Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

https://bic.berkeley.edu/sites/default/files/Rossi_09_TMS%20safety%20review.pdf

Safety, ethical considerations, and application guidelines for the use of transcranial magnetic stimulation in clinical practice and research

Four adenosine receptors have been cloned and characterized from several mammalian species. The receptors are named adenosine A(1), A(2A), A(2B), and A(3). The A(2A) and A(2B) receptors preferably interact with members of the G(s) family of G proteins and the A(1) and A(3) receptors with G(i/o) proteins. However, other G protein interactions have also been described. Adenosine is the preferred endogenous agonist at all these receptors, but inosine can also activate the A(3) receptor. The levels of adenosine seen under basal conditions are sufficient to cause some activation of all the receptors, at least where they are abundantly expressed. Adenosine levels during, e.g., ischemia can activate all receptors even when expressed in low abundance. Accordingly, experiments with receptor antagonists and mice with targeted disruption of adenosine A(1), A(2A), and A(3) expression reveal roles for these receptors under physiological and particularly pathophysiological conditions. There are pharmacological tools that can be used to classify A(1), A(2A), and A(3) receptors but few drugs that interact selectively with A(2B) receptors. Testable models of the interaction of these drugs with their receptors have been generated by site-directed mutagenesis and homology-based modelling. Both agonists and antagonists are being developed as potential drugs.

https://pharmrev.aspetjournals.org/content/pharmrev/53/4/527.full.pdf

International Union of Pharmacology. XXV. Nomenclature and Classification of Adenosine Receptors

Nitric oxide (NO) was first recognized as a messenger molecule in the central nervous system (eNS) in 1988 (52), when it was identified as the unstable intercellular factor that had been hypothesized, a year earlier (53), to mediate the increased cyclic GMP (cGMP) levels that occur on activation of glutamate receptors, particularly those of the NMDA (N-methyl-D-aspartate) subtype. The presence of an NO-forming enzyme (NO synthase, or NOS) in the brain was later confirmed (74), and this enzyme was subsequently purified (14) and its cDNA cloned and sequenced (12). The discovery that NO functions as a signaling molecule in the brain opened a new dimension in our concept of neural communication, one overlaying the classical picture of chemical neurotransmission, where information is passed between neuronal elements at discrete loci (synapses), and in one direction, with a diffusive type of signal that disregards the spatial constraints on neu­ rotransmitter activity normally imposed by membranes, transporters, and in­ activating enzymes. In principle, NO could spread out from its site of produc­ tion to influence many different tissue elements (neuronal, glial, and vascular) that are not necessarily in close anatomical juxtaposition. During the past few years, much information on the enzymology and mo­ lecular characteristics of NO synthesis has accrued, as reviewed in other articles in this volume. Furthermore, data from immunocytochemistry, in situ hybridization, and NADPH diaphorase histochemistry have combined to give

Nitric oxide signaling in the central nervous system.

http://www.mag2health.com/wp-content/uploads/CLINPH-Guidelines-rTMS.pdf

Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS)

Nitric oxide as modulator of neuronal function

Release of neurotransmitters in the locus coeruleus

Nitric oxide releases acetylcholine in the basal forebrain.

Using intracerebral microdialysis in urethane-anaesthetized adult male Wistar rats, we monitored the effects of acute repetitive transcranial magnetic stimulation (rTMS; 20 trains of 20 Hz, 2.5 s) on the intrahypothalamic release of arginine vasopressin (AVP) and selected amino acids (glutamate, glutamine, aspartate, serine, arginine, taurine, gamma-aminobutyric acid) and the intrahippocampal release of monoamines (dopamine, noradrenaline, serotonin) and their metabolites (homovanillic acid, 3,4-dihydroxyphenylacetic acid, 5-hydroxyindoleacetic acid). The stimulation parameters were adjusted according to the results of accurate computer reconstructions of the current density distributions induced by rTMS in the rat and human brains, ensuring similar stimulation patterns in both cases. There was a continuous reduction in AVP release of up to 50% within the hypothalamic paraventricular nucleus in response to rTMS. In contrast, the release of taurine, aspartate and serine was selectively stimulated within this nucleus by rTMS. Furthermore, in the dorsal hippocampus the extracellular concentration of dopamine was elevated in response to rTMS. Taken together, these data provide the first in vivo evidence that acute rTMS of frontal brain regions has a differentiated modulatory effect on selected neurotransmitter/neuromodulator systems in distinct brain areas.

Acute transcranial magnetic stimulation of frontal brain regions selectively modulates the release of vasopressin, biogenic amines and amino acids in the rat brain

Athineos Philippu

Papers

Nitric oxide as modulator of neuronal function

Release of neurotransmitters in the locus coeruleus

Nitric oxide releases acetylcholine in the basal forebrain.

Acute transcranial magnetic stimulation of frontal brain regions selectively modulates the release of vasopressin, biogenic amines and amino acids in the rat brain

Histaminergic neurons facilitate social memory in rats