Noradrenaline synaptic pharmacology

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. 

As outlined previously, initial biological hypotheses of mood disorders were derived from the pharmacological actions of antidepressant drugs, which increase synaptic concentrations of noradrenaline (NA] and/or serotonin. Consequently, the biogenic amine hypothesis was formulated, but it lacks consistent proof that NA and/or serotonin release is indeed diminished. This failure is in part a result of the limited access to relevant brain areas. Measurements of NA and serotonin and their metabolites in blood, urine, and CSF... 

Psychostimulant pharmacology involves an augmented release of noradrenaline and dopamine into the synaptic cleft. The presence of monoamine neurotransmitters in the synaptic cleft is regulated in a variety of ways in response to an action potential. Around 70-80% of all transmitter molecules return into the presynaptic neuron by uptake using an energy-dependent reuptake transport protein that is embedded in the neuronal membrane. A smaller fraction... 

Psychostimulants are able to induce a number of dose-dependent behaviour-activating features including the activation of fight-or-flight-type responses. A fine line can exist between therapy and potential for misuse or abuse and sometimes the differentiation appears to be somewhat arbitrary. Psychomotor stimulant pharmacology involves an augmented release of noradrenaline, dopamine, and to a lesser extent serotonin, into the synaptic cleft. Increased availability of monoamines is predominantly caused by inhibition of the corresponding monoamine... 

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