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Neuronal Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
By altering the postsynaptic membrane permeability, the transmitter produces a local potential change resulting in either depolarization or hyperpolarization. As depolarization leads to excitation of a neuron, it is called an excitatory postsynaptic potential (EPSP). An EPSP is a depolarization of a few millivolts resulting from an increased postsynaptic membrane conductance to Na+ and K+ ions. Na+ ions move into the cell, and K+ ions move out. As the movement of Na+ ions predominates, the net effect is a small depolarization of the postsynaptic membrane, bringing the membrane potential closer to the threshold required for opening of its voltage-gated channels so that an action potential is more likely to be triggered.
Cholinergic Antagonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Vishal S. Gulecha, Manoj S. Mahajan, Aman Upaganlawar, Abdulla Sherikar, Chandrashekhar Upasani
A tricyclic antimuscarinic drug, pirenzepine, is an M1-receptor selective agent (Caulfield and Birdsall, 1998). It has a higher affinity for M1 receptors, specifically in the cerebral cortex and sympathetic ganglia. Pirenzepine shows minimal binding toward involuntary muscles (cardiac and smooth muscle) and glands at very low concentration. The drug is responsible for blocking the excitatory postsynaptic potential (EPSP) due to binding of ACh and other cholinergic agonists at ganglionic M1 receptor thereby altering the functions of these M1 receptors (Eglen et al., 1996; Caulfield and Birdsall, 1998). Pirenzepine, at low concentration, reduces the secretion of gastric acid and muscle spasm; therefore, it is used in the management of peptic ulcer. Pirenzepine also showed the contraction of lower esophageal sphincter due to blockade of ganglionic receptors (Wellstein and Pitschner, 1988). Adverse effects such as dry mouth, distorted visualization, and central muscarinic disturbances of other anti-mucarinics are observed to a lower extent with pirenzepine at therapeutic concentration. At a curative dose (100–150 mg/day), pirenzepine cure the duodenal and gastric ulcers as cimetidine and ranitidine which are H2-receptor blockers (Carmine and Brogden, 1985; Tryba and Cook, 1997).
Baroreceptor and Chemoreceptor Afferent Processing in the Solitary Tract Nucleus
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Robert B. Felder, Steven W. Mifflin
Early extracellular and intracellular studies demonstrated that low-frequency (approximately 1 Hz) stimulation of visceral afferent nerves projecting to the NTS could excite or inhibit the discharge of single neurons. Exhaustive cataloguing of neurons recorded with regard to location and excitatory or inhibitory responses has not generally been undertaken, so that the ratio of neurons in NTS excited or inhibited by electrical stimulation remains uncertain. One study17 reported predominantly excitatory responses to electrical stimulation of carotid sinus, aortic, or cervical vagus nerves, but intracellular recording techniques which would permit the observation of inhibitory postsynaptic potentials (IPSPs) were not employed in all instances. In that study, inhibitory responses in extra-cellularly recorded neurons were demonstrated by an interruption of ongoing spontaneous activity by the evoking stimulus. Another study,48 in which all recordings were made intracellularly and the carotid sinus nerve was the only nerve stimulated, found more IPSP than excitatory postsynaptic potential (EPSP) responses. In that study, the EPSP responses were decidedly shorter in latency (2 to 4 ms range) when compared with the IPSP latencies (4 to 9 ms range). Neither study examined the responses of these neurons to selective stimulation of baroreceptors, chemoreceptors, or cardiac receptors.
Depletion of dietary phytoestrogens reduces hippocampal plasticity and contextual fear memory stability in adult male mouse
Published in Nutritional Neuroscience, 2021
Gürsel Çalışkan, Syed Ahsan Raza, Yunus E. Demiray, Emre Kul, Kiran V. Sandhu, Oliver Stork
The stimulation electrode was placed on the Schaffer collaterals (SC) at the border of areas CA2 and CA1 whereas the recording electrode was placed at the stratum radiatum (SR) of area CA1. First, baseline responses were recorded about 10–20 min until they had been stabilized. Then, an input-output (I–O) curve was recorded (inter-stimulus interval: 30 s, stimulation duration: 100 µs) using intensities ranging from 10 to 50 µA after which paired-pulse responses were recorded with intervals ranging from 10 to 500 ms. Before induction of LTP (100 Hz, 100 (for VH) or 50 (for DH) pulses repeated 2 times with 20 s interval) baseline responses were recorded for another 20 min. For the experiments testing the effect of equol (purchased from APExBIO, Houston, TX) on baseline transmission and LTP, the baseline responses were recorded for 30 min and 1 µM equol was continuously bath applied after the initial 5 min baseline recording for the duration of the whole experiment. After LTP induction, another set of test pulses were recorded for 40 min (0.033 Hz). Evoked potentials were analyzed using MATLAB-based analysis tools (MathWorks, Natick, MA). The slope of field excitatory postsynaptic potentials (EPSPs) were analyzed by calculating the slope (V/s) between the 20 and 80% of the fEPSP amplitudes. Paired-pulse responses were analyzed by dividing the slope of the second fEPSP to the first one. For the analysis of LTP and LTD experiments, the data were normalized to baseline responses obtained for 20 min before LTP induction.
Acute enhancing effect of a standardized extract of Centella asiatica (ECa 233) on synaptic plasticity: an investigation via hippocampal long-term potentiation
Published in Pharmaceutical Biology, 2021
Yingrak Boondam, Mayuree H. Tantisira, Kanokwan Tilokskulchai, Sompol Tapechum, Narawut Pakaprot
The communication between neurons requires normal basal synaptic transmission, which starts when Ca2+ ions influx into the cells, triggering the release of neurotransmitters from the presynaptic membrane. Memory formation requires the release of glutamate, which is a major excitatory neurotransmitter in the nervous system. These glutamates bind to specific receptors such as ionotropic glutamate receptor (NMDAR and AMPAR) and metabotropic glutamate receptor (mGluR) on the postsynaptic membrane. After binding, excitatory postsynaptic potentials (EPSPs) are generated. The binding of glutamate to NMDARs also induces Ca2+-dependent signalling cascades, which mediate many neurotrophic protein transcriptions and synaptic plasticity (Sweatt 2010). As mentioned, the LTP model is generally used to study synaptic plasticity (Hölscher 1999), representing the mechanism of the episodic memory encoding and consolidation in the hippocampus (Clopath 2012). Therefore, LTP magnitude enhancement indicates the increased capability of hippocampal synapses to encode and consolidate information, which is important for learning and memory.
Effects of long-term exercise and low-level inhibition of GABAergic synapses on motor control and the expression of BDNF in the motor related cortex
Published in Neurological Research, 2018
Takahiro Inoue, Shuta Ninuma, Masataka Hayashi, Akane Okuda, Tadayoshi Asaka, Hiroshi Maejima
Neuronal activity involves excitatory post-synaptic potentials (EPSPs) and inhibitory post-synaptic potentials (IPSPs). Glutamatergic synapses expressing N-methyl-D-aspartate (NMDA) receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors mainly regulate EPSPs, whereas GABAergic inputs from interneurons produce IPSPs. In a clinical trial designed to control the balance between motor-related EPSPs and IPSPs, transcranial direct current stimulation (tDCS) to the cortex was used to enhance the motor recovery of patients with cerebrovascular accident (CVA) receiving kinesiotherapy [12]. The application of tDCS to the motor-related cortex enhances motor learning [12], inhibiting GABAergic neurons and reducing IPSPs to enhance the excitability of the target neuronal network [13,14].