No abstract

No abstract

Return of sensory nerve function in rat molars following cut or crush injury to the inferior alveolar nerve (IAN) was measured by observing the jaw opening reflex (JOR) response of the digastric muscle to electrical stimulation of individual molars or the gingiva. The IAN was injured from a lateral approach to the mandibular ramus at a site approximately 2 mm proximal to the incisor apex. Following nerve injury, the JOR threshold to stimulation of the first molars increased 6-fold: preoperative threshold mean = 47.4 +/- 21.3 microA (n = 27), postoperative threshold mean = 248.5 +/- 127.1 microA (n = 25). A 4-fold postoperative increase in JOR threshold was found for the second molars, and the thresholds were not significantly affected for third molars or gingiva. These postoperative results indicated that the major pathway of sensory innervation to the first and second molars was affected by the IAN injury, whereas the third molars and gingiva had alternate sources of innervation which remained unaffected by the IAN injury. At 1 week following injury, there was partial return of sensitivity, by 3 weeks there was approximately 50% recovery, and by 6 weeks complete return to normal JOR thresholds was found. The degree of sensory deficit, as reflected in JOR inhibition, and the rate of recovery were not significantly different after cut or crush injury in these experiments; however, there was a tendency for greater sensory loss and for more rapid recovery after crush injury. This study forms the basis for a subsequent autoradiographic analysis of nerve location in rat molars of known sensory deficit, partial recovery, or full sensory recovery.

No abstract

The preparation of 8-bromo-9-(2,3,5-tr~~-acetyl-~-~-arabinofuranosyl)aden~ne (3) was accomplished by the bromination of 9-(2,3,5-tri-0-acetyl-~-~-arabinofuranosyl)adenine (2). The reaction of 3 with basic nucleophiles such as sodium methoxide and ammonia effected an intramolecular displacement of bromide to give 8,2'anhydro-S-hydroxy-9-(8-D-arabinofuranosyl)adenine (9). Displacement of the bromine of 3 by the nonbasic nucleophiles, thiourea and sodium azide, gave the %thiol and &azide. A similar set of reactions was carried out starting from 9-(2,3,5-tri-O-acetyl-p-~-xylofuranosyl)adenine (12). The displacement of bromide from &bromo-9-(2,3,5-tri-O-acety~-p-~-xy~ofuranosyl)adenine (13) by both neutral and basic nucleophiles proceeded normally to give the appropriate 8-substituted purine xylofuranoside. There was no evidence for an intramolecular displacement of bromide to give 8,3 '-anhydro nucleosides.Enzymic hydroxylation of 6-methylthiopurine by hepatic aldehyde oxidase to give 6-methylthio-8-hydroxypurine was described in a recent paper.2 It was