General Psychopharmacology

Mapping Intimacies ◽

10.2310/psych.13063 ◽

2018 ◽

Author(s):

Shadi Doroudgar ◽

Paul Perry

Keyword(s):

Butyric Acid ◽

Synaptic Cleft ◽

Terminal Segment ◽

Clinical Effects ◽

Postsynaptic Neuron ◽

Presynaptic Neuron ◽

Initial Development ◽

Amino Butyric Acid ◽

Enzyme Degradation ◽

Selection Of

Initial development of neuropsychiatric medications relied heavily on serendipitous discovery rather than targeted drug designs. Nowadays, drug discovery targets include receptors, enzymes, and transporters. The human brain comprises many neurons, each being connected to other neurons via synapses. Neurotransmission occurs when a presynaptic neuron projects its terminal segment to form a connection or synapse with an adjacent postsynaptic neuron. When stimulated, neurotransmitters that are stored in small vesicles in the presynaptic neuron are released into an interneuronal gap called the synaptic cleft. Serotonin, dopamine, norepinephrine, γ-amino butyric acid, glutamate, and acetylcholine are among the primary neurotransmitters and chemicals that play important roles in neuropsychiatric functions. As such, they are often common targets of drug development. Grasping the basics of neurotransmission, enzyme degradation, and receptor and transporter pharmacology is essential in understanding today’s FDA-approved pharmaceuticals. This neuropharmacology primer will allow the rational and appropriate clinical selection of pharmacotherapy and accurate anticipation of clinical effects following use. This review contains 1 figure and 45 references Key Words: acetylcholine, dopamine, γ-amino butyric acid, glutamate, neurotransmission, norepinephrine, pharmacology, psychiatric medications, psychopharmacology, receptor, serotonin

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The role of epigenetic-related codes in neurocomputation: dynamic hardware in the brain

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2013.0519 ◽

2014 ◽

Vol 369 (1652) ◽

pp. 20130519 ◽

Cited By ~ 8

Author(s):

Lawrence Edelstein ◽

John Smythies

Keyword(s):

Transcription Factor ◽

Second Messengers ◽

Synaptic Cleft ◽

Postsynaptic Neuron ◽

Presynaptic Neuron ◽

Signalling Molecules ◽

Primary Sensory Cortex ◽

Direct Cell ◽

A Chain ◽

The Brain

This paper presents a review of recent work on the role that two epigenetic-related systems may play in information processing mechanisms in the brain. The first consists of exosomes that transport epigenetic-related molecules between neurons. The second consists of homeoproteins like Otx2 that carry information from sense organs to primary sensory cortex. There is developing evidence that presynaptic neurons may be able to modulate the fine microanatomical structure in the postsynaptic neuron. This may be conducted by three mechanisms, of which the first is well established and the latter two are novel. (i) By the well-established activation of receptors that trigger a chain of signalling molecules (second messengers) that result in the upregulation and/or activation of a transcription factor. The two novel systems are the exosome system and homeoproteins. (ii) Exosomes are small vesicles that are released upon activation of the axon terminal, traverse the synaptic cleft, probably via astrocytes and are taken up by the postsynaptic neuron. They carry a load of signalling proteins and a variety of forms of RNA. These loads may then be transported widely throughout the postsynaptic neuron and engineer modulations in the fine structure of computational machinery by epigenetic-related processes. (iii) Otx2 is a transcription factor that, inter alia , controls the development and survival of PV+ GABAergic interneurons (PV cells) in the primary visual cortex. It is synthesized in the retina and is transported to the cortex by a presently unknown mechanism that probably includes direct cell-to-cell transfer, and may, or may not, include transfer by the dynein and exosome systems in addition. These three mechanisms explain a quantity of data from the field of de- and reafferentation plasticity. These data show that the modality of the presynaptic neuron controls to a large extent the modality of the postsynaptic neuron. However, the mechanism that effects this is currently unknown. The exosome and the homeoprotein hypotheses provide novel explanations to add to the well-established earlier mechanism described above.

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