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Transmitter/Receptor Mechanisms in Cardiovascular Control by the NTS: Excitatory Amino Acids, Acetylcholine, and Substance P
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
The role of glutamate as a transmitter was recently questioned because several investigators (with some exceptions)25 reported that microinjections of kynurenate into the NTS failed to abolish the depressor responses to microinjections of l-glutamate at the same site.26,27 However, this controversy has been resolved by the pharmacological demonstration of kynurenate-insensitive ACPD receptors in NTS; activation of these receptors by exogenously applied glutamate is not attenuated or abolished by kynurenate.34 The role of glutamate as the transmitter of baroreceptor afferents in the NTS is further supported by the observations that bilateral microinjections of kynurenate into the NTS block the responses to baroreceptor activation following the aortic nerve stimulation or phenylephrine injections.25-27,30
Glutathione and Glutathione Derivatives: Possible Modulators of Ionotropic Glutamate Receptors
Published in Christopher A. Shaw, Glutathione in the Nervous System, 2018
Réka Janáky, Vince Varga, Zsolt Jenei, Pirjo Saransaari, Simo S. Oja
The slight enhancing effect (20 ± 4 percent, mean ± SD, n = 12) of NMDA observed in 0.1 mM Mg2+ medium in the presence of 50 μM glycine is not discernible in standard Krebs–Ringer–Hepes solution (Table 4). This block is relieved in the presence of GSH, but not GSSG (Janáky et al., unpublished results). The release evoked by 1 mM kainate is enhanced by GSSG (Table 5), but only during the late stimulation phase by GSH. It is inhibited by CNQX and DNQX, NBQX being without effect (Janáky et al. 1997). The release evoked by 0.5 mM AMPA is enhanced by GSSG, GSH being ineffective (Table 5). t-ACPD fails to influence the release of dopamine in all conditions (Janáky et al. 1997).
A Neurochemical Approach to Elucidate Metabotropic vs. Ionotropic Glutamate Receptor Activities in Rat Hippocampal Slices
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Darryle D. Schoepp, Manisha A. Desai
The use of brain slices for biochemical assays has also aided in the characterization of metabotropic glutamate receptors in the hippocampal formation. Although a number of electrophysiological studies suggested the existence of G-protein-coupled glutamate receptors, biochemical studies provided the best evidence of this. Glutamate was first reported to stimulate phosphoinositide hydrolysis in primary cultures of rat striatal neurons,31 resulting in the formation of the second messengers inositol trisphosphate and diacylglycerol. Excitatory amino acid-induced activation of phosphoinositide hydrolysis was later reported in hippocampal slices.32,36,57 For purposes of comparison, we show the effects in Figure 3 of the five excitatory amino acid agonists described in Figures 1 and 2 on phosphoinositide hydrolysis as measured from adult rat hippocampal slices. As discussed previously, NMDA, kainate, and AMPA are selective for ionotropic glutamate receptors and have no activity at metabotropic glutamate receptors. In contrast, 1S,3R-ACPD is selective for metabotropic glutamate receptors relative to ionotropic glutamate receptors. Quisqualate is a nonselective agonist at ionotropic and metabotropic glutamate receptors. Consistent with this, Figure 3 shows that none of the selective ionotropic glutamate receptor agonists stimulates phosphoinositide hydrolysis in slices of rat hippocampus. However, 1S,3R-ACPD does stimulate phosphoinositide hydrolysis. Quisqualate, which is a partial agonist at metabotropic glutamate receptors, also stimulates phosphoinositide hydrolysis; however, it is not as efficacious as the full agonist, 1S,3R-ACPD (Figure 3).
Patterns of buprenorphine/naloxone prescribing: an analysis of claims data from Massachusetts
Published in The American Journal of Drug and Alcohol Abuse, 2020
Richard Paulsen, Alicia Sasser Modestino, Md Mahmudul Hasan, Md. Noor-E-Alam, Leonard D. Young, Gary J. Young
The source of data for this study was the Massachusetts All-Payer Claims Database (APCD). These data are collected by the Center for Health Information and Analysis (CHIA). The APCD contains pharmacy, medical and dental claims from private health insurers. For our analysis, we used all commercially insured pharmacy and medical claims, which included Medicare Advantage and Medigap plans, for years 2011 to 2015. During this time frame, the APCD included claims for coverage and services for virtually all Massachusetts residents with commercial insurance. Two exceptions are claims covered by Workers’ Compensation and claims covered by a health insurer with less than 1,000 covered lives (10). The pharmacy file contains information related to the date the prescription is filled, the drug name and quantity, information about the prescribing physician, patient, and pharmacy (11). The medical claims file contains information regarding diagnosis, date of service, and location. There is also a member file that contains information for individuals who are commercially insured including gender, age, and type of insurance (e.g., HMO or PPO).
Inhibitory effects of fucoidan on NMDA receptors and l -type Ca2+ channels regulating the Ca2+ responses in rat neurons
Published in Pharmaceutical Biology, 2019
Hong Wu, Shuibo Gao, Susumu Terakawa
To elucidate the source of Ca2+ responses remaining after exposure to fucoidan, we examined the effect of fucoidan on [Ca2+]i in cortical neurons in the absence of extracellular calcium ions. Results showed that when calcium ions were removed from the extracellular medium by Ca2+ chelator, EGTA (1 mM), treatment of glutamate has no significant influence on [Ca2+]i in cortical neurons within the concentration range of 50–1000 µM (data not shown). Interestingly, glutamate (50 µM) could induce the Ca2+ responses in hippocampal neurons in the absence of extracellular Ca2+ (Figure 2(A,C)). Application of ACPD (100 µM), which activates both group I and II mGluRs (Irving et al. 1990; Conn and Pin 1997), did not induce Ca2+ transients either in the presence or absence of calcium in the cortical neurons (data not shown), but it did in the hippocampal neurons (Figure 2(B,C)). This was consistent with that of glutamate administration in the absence of extracellular Ca2+. These findings showed that glutamate or ACPD can induce Ca2+ releases from intracellular stores via activation of mGluRs which are expressed on the cell membrane of hippocampal. The increasing responses of [Ca2+]i induced by glutamate or ACPD in the absence of extracellular Ca2+ were insensitive to fucoidan treatment (0.5 mg/mL) (Figure 2(A–C)).
US budget impact of increased payer adoption of the Flexitouch advanced pneumatic compression device in lymphedema patients with advanced chronic venous insufficiency and multiple infections
Published in Journal of Medical Economics, 2018
Adam Cohen, Julia A. Gaebler, Jessica Izhakoff, Laura Gullett, Timothy Niecko, Thomas O’Donnell
APCDs have been found to provide significant clinical benefit, including reduced edema9 and lower incidence of cellulitis21. In addition, side-effects of PCD use are rare22 and newer APCDs may reduce the risk of complications, such as genital edema, observed with older devices23. A specific APCD, Flexitouch (Tactile Medical), was chosen for evaluation in this study due to its robust efficacy data9,21, including proof of its ability to stimulate the lymphatic system, which has not been proven for any other PCDs14. The efficacy of Flexitouch has been hypothesized to be related to its design, which includes up to 32 inflatable chambers (compared to eight chambers with other APCDs) and 18 treatment program options, as well as its unique compression therapy profile, which closely simulates the optimally-performed MLD technique (compared to the higher pressure “squeeze-and-hold” technique employed by other devices)24. In this study, we sought to evaluate the budget impact of treating specific LE patient populations with Flexitouch, instead of with other APCDs, SPCDs, or conservative therapy alone in a representative, privately insured US population.