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Reduced transmittance

Inserting aluminum foil (0.0254 cm thick) reduced transmittance to 83.8% of its value for cell 5 alone. With aid of published data for aluminum, one obtains 0.556 A for effective wavelength of polychromatic beam. [Pg.88]

The best-understood sites of action of morphine are at spinal and brainstem/ midbrain loci, producing both the wanted and unwanted effects of the opioid. The spinal actions of opioids and their mechanisms of analgesia involve (1) reduced transmitter release from nociceptive C-fibres so that spinal neurons are less excited by incoming painful messages, and (2) postsynaptic inhibitions of neurons conveying information from the spinal cord to the brain. This dual action of opioids can result in a... [Pg.258]

Opioids act in the brain and within the dorsal horn of the spinal cord, where their actions are better understood. The actions of opioids important for analgesia and their side-effects involve pre- and postsynaptic effects (1) reduced transmitter release from nerve terminals so that neurons are less excited by excitatory transmitters, and (2) direct inhibitions of neuronal firing so that the information flow from the neuron is reduced but also inhibitions of inhibitory neurons leading to disinhibition. This dual action of opioids can result in a total block of sensory inputs as they arrive in the spinal cord (Fig. 21.5). Thus any new drug would have to equal this dual action in controlling both transmitter release and neuronal firing. [Pg.469]

Figure 21.5 Mechanisms of opioid analgesia at the spinal level. Action potentials in nociceptive afferent fibres invade the terminal and by opening calcium channels (L, N and P-type) cause the release of glutamate and peptides that further transmit pain subsequent to activation of their postsynaptic receptors. Presynaptic opioid receptor activation (mu- and delta-mediated effects have been most clearly shown) opens potassium channels which hyperpolarise the terminal, so reducing transmitter release and inhibiting the postsynaptic neuron... Figure 21.5 Mechanisms of opioid analgesia at the spinal level. Action potentials in nociceptive afferent fibres invade the terminal and by opening calcium channels (L, N and P-type) cause the release of glutamate and peptides that further transmit pain subsequent to activation of their postsynaptic receptors. Presynaptic opioid receptor activation (mu- and delta-mediated effects have been most clearly shown) opens potassium channels which hyperpolarise the terminal, so reducing transmitter release and inhibiting the postsynaptic neuron...
Spinal sites of opioid action. Mu (v), delta (5), and kappa ( ) agonists reduce transmitter release from presynaptic terminals of nociceptive primary afferents. Mu-agonists also hyperpolarize second-order pain transmission neurons by increasing K+ conductance, evoking an inhibitory postsynaptic potential. [Pg.696]

Postsynaptic, excitatory, linked to formation of IP3 Presynaptic, reduce transmitter release, reduce calcium entry Postsynaptic, depressive, ... [Pg.193]

The pitch is indicated by the spectral position of the selective-reflection or reduced-transmittance band ... [Pg.339]

The aminoglycosides have a magnesium-like effect, acting prejunctionaUy to reduce transmitter release and post-junctionally to increase transmitter release they also reduce postjunctional sensitivity to acetylcholine. In most cases their effects can be reversed, partly at least by calcium or 4-aminopyridine. Tobramycin is thought also to have a direct effect on muscle. [Pg.2493]

The tetracyclines produce a small effect, partly by calcium chelation, thus reducing transmitter release. Reversal is usually, but inconsistently, obtained with calcium or neostigmine. [Pg.2493]


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See also in sourсe #XX -- [ Pg.527 ]




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