention or rehabilitation of alcohohsm are 1) direct efforts to reduce or stop drinking behavior by producing adverse effects when alcohol is consumed or by modifying the neurotransmitter systems that mediate alcohol reinforcement, and 2) the treatment of persistent psychiatric symptoms, with the aim of reducing the risk of relapse by reducing the motivation to use alcohol to self-medicate such symptoms. 

As reviewed earlier in the section on the pharmacology of ethanol, several neurotransmitter systems appear to influence the reinforcing or discriminative stimulus effects of ethanol. Although these systems appear to function interactively in their influences on drinking behavior, the medications that have been employed to treat alcohol dependence affect neurotransmitter systems relatively selectively. Consequently, these systems will be discussed individually here. 

Despite recent advances in understanding the neuropharmacological basis of inhalant dependence, there are no published studies examining the effects of potentially efficacious medications in the treatment of this condition. In the following sections, we discuss psychopharmacological agents that, because of their known effects on the neurotransmitter systems that mediate inhalants reinforcing effects, may assist inhalant abusers achieve abstinence. 

After an overview of neurotransmitter systems and function and a consideration of which substances can be classified as neurotransmitters, section A deals with their release, effects on neuronal excitability and receptor interaction. The synaptic physiology and pharmacology and possible brain function of each neurotransmitter is then covered in some detail (section B). Special attention is given to acetylcholine, glutamate, GABA, noradrenaline, dopamine, 5-hydroxytryptamine and the peptides but the purines, histamine, steroids and nitric oxide are not forgotten and there is a brief overview of appropriate basic pharmacology. 

One problem with both these theories is that disruption of noradrenergic transmission by selective adrenoceptor antagonists has little impact on the development of escape deficits. However, such antagonists do prevent the reversal of learned helplessness by antidepressants (reviewed by Stanford 1995). Also, it would be most unlikely that a deficit in only one neurotransmitter system fully accounts for learned helplessness. Indeed, there is plenty of evidence for a role for 5-HT in learned helplessness for instance, this behaviour is reversed by microinjection of 5-HT into the prefrontal cortex (Davis et al. 1999). Finally, it is clear that opioid, GABAergic and cholinergic systems (among others) are all linked with this behavioural deficit and even dihydropyridine antagonists of Ca + channels prevent its development. 

In short, the widespread neurochemical disruption during learned helplessness suggests that antidepressant drugs could prevent this syndrome by targeting any of several different neurotransmitter systems. 

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