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Potentials, electric inhibitory

Postictal inhibition has been demonstrated after bilateral ECS through ear-clip electrodes as well as after direct electrical stimulation of specific brain areas [for review, see Krauss and Fisher 1993]. TMS might exert anticonvulsive effects by stimulation of brain areas that are responsible for seizure inhibition. Alternatively, TMS might inhibit by direct inhibition of neural excitability in brain regions that are responsible for seizure initiation and spreading. Indeed, the TMS-induced decrease in postsynaptic action potentials hints that TMS might generate direct inhibitory mechanisms on neural excitability. [Pg.195]

Recently, a method for TMS of the brain has been developed. By using TMS it is possible to noninvasively depolarize neurons located deep in the brain without induction of seizures or pain. Thus, it may be possible to compare behavioral effects of TMS and known effects of repeated ECS and other antidepressants in rats. ECS reverses behavioral despair in the swim test and enhances apomorphine hyperactivity and stereotypy. TMS appears to have similar effects to ECS on reversal of the despair in the swim test. Rapid [25-Hz] TMS but not slow (0.2-Hz) TMS potentiated apomorphine stereotypy. ECS is followed by a postictal inhibitory period for further seizures. In this study, TMS as well as ECS increased the seizure threshold for subsequent stimulation and decreased the duration of subsequent seizure. Rapid [25-Hz] TMS but not slow [5- or 1-Hz) TMS decreases the duration of seizure induced by electrical current. [Pg.196]

Neurons communicate with each other at regions of contiguity called synapses. Foster and Sherrington first coined this term in 1897 (Foster and Sherrington, 1897). The synapse is where the axon terminal of one cell links to a dendrite or soma of another. Neurons may have more than 1000 dendrites that connect to even more cells. Synapses function as excitatory or inhibitory in how they affect neuronal activity. When an action potential engages the axonal termini it opens voltagegated calcium channels. Calcium then enters which causes neurotransmitters within vesicles to be released into the synaptic cleft that then activates postsynaptic neuronal receptors. In mammals, the majority of synapses are chemical rather than electrical. Substances called neurotransmitters and neuromodulators - either a gas or, more commonly, a liquid, rather than... [Pg.172]

Another example of an effect apparently unrelated to ChE Inhibition Is found in studies of the actions of ChE Inhibitors on ionic conductances of electrically excitable membranes. When single frog nerve fibers were used, physostlgraine (1-10 mM) attenuated action potential and current, markedly prolonged the duration of the current, and slowed conduction. This mechanism might be involved in functional sensory deficit and—If selective for Inhibitory fibers, as Is the case with local anesthetics (65)--might play a role In generation of facilitation before depression. [Pg.27]

Inhibitory neurotransmitters cause membrane changes that result in a movement of ions across the postsynaptic neural cell membrane that move the electrical potential away from the threshold potential. [Pg.516]

Phenobarbital is the most commonly used anticonvulsant in horses as it has effects at doses lower than those that produce sedahon. It potentiates the actions of gamma-aminobutyric acid (GABA), the inhibitory neurotransmitter in the CNS. Neuronal stabilization by GABA in postsynaptic neurons occurs from increased intracellular chloride conductance, which hyperpolarizes the membrane the overall result is an increase in the seizure threshold and a decrease in the electrical activity of the seizure focus. [Pg.149]

Some synapses deliver transmitter substances that do not decrease the membrane potential at the postsynaptic membrane but, on the contrary, increase it by binding to receptor sites at other specific channel proteins. These synapses are said to be inhibitory because, when activated, they inhibit the transfer of signals from the excitatory synapses, like the cholinergic ones. Most channels for chloride are of this type. Although chloride ions cannot flux freely across the membrane, the outside and inside concentrations of chloride are as if they could do this. Because of the voltage difference, the outside-inside concentration difference may be substantial (e.g., 570 pM outside and 40 pM inside). The concentrations are said to be at equilibrium at the resting electrical potential. Opening of the chloride channels makes it... [Pg.126]

Receptors for several neurotransmitters form ion-selective channels in the plasma membrane and diffuse their signals by altering the cell s membrane potential or the cytoplasmic ionic composition. This subfamily of receptors included the well-characterized nicotinic acetylcholine receptor from electric organ, muscle and brain, the receptors for the excitatory amino acids (aspartate and glutamate), the inhibitory amino acids (7-aminobutyrate (GABA), glycine). [Pg.53]


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Electrical potential

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