Neuropharmacology
Neuropharmacology is the study of how drugs affect function in the nervous system, and the neural mechanisms through which they influence behavior.
[2] Molecular neuropharmacology involves the study of neurons and their neurochemical interactions, with the overall goal of developing drugs that have beneficial effects on neurological function.
Both of these fields are closely connected, since both are concerned with the interactions of neurotransmitters, neuropeptides, neurohormones, neuromodulators, enzymes, second messengers, co-transporters, ion channels, and receptor proteins in the central and peripheral nervous systems.
Neuropharmacology did not appear in the scientific field until, in the early part of the 20th century, scientists were able to figure out a basic understanding of the nervous system and how nerves communicate between one another.
In the 1930s, French scientists began working with a compound called phenothiazine in the hope of synthesizing a drug that would be able to combat malaria.
This black box method, wherein an investigator would administer a drug and examine the response without knowing how to relate drug action to patient response, was the main approach to this field, until, in the late 1940s and early 1950s, scientists were able to identify specific neurotransmitters, such as norepinephrine (involved in the constriction of blood vessels and the increase in heart rate and blood pressure), dopamine (the chemical whose shortage is involved in Parkinson's disease), and serotonin (soon to be recognized as deeply connected to depression[citation needed]).
[citation needed] Neuropharmacology is a very broad region of science that encompasses many aspects of the nervous system from single neuron manipulation to entire areas of the brain, spinal cord, and peripheral nerves.
The calcium ions will then cause vesicles, small packets filled with neurotransmitters, to bind to the cell membrane and release its contents into the synapse.
Once the neurotransmitter binds to the GPCR protein, it causes a cascade of intracellular interactions that can lead to many different types of changes in cellular biochemistry, physiology, and gene expression.
Neurotransmitter/receptor interactions in the field of neuropharmacology are extremely important because many drugs that are developed today have to do with disrupting this binding process.
There are a few technical words that must be defined when relating neurotransmission to receptor action:[citation needed] The following neurotransmitter/receptor interactions can be affected by synthetic compounds that act as one of the three above.
[citation needed] The GABA neurotransmitter mediates the fast synaptic inhibition in the central nervous system.
[citation needed] This GABAA receptor contains many binding sites that allow conformational changes and are the primary target for drug development.
The excitatory or inhibitory post-synaptic effects of serotonin are determined by the type of receptor expressed in a given brain region.
Monoamine oxidase inhibitors (MAOIs) increased the amount of serotonin in the synapse, but had many side-effects including intense migraines and high blood pressure.
Most research has shown that the major part of the brain that reinforces addiction through neurochemical reward is the nucleus accumbens.
[12][13] With acute alcohol consumption, dopamine is released in the synapses of the mesolimbic pathway, in turn heightening activation of postsynaptic D1 receptors.
[10] These modifications to CREB function in the mesolimbic pathway induce expression (i.e., increase gene expression) of ΔFosB in the NAcc,[10] where ΔFosB is the "master control protein" that, when overexpressed in the NAcc, is necessary and sufficient for the development and maintenance of an addictive state (i.e., its overexpression in the nucleus accumbens produces and then directly modulates compulsive alcohol consumption).
The excessive stimulation of muscarinic and nicotinic receptors by acetylcholine may contribute to the side effects that anticholinesterases have.
