Neuronal Function
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
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.
Pharmacological MRI as a Molecular Imaging Technique
Michel M. J. Modo, Jeff W. M. Bulte in Molecular and Cellular MR Imaging, 2007
Performing a simple sensory, motor, or cognitive task requires complicated neuronal interactions involving evoking and modulating activity from the molecular to the structural level. For example, finger tapping is the result of coordinating neuronal activity in the ascending sensory and descending motor pathways involving the thalamus, the basal ganglia feedback loop, and sensory, premotor, and motor cortices. The cascading neuronal activity traveling through those functional units reflects a series of neurotransmitter-mediating synaptic transmission and modulation. When a neuronal signal is transmitted at the synapse, it can either evoke or suppress the postsynaptic neuron. For example, glutamate, which induces excitatory postsynaptic potentials (EPSPs), is a major excitatory neurotransmitter in the brain. GABA, which induces inhibitory postsynaptic potentials (IPSPs), is a major inhibitory neurotransmitter. Both glutamate and GABA can be released into the same synapse and alter the function of the postsynaptic neuron competitively. They can also innervate each other to boost (glutamate on GABAergic neuron) or attenuate (GABA on glutamatergic neuron) their ability of releasing the GABA and glutamate neurotransmitters, respectively.
The cell
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella in Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
At an excitatory synapse, binding of the neurotransmitter to its receptor causes an increase in the permeability of the membrane to Na+ ions and K+ ions through chemical messenger-gated channels that are closely associated with the receptor. Na+ ions enter the cell down both their concentration and electrical gradients, and K+ ions leave the cell down their concentration gradient only. Because there are two forces causing the inward diffusion of sodium and only one force causing the outward diffusion of potassium, the influx of Na+ ions is significantly greater than the efflux of K+ ions. This greater movement of (+) charges into the cell results in a small depolarization of the neuron and is referred to as an excitatory postsynaptic potential (EPSP). An EPSP is a graded potential only. A single action potential occurring at a single excitatory synapse opens too few Na+ channels to depolarize the membrane all the way to threshold; however, it does bring the membrane potential closer toward it. This increases the likelihood that subsequent stimuli will continue the depolarization to threshold and that an action potential will be generated by the postsynaptic neuron.
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.
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.
Vanillic acid attenuates amyloid β1-40-induced long-term potentiation deficit in male rats: an in vivo investigation
Published in Neurological Research, 2021
Nesa Ahmadi, Naser Mirazi, Alireza Komaki, Samaneh Safari, Abdolkarim Hosseini
In the DG, field excitatory postsynaptic potential (fEPSP) and PS were the two components of the evoked field potentials. During the electrophysiological recordings, fEPSP slopes and alterations in the PS amplitudes were assessed. The slope functions of fEPSP were measured as the slope of the line which connects the beginning of the evoked potential’s initial positive deflection with the peak of the deflection in the second positive evoked potential. We measured the PS amplitudes from the first deflection’s peak which was positive in the evoked potential to the peak of the next potential which was negative [22,23]. The slope measurements of fEPSP were taken between 20% and 80% of the peak amplitude. In the current study, in order to evoke potentials, the adjustment of the stimulation intensity was implemented which included 40% of the maximum PS amplitude, specified by a curve of input/output [18].
Related Knowledge Centers
- Action Potential
- Inhibitory Postsynaptic Potential
- Membrane Potential
- Neurotransmitter Receptor
- Postsynaptic Potential
- Neurotransmitter
- Ion Channel
- Neuroscience
- Ion
- Ligand-Gated Ion Channel