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Suxamethonium chloride, also known as suxamethonium or succinylcholine, is a medication used to cause short-term paralysis as part of general anesthesia. This is done to help with tracheal intubation or electroconvulsive therapy. It is given either by injection into a vein or muscle. When used in a vein onset of action is generally within one minute and effects last for up to 10 minutes.
The contraction of cardiac muscle in all animals is initiated by electrical impulses known as action potentials. The rate at which these impulses fire, controls the rate of cardiac contraction, that is, the heart rate. The cells that create these rhythmic impulses, setting the pace for blood pumping, are called pacemaker cells, and they directly control the heart rate. They make up the cardiac pacemaker, that is, the natural pacemaker of the heart. In most humans, the concentration of pacemaker cells in the sinoatrial (SA) node is the natural pacemaker, and the resultant rhythm is a sinus rhythm.
In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.
A tetanic contraction is a sustained muscle contraction evoked when the motor nerve that innervates a skeletal muscle emits action potentials at a very high rate. During this state, a motor unit has been maximally stimulated by its motor neuron and remains that way for some time. This occurs when a muscle's motor unit is stimulated by multiple impulses at a sufficiently high frequency. Each stimulus causes a twitch. If stimuli are delivered slowly enough, the tension in the muscle will relax between successive twitches. If stimuli are delivered at high frequency, the twitches will overlap, resulting in tetanic contraction. A tetanic contraction can be either unfused (incomplete) or fused (complete). An unfused tetanus is when the muscle fibers do not completely relax before the next stimulus because they are being stimulated at a fast rate; however there is a partial relaxation of the muscle fibers between the twitches. Fused tetanus is when there is no relaxation of the muscle fibers between stimuli and it occurs during a high rate of stimulation. A fused tetanic contraction is the strongest single-unit twitch in contraction. When tetanized, the contracting tension in the muscle remains constant in a steady state. This is the maximal possible contraction. During tetanic contractions, muscles can shorten, lengthen or remain constant length.
In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity.
In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.
In neuroscience, a silent synapse is an excitatory glutamatergic synapse whose postsynaptic membrane contains NMDA-type glutamate receptors but no AMPA-type glutamate receptors. These synapses are named "silent" because normal AMPA receptor-mediated signaling is not present, rendering the synapse inactive under typical conditions. Silent synapses are typically considered to be immature glutamatergic synapses. As the brain matures, the relative number of silent synapses decreases. However, recent research on hippocampal silent synapses shows that while they may indeed be a developmental landmark in the formation of a synapse, that synapses can be "silenced" by activity, even once they have acquired AMPA receptors. Thus, silence may be a state that synapses can visit many times during their lifetimes.
Muscle contraction is the activation of tension-generating sites within muscle fibers. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length such as holding a heavy book or a dumbbell at the same position. The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state.
End plate potentials (EPPs) are the voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction. They are called "end plates" because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. When an action potential reaches the axon terminal of a motor neuron, vesicles carrying neurotransmitters are exocytosed and the contents are released into the neuromuscular junction. These neurotransmitters bind to receptors on the postsynaptic membrane and lead to its depolarization. In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small depolarizations in the postsynaptic membrane. This small response (~0.4mV) is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. It represents the smallest possible depolarization which can be induced in a muscle.
The induction of NMDA receptor-dependent long-term potentiation (LTP) in chemical synapses in the brain occurs via a fairly straightforward mechanism. A substantial and rapid rise in calcium ion concentration inside the postsynaptic cell is most possibly all that is required to induce LTP. But the mechanism of calcium delivery to the postsynaptic cell in inducing LTP is more complicated.
Neuromuscular-blocking drugs block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. This is accomplished via their action on the post-synaptic acetylcholine (Nm) receptors.
Myocardial contractility represents the innate ability of the heart muscle (cardiac muscle or myocardium) to contract. The ability to produce changes in force during contraction result from incremental degrees of binding between different types of tissue, that is, between filaments of myosin (thick) and actin (thin) tissue. The degree of binding depends upon the concentration of calcium ions in the cell. Within an in vivo intact heart, the action/response of the sympathetic nervous system is driven by precisely timed releases of a catecholamine, which is a process that determines the concentration of calcium ions in the cytosol of cardiac muscle cells. The factors causing an increase in contractility work by causing an increase in intracellular calcium ions (Ca++) during contraction.
Neural facilitation, also known as paired pulse facilitation (PPF), is a phenomenon in neuroscience in which postsynaptic potentials (PSPs) evoked by an impulse are increased when that impulse closely follows a prior impulse. PPF is thus a form of short-term synaptic plasticity. The mechanisms underlying neural facilitation are exclusively pre-synaptic; broadly speaking, PPF arises due to increased presynaptic Ca2+
concentration leading to a greater release of neurotransmitter-containing synaptic vesicles. Neural facilitation may be involved in several neuronal tasks, including simple learning, information processing, and sound-source localization.
Tetany or tetanic seizure is a medical sign consisting of the involuntary contraction of muscles, which may be caused by disorders that increase the action potential frequency of muscle cells or the nerves that innervate them.
The basal or basic electrical rhythm (BER) or electrical control activity (ECA) is the spontaneous depolarization and repolarization of pacemaker cells in the smooth muscle of the stomach, small intestine, and large intestine. This electrical rhythm is spread through gap junctions in the smooth muscle of the GI tract. These pacemaker cells, also called the interstitial cells of Cajal, control the frequency of contractions in the gastrointestinal tract. The cells can be located in either the circular or longitudinal layer of the smooth muscle in the GI tract; circular for the small and large intestine, longitudinal for the stomach. The frequency of contraction differs at each location in the GI tract beginning with 3 per minute in the stomach, then 12 per minute in the duodenum, 9 per minute in the ileum, and a normally low one contraction per 30 minutes in the large intestines that increases 3 to 4 times a day due to a phenomenon called mass movement. The basal electrical rhythm controls the frequency of contraction but additional neuronal and hormonal controls regulate the strength of each contraction.
Bathmotropic often refers to modifying the degree of excitability specifically of the heart; in general, it refers to modification of the degree of excitability of musculature in general, including the heart. It especially is used to describe the effects of the cardiac nerves on cardiac excitability. Positive bathmotropic effects increase the response of muscle to stimulation, whereas negative bathmotropic effects decrease the response of muscle to stimulation. In a whole, it is the heart's reaction to catecholamines. Conditions that decrease bathmotropy cause the heart to be less responsive to catecholaminergic drugs. A substance that has a bathmotropic effect is known as a bathmotrope.
Summation, which includes both spatial and temporal summation, is the process that determines whether or not an action potential will be generated by the combined effects of excitatory and inhibitory signals, both from multiple simultaneous inputs, and from repeated inputs. Depending on the sum total of many individual inputs, summation may or may not reach the threshold voltage to trigger an action potential.
Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.
Post-tetanic potentiation (PTP) is a form of synaptic plasticity which is short-lived and results in increased frequency of miniature excitatory postsynaptic potentials (mEPSPs) or currents (EPSCs) with no effect on amplitude in the spontaneous postsynaptic potential. It usually lasts in the range of several minutes. PTPs are observed when synapses are stimulated with repetitive (tetanic) pulses, by means of prolonged trains of stimuli applied at high frequencies.
Plasticity Product is a term coined by Jerry Rudy to refer to mRNA genetic artifacts and protein products triggered by transcription factors leading to long-lasting long term potentiation.
References
- ↑ Livingston, Churchill. "Chapter 36:Tetanic stimulation". Sultan Qaboos University.
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