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Excitatory Amino Acid Receptors and Afferent Synaptic Transmission in the Nucleus Tractus Solitarius
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Michael C. Andresen, Mingyong Yang
Injections of NMDA agonists and antagonists into mNTS cause marked changes in blood pressure.17,18,30,31 To examine possible NMDA receptor contributions to synaptic responses to afferent activation, we tested the effects of AP5 on the short-latency EPSP. High concentrations of CNQX can also inhibit NMDA responses. Methods were similar to the CNQX series. AP5 was without effect on the EPSP until very high concentrations were reached (Figure 3). The depression of the EPSP at these high concentrations is likely due to nonspecific effects rather than actions at the NMDA receptor type. Addition of CNQX during AP5 reduced the EPSP amplitude in a similar manner to CNQX alone (Figure 3). Responses to high-frequency stimulation (up to 100 Hz) were not attenuated by application of the NMDA ionophore blocker MK-801 (Figure 4). Together, these experiments suggest that excitatory afferent synapses on mNTS neurons are mediated by EAA acting at non-NMDA receptors. We could find no evidence for a contribution of NMDA receptors to the electrical activation of solitary tract afferents. Results were uniform across all neurons tested. A recent report on reflex responses to aortic nerve stimulation found that NMDA-dependent responses are associated with high stimulation frequencies and concluded that non-NMDA receptors are the primary mediator of aortic baroreflexes.38
Transmitter Regulation of Mesencephalic Dopamine Cells
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Vincent Seutin, R. Alan North, Steven W. Johnson
Synaptic potentials mediated by excitatory amino acids can be detected in both principal and secondary cells of the VTA7,26,40 (Figure 1). These synaptic potentials are depolarizing at the resting potential of the cell; the underlying current rises to its peak in about 1 msec. The current reverses polarity at about 0 mV.40 In most cells, the synaptic potential or underlying synaptic current declines from its peak biphasically. The time constants for the current decay are about 4 msec and 40 msec. The slower component is enhanced in magnesium-free solutions, disappears with hyperpolarization, and is blocked by APV; it results from activation of NMDA receptors. The faster component is blocked by CNQX; it results from activation of non-NMDA receptors.
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).
NBQX attenuates relapse of nicotine seeking but not nicotine and methamphetamine self-administration in rats
Published in The World Journal of Biological Psychiatry, 2021
Jana Ruda-Kucerova, Petra Amchova, Filip Siska, Yousef Tizabi
Notably, there is a large spectrum of AMPA/kainate allosteric modulators or antagonists where their selectivity and pharmacodynamic profiles differ substantially from each other (Lees 2000; Gass and Olive 2008). Even the class of quinoxalinediones ligands has a variable mechanism of action. Thus, DNQX and CNQX also possess weak partial agonists at both AMPA and kainate receptors and may antagonise the NMDA receptor’s glycine site (Kessler et al. 1989). NBQX, on the other hand, seems to be most selective for AMPA receptors, with 30- to 60-fold greater selectivity over kainate receptors (Lees 2000). There is a study showing that CNQX but not NBQX can suppress amphetamine-induced conditioned place preference, which may be explained by the NMDA antagonistic effect of CNQX (Mead and Stephens 1999). Hence, the presumed selectivity of the ligands has to be carefully verified. For example, it may be that the NMDA antagonism is truly responsible for numerous anti-addiction effects of the compounds (Jones et al. 2018). Nonetheless, a role of kainate antagonism against alcohol drinking was also recently suggested (Van Nest et al. 2017). Similarly, the investigation of selective AMPA receptor modulators in drug addiction is worth exploring as a recent study has demonstrated potential antidepressant effects of such ligands in an animal model (Gordillo-Salas et al. 2020).
Interaction between leptin and glutamatergic system on food intake regulation in neonatal chicken: role of NMDA and AMPA receptors
Published in International Journal of Neuroscience, 2020
Amin Adeli, Morteza Zendehdel, Vahab Babapour, Negar Panahi
To investigate the interconnections of glutamatergic system with leptin on cumulative food intake in neonatal broiler chicken, nine experiments designed (each experiment contains four groups (i–iv) within 11 replicates in each group). FD3 chicken received ICV injection of control solution (group i) and 2.5, 5 and 10 µg of leptin (groups ii-iv). In experiment 2, FD3 chicken were ICV injected with (group i) control solution and groups ii–iv with 2.5, 5 and 10 nmol of AG-490 (JAK2 antagonist). In experiment 3, chicken received ICV injections of (i) control solution, (ii) leptin (10 µg), (iii) AG-490 (2.5 nmol) and (iv) leptin + AG-490. In experiment 4, birds were ICV injected with (i) control solution, (ii) leptin (10 µg), (iii) MK-801 (NMDA glutamate receptors antagonist; 15 nmol) and (iv) leptin + MK-801. In experiment 5, injection were (i) control solution, (ii) leptin (10 µg), (iii) CNQX (AMPA glutamate receptors antagonist; 390 nmol) and (iv) leptin + AMPA. In experiment 6, chicken received ICV injection of (i) control solution, (ii) leptin (10 µg), (iii) UBP-302 (Kainate glutamate receptors antagonist; 390 nmol) and (iv) leptin + UBP-302. In experiment 7, injections were (i) control solution, (ii) leptin (10 µg), (iii) AIDA (mGLUR1 glutamate receptors antagonist; 2 nmol) and (iv) leptin + AIDA. In experiment 8, birds received ICV injections of (i) control solution, (ii) leptin (10 µg), (iii) LY341495 (mGLUR2 glutamate receptors antagonist; 150 nmol) and (iv) leptin + LY341495. In experiment 9, injections were (i) control solution, (ii) leptin (10 µg), (iii) UBP1112 (mGLUR3 glutamate receptors antagonist; 2 nmol) and (iv) leptin + UBP1112. Illustration of experimental procedures and treatments during the study are shown in Table 2. Each bird was injected once only. These doses of drugs were calculated based on previous [7,12–14,26] and our pilot experiments (un-published data). Right away after injection, chickens were returned to their individual cages and were provided ad libitum food (pre-weighed) and water. Cumulative food intake recorded at 30, 60 and 120 min’ post injections.