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Mechanisms of action for estrogen in cardioprotection
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
In their study, Michel and Smith101 also determined the role of nitric oxide in affecting rate of contraction of isolated rat ventricular myocytes. Carbachol (muscarinic agonist) produced slowing of contractions in a dose-related manner. This effect correlates well with cholinergic-induced bradycardia in vivo. Addition of L-NMMA (an inhibitor of nitric oxide synthase) abolished the effect of carbachol, suggesting that nitric oxide may be an important mediator of muscarinic stimulation of cardiac bradycardia. If a similar mechanism operates in vivo, it is possible that the estrogen-induced bradycardia is mediated by up-regulation of nitric oxide mechanisms in cardiac myocytes.
Inflammation Alters Smooth Muscle Function in the Gut: Studies on the Nematode-Infected Rat
Published in William J. Snape, Stephen M. Collins, Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves, 2020
S.M. Collins, D.L. Vermillion, J.D. Huizinga, M.J. Muller
At the level of the muscle cell, both the results of contractility and radioligand binding studies suggest that changes are not mediated by receptors for contractile stimuli. First, increased responses were observed with two pharmacologically distinct stimuli (carbachol and 5-HT). Second, small changes observed in the ligand binding studies are both qualitatively and quantitatively insufficient to explain the changes in contraction. However, given the decrease in the ED50 value for 5-HT-induced contraction in nematode-infected rat jejunum, a change in the affinity of the 5-HT receptor for its ligand cannot be ruled out.
Limbic Cortico-Striato-Pallido-Pontine Substrates of Sensorimotor Gating in Animal Models and Psychiatric Disorders
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Neal R. Swerdlow, David L. Braff, S. Barak Caine, Mark A. Geyer
Sensory gating of auditory evoked potentials has been demonstrated in hippocampal neurons in rats.29 A role for the HPC in modulating PPI is suggested by our findings that PPI is blocked by intra-HPC infusion of carbachol,30 but not by infusions of carbachol into parietal cortex. Intra-HPC carbachol infusion disrupts PPI of both acoustic and tactile startle. The effects on PPI of acoustic startle are most evident after infusion into the dentate gyrus (DG) or region CA1, and are weaker, although statistically significant, after infusion into the ventral subiculum. These effects of carbachol appear to be mediated through its action at muscarinic receptors since they are reversed by concomitant administration of the antimuscarinic atropine.31
Gαs and Gαq/11 protein coupling bias of two AVPR2 mutants (R68W and V162A) that cause nephrogenic diabetes insipidus
Published in Journal of Receptors and Signal Transduction, 2022
Fluo-8 Calcium Flux Assay-No Wash (Abcam) was used for the measurement of calcium amount in the cell after the stimulation with agonists. After the media were removed, cells were washed with Hank’s Buffer with HEPES (HHBS) solution and assay reagents were added to the wells according to the manufacturer’s protocol. Cells were incubated first at 37 °C in 5% CO2 in the air for 30 min, then at room temperature for 30 min at dark. After the incubations, different concentrations of agonists were added and Ca2+ release to the cytoplasm was immediately measured at 10, 30, and 60 s-time points. Fluorescence intensities were read at Ex/Em= 490/525 nm on the EnSight™ Multimode plate reader (PerkinElmer Inc.). Carbachol was used as a positive control since it induces agonist-mediated calcium release in cells. All data were analyzed using GraphPad Prism 8 for macOS (Version 8.4.3., GraphPad Software, LLC).
Stimulatory and inhibitory effects of morphine on pentylenetetrazol-induced epileptic activity in rat
Published in International Journal of Neuroscience, 2021
Samrand Rashan, Yousef Panahi, Emad Khalilzadeh
In the present study, the administration of naloxone at a dose of 1 mg/kg for 25 min before the PTZ injection enhanced spike amplitude significantly (p < 0.001) while in the morphine groups, in comparison with control animals, there was not a significant difference (p > 0.05) between amplitude of spikes. Similar to this study, Stach et al. reported that naloxone is given intravenously (10 mg/kg) or intracaudally (2 micrograms) prolonged the duration and increased the amplitude of bioelectrical epileptiform activity induced by intracaudal carbachol application [29]. Vaughan et al. reported that selective mu and k-receptor agonists can reduce the amplitudes of evoked inhibitory postsynaptic currents [30]. Because significant postsynaptic effects of the opioid peptides could be excluded, their depressant action on EPSC amplitudes might be explained either by presynaptic inhibition of glutamate release or by a postsynaptic interaction between opioid receptors and glutamate receptors [31]. Besides that, rapid changes in amplitude within a train may be related to the activation and inactivation properties of a cell’s ion channels and changes in the membrane potential of the cell [32]. Thus, more specific pharmacological and or genetic manipulations are necessary to determine the exact mechanism responsible for changes in spike amplitude attenuation in vivo.
Should “Retro-ocular Pain, Photophobia and Visual Acuity Loss” Be Recognised as a Distinct Entity? The ROPPVAL Syndrome
Published in Neuro-Ophthalmology, 2021
Francesco Pellegrini, Erika Mandarà, Daniele Brocca
In 2017 Shelukhina et al. found an increase in nociceptive firing recorded by suction electrodes in peripheral terminal of meningeal trigeminal nerves of rats after administration of Ach and Ach receptor agonists. Moreover, nociceptive firing induced by carbachol was reduced by atropine. Interestingly, carbachol but not nicotine caused a massive degranulation of meningeal mast cells releasing multiple pro-nociceptive mediators. The authors concluded that “trigeminal nerve terminals in meninges, as well as dural mast cells and trigeminal ganglion neurons express a reservoir of pro-nociceptive nicotinic and muscarinic Ach receptors, which are activated by Ach released from parasympathetic nerves. These receptors represent a potential target for novel therapeutic interventions in trigeminal pain and probably in migraine”.17 The exact mechanism(s) by which cycloplegia may reduce pain and photophobia in ROPPVAL syndrome has still to be understood but we may speculate that induction of cycloplegia may interrupt a vicious cycle in which the trigeminal nerve could play a role through the ciliary muscle.