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Basic psychopharmacology
Published in Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson, Pocket Prescriber Psychiatry, 2019
Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson
Neurotransmission starts with an electrical impulse in an axon. This causes calcium influx in the presynaptic terminal, resulting in exocytosis of vesicles containing neurotransmitters. These neurotransmitters may cross the synapse and bind to postsynaptic or presynaptic receptors. The receptor may open an ion channel or activate a G-protein, resulting in an intracellular enzyme cascade. Neurotransmitter is removed from the synapse, either by breakdown by an enzyme or by re-uptake into the presynaptic terminal. Breakdown may also occur in the presynaptic neuron. Neurotransmitters in the presynaptic terminal can then be packaged into vesicles ready for exocytosis.
Neuroimaging Applications for the Study of Alzheimer’s Disease
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
Many neurochemical systems are abnormal in AD, including the well-described cholinergic and somatostatinergic systems as well as the biogenic amine systems (norepinephrine, serotonin, and dopamine). In each neurotransmitter system, considerable evidence suggests that the abnormality involves the presynaptic neuron. For example, the presynaptic nature of the cholinergic deficit is strongly supported by the frequently reported degeneration of basal forebrain projections. Each biogenic amine system studied in AD patients shows degeneration of the subcortical projection system, e.g., the locus ceruleus, raphe nucleus, and ventral tegmental area associated with evidence of loss of the corresponding projections to cerebral cortex, noradrenaline, serotonin, and dopamine. These presynaptic losses generally stand in distinct contrast to the more conflicting data regarding changes in postsynaptic receptors in the cholinergic, serotonergic, and adrenergic systems, where variable increases, decreases, or lack of change in the receptors have been noted.
The cell
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Most neurons, particularly in the CNS, receive thousands of inputs. The function of a neuron is to communicate or relay information to another cell by way of an electrical impulse. A synapse is the site where the impulse is transmitted from one cell to the next. A neuron may terminate on a muscle cell, a glandular cell or another neuron. The discussion in this chapter will focus on neuron-to-neuron transmission. At these types of synapses, the presynaptic neuron transmits the impulse toward the synapse and the postsynaptic neuron transmits the impulse away from the synapse. Specifically, it is the axon terminal of the presynaptic neuron that synapses with the cell body or the dendrites of the postsynaptic neuron. As will become evident, the transmission of the impulse at the synapse is unidirectional and the presynaptic neuron influences the activity of the postsynaptic neuron only.
A potential paradigm shift in opioid crisis management: The role of pharmacogenomics
Published in The World Journal of Biological Psychiatry, 2022
David Eapen-John, Ayeshah G. Mohiuddin, James L. Kennedy
Serotonin released from the median raphe nucleus acts on dopaminergic centres in the limbic system. Serotonin is known to have numerous effects in the brain, but it is hypothesised that serotonin and dopamine serve reciprocal functions, with dopamine inducing appetitive or seeking behaviours, and serotonin countering these effects by inhibiting dopaminergic activity (Esposito et al. 2008). A major point of serotonin regulation is at the serotonin transporter (SERT), encoded by the gene SLC6A4. This transporter protein serves to remove serotonin from the synaptic cleft and recycle it into storage in the presynaptic neuron (Yuferov et al. 2021). Variation in dopamine receptor genes and serotonin transporter genes may alter an individual’s tendency for addictive behaviours, such as opioid abuse and may provide useful information regarding the individualised risk of opioid prescription for pain management.
Immune to addiction: how immunotherapies can be used to combat methamphetamine addiction
Published in Expert Review of Vaccines, 2021
Md Kamal Hossain, Majid Hassanzadeganroudsari, Erica Kypreos, Jack Feehan, Vasso Apostolopoulos
In the setting of the natural reward mechanism, dopamine is secreted from presynaptic neuron into the synaptic cleft (Figure 2). The released dopamine stays in the synaptic cleft for a short duration and transmits a signal by propagating an action potential to the postsynaptic neuron. The dopamine is then returned to the presynaptic neuron by a specific dopamine transporter. With application of METH, dopamine remains in the synaptic cleft for 8 to 12 hours, causing ongoing stimulation of the postsynaptic neuron, and extended feelings of euphoria. The critical action of METH on this mechanism is to block the action of the dopamine transporter, leading to the inability to remove the neurotransmitter and subsequent increased concentration in the synaptic cleft. With this large amount of dopamine, and its sustained action on the reward center, the individual experiences an extreme peak of euphoria, leading to addiction [20,24].
The World Federation of Societies of Biological Psychiatry (WFSBP) 2020 guidelines for the pharmacological treatment of paraphilic disorders
Published in The World Journal of Biological Psychiatry, 2020
Florence Thibaut, Paul Cosyns, John Paul Fedoroff, Peer Briken, Kris Goethals, John M. W. Bradford
Serotonin and dopamine affect, to a lesser extent, sexual behaviour, as shown in animal and human studies (Bradford 1999, 2001; Kafka 2006). Dopamine agonist treatments may be associated with hypersexual behaviours and, in some cases, with sexual delinquency (see also Chapter 6.4.1.1). Levels of norepinephrine, dopamine, dihydroxyphenylalanine and dihydroxyphenylacetic acid were significantly higher and serotonin levels were lower in patients with paraphilias with compulsive symptoms. Thus neurotransmitters levels seem to be more relevant to control on sexual behaviour but not on paraphilia itself (Kogan et al. 1995). Maes et al. (2001) have reported that paedophilia was accompanied by increased plasma concentrations of catecholamines. Nine men with paedophilia had higher cortisone and prolactin levels in response to meta-chlorophenylpiperazine (a serotonin (5HT) agonist) as compared to controls. This may be a marker of serotoninergic disturbance in paedophilia. The results suggest that there is a decreased activity of the serotoninergic presynaptic neuron and a 5-HT2 postsynaptic receptor hyperresponsivity in paedophilic subjects (Maes et al. 2001). Bradford (1996) has speculated that serotonin may be the most critical neurotransmitter in forensic mental health.