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Targeting the Nervous System
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
The hormone adrenaline is closely related to a range of vital neurotransmitters, each of which have an important role in determining mood and behaviour. Intriguingly, all of these neurotransmitters are structurally related, with only subtle differences to optimise their binding to specific receptors. Noradrenaline is the most closely related to adrenaline, and is responsible for the amount of stimulation experienced. Dopamine is associated with the sense of ‘reward’ when performing a task, and serotonin is involved in mediating the biochemical processes of feeling good; so called ‘euphoria’. In order to carry out their roles in the brain, these neurotransmitters must dock with key enzymes, which catalyse the biochemical processes associated with mood and behaviour. The structures of the neurotransmitters dopamine and serotonin are shown in Figure 8 of the Supporting Material∗. Evident from structural analysis, amino-carboxylate interactions, in combination with hydrophobic interactions with the aromatic rings, are vital for the general mode of action of neurotransmitters in conjunction with enzyme binding. Other aspects of the molecular structure can be subtly varied to tune the precise activity profile. This means that this family of compounds can easily be used to control mood.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Neurotransmitters are chemicals that excite, inhibit or modify the response of another cell. They are classified by their molecular size into small-molecule neurotransmitters and neuropeptides (Tortora and Derrickson 2017). Small molecule neurotransmitters include acetylcholine, norepinephrine, epinephrine and dopamine. Acetylcholine (ACh), an important neurotransmitter in both the PNS and the CNS, is inactivated by the enzyme acetylcholinesterase (AChE).
Brain Motor Centers and Pathways
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The basal ganglia have been implicated in a wide range of functions, as evidenced by the distribution of the inputs they receive. Practically all areas of the cerebral cortex project essentially topographically to the dorsal striatum, thence to other nuclei, and back through the feedback loops via the thalamus to the same cortical areas of origin of the given input to the basal ganglia. The dorsal striatum also receives: (i) feedback input from thalamic nuclei, (ii) dopaminergic input from the ventral tegmental area of the midbrain, which is believed to be part of the “reward” system in the brain, and (iii) serotonergic input from the raphe nuclei, which are a group of nuclei in the brainstem that are a major source of serotonin to the rest of the brain. Serotonin is a neurotransmitter that influences many brain functions, including mood, behavior, sleep, memory, and learning.
Pharmacological management of dementia with Lewy bodies with a focus on zonisamide for treating parkinsonism
Published in Expert Opinion on Pharmacotherapy, 2021
Francesco Panza, Madia Lozupone, Mark Watling, Bruno P. Imbimbo
Neuropathological and imaging studies have shown that in the DLB brain there is degeneration of cholinergic neurons in ventral forebrain nuclei [63], similar to that seen in the AD brain [64], and impaired midbrain dopamine neuron projections to limbic and cognitive brain regions, such as the caudate and anterior cingulate [65]. Therefore, for cognitive symptoms in DLB, acetylcholinesterase inhibitors (AChEIs) (rivastigmine, galantamine, and donepezil) have been shown to ameliorate cognitive and neuropsychiatric symptoms (NPS) in DLB without worsening motor function [66–72]. Glutamate is the main excitatory neurotransmitter in the brain. Animal models of parkinsonism and other neurodegenerative diseases have shown evidence for glutaminergic overactivity in cortical synapses [73]. Memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist approved for the treatment of moderate-to-severe AD patients, is believed to work by preventing brain glutaminergic overactivity. Memantine was shown to improve clinical global status of patients with DLB [74,75]. However, memantine did not improve cognitive performance in these patients [76,77], or improved only some cognitive domains [78].
Effects of glutamate-related drugs on anxiety and compulsive behavior in rats with obsessive-compulsive disorder
Published in International Journal of Neuroscience, 2020
Yuhua Zhan, Jing Xia, Xumei Wang
Obsessive-compulsive disorder (OCD) is a chronic and debilitating psychiatric disorder characterized by recurrent, intrusive, and unwanted thoughts (obsessions) and/or repetitive ritualistic (compulsions) behaviors [1,2]. It is reported to have a worldwide prevalence of 1–3% [3,4]. The glutamate system is the major excitatory neurotransmitter system in the brain and is essential for cognitive processing. Increasing clinical evidence indicates that glutamatergic abnormalities are associated with OCD symptoms [5,6]. Specifically, elevated glutamate levels were found in the cerebrospinal fluid (CSF) of OCD patients [7]. And symptom severity was found to correlate with the level of glutamatergic neurotransmitters in various brain regions implicated of OCD patients, including the caudate nuclei, the prefrontal cortex, and the cingulate cortex [8–10].
Cannabis for cancer – illusion or the tip of an iceberg: a review of the evidence for the use of Cannabis and synthetic cannabinoids in oncology
Published in Expert Opinion on Investigational Drugs, 2019
Emesis results from stimulation of complex reflex pathways controlled by the brain. Neurotransmitters such as dopamine, histamine, acetylcholine, serotonin, and substance P are common targets for anti-emetic medicines, each affecting a distinct aspect of the emetic pathways [18]. Endocannabinoid receptors richly populate these very neuronal tracts, thereby signifying an additional target for treating CINV. The dorsal vagal complex is a region in the brain associated with gastrointestinal function and pathophysiology, and at the root of emesis regulation. This region includes the area postrema, the nucleus of the solitary tract (nTS) and the dorsal motor nucleus of the vagus, and contains vagal outputs in the gastrointestinal tract – all of which contain CB-1 receptors that have demonstrated anti-emetic effects when activated by Δ9-THC [18]. In contrast, serotonin agonists that induce nausea have shown opposite effects on the nTS compared to Δ9-THC [19]. Located just outside the blood-brain barrier in the fourth ventricle of the brain, the area postrema provides direct communication between blood-borne signals such as chemotherapy and the autonomic neurons that elicit emesis [18].