PubMed · 8917152
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J W Richards. 1996. Cryptic tonsillitis.. https://pubmed.ncbi.nlm.nih.gov/8917152/
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Optic nerve section in the newborn rat results in a rapid apoptotic degeneration of most axotomized retinal ganglion cells (RGCs). This massive process of neuronal death has been ascribed mainly to the interruption of a trophic factor supply from target structures rather than to the axonal damage per se. To distinguish between these two possibilities, we induced a reversible axonal transport blockade in the developing optic nerve by topical application of a local anesthetic (lidocaine). Light and electron microscopy showed no alterations in the fine structure of treated optic nerves. Retinae of treated and control rats were stained with cresyl violet and examined at different times after surgery. We found that axonal transport blockade induced only a limited number of pyknotic RGCs. Degeneration of these cells was completely prevented by inhibiting protein synthesis during lidocaine application. We conclude that the rapid degeneration of RGCs after axotomy can be ascribed only partly to the loss of retrogradely transported trophic factors.
1. The effects of tetracaine were studied on voltage-clamped rat ventricular myocytes, which exhibited Ca2+ overload as identified by spontaneous Ca2+ release from the sarcoplasmic reticulum (SR) as shown by the associated contractions. This Ca2+ release was initially abolished by tetracaine before returning at a lower frequency, but greater amplitude, than the control. On removal of tetracaine, there was a burst of spontaneous Ca2+ release activity. All these effects were dose dependent, from 25 to 200 microM tetracaine. 2. The spontaneous Ca2+ release activated an inward Na(+)-Ca2+ exchange current as Ca2+ was pumped out of the cell. The integral of this current (i.e. the Ca2+ efflux) was increased in the presence of tetracaine. The calcium efflux per unit time was unaffected by tetracaine. 3. The SR Ca2+ content was increased by tetracaine, as shown by the integral of the caffeine-evoked Na(+)-Ca2+ exchange current. The increase of SR Ca2+ content was equal to the extra Ca2+ lost from the cell during the burst on removal of tetracaine, and to estimates of the extra calcium gained over the quiescent period following addition of tetracaine. 4. It is concluded that partial inhibition of calcium-induced calcium release increases SR Ca2+ content. In the steady state, cell Ca2+ balance is maintained as the lower frequency of spontaneous release (that activates efflux) is compensated for by their greater size.
The antinociceptive potential of mazindol, an anorectic drug, and lidocaine, an amide-type local anesthetic, were investigated in the mouse formalin test with concurrent motor function assessment. In addition, the role of dopamine and opioid receptors in mediation of the antinociceptive action of these drugs was examined. The i.p. injection of mazindol (1.25-10 mg/kg) and lidocaine (10-30 mg/kg) induced significant antinociceptive responses in both phases of the test. Cocaine (20 mg/kg, i.p.), used as positive control, also inhibited the pain responses caused by formalin. Haloperidol (0.2 mg/kg, i.p.), and sulpiride (5 mg/kg, i.p.), a dopamine D2 receptor antagonist, reduced the antinociceptive actions of mazindol and cocaine, while SCH 23390, R(+)-7-chloro 8-hydroxy-3methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3 benzazepine (0.03 mg/kg, i.p.), a dopamine D1 receptor antagonist, did not affect these responses. Only the antinociception associated with mazindol was reversed by naloxone (2 mg/kg, i.p.). The same pretreatments failed to modify lidocaine-induced antinociception. The drug conditions used in this study did not reveal any motor impairment in the rotarod test. These observations suggest an involvement of dopaminergic mechanisms, mainly via dopamine D2 receptors, in the antinociceptive action of mazindol in the formalin test, but the nature of mechanisms involved in the lidocaine responses remains unsolved.