Nicotine induced c-fos expression in the striatum is mediated mostly by dopamine D1 receptor and is dependent on NMDA stimulation.

The powerful psychostimulant and positive reinforcing effects of nicotine have been speculated to be mediated by the dopaminergic neurons of the ventral tegemental area (VTA) and their terminals in the nucleus accumbens. To extend our understanding of nicotine and dopamine interactions, we mapped the pattern of c-fos expression in the striatum as an important marker of some of the earliest changes that occur at gene transcription level. Acute nicotine injections in rats led to Fos expression more prominently in the caudatoputamen than in the nucleus accumbens in a dose-dependent fashion. Fos-reactive cells were more prominent in the central and dorsomedial limbic caudatoputamen than in the dorsolateral sensory-motor striatum. Injections of mecamylamine completely blocked nicotine-induced Fos expression. Injections of the selective dopamine D1 antagonist SCH 23390, but not D2 antagonist YM 09151-2 or Clozapine, a drug with high affinity to D4 receptors, before nicotine injections, completely blocked Fos expression in the striatum. Nicotine induced Fos expression was also blocked completely by the NMDA receptor antagonists MK-801 and CPP. These results suggest that nicotine-induced Fos expression in the striatum is mediated mostly by dopamine D1 receptors and that the Fos expression is also dependent on N-methyl-D-aspartate (NMDA) stimulation.

Acute nicotine injections induce c-fos mostly in non-dopaminergic neurons of the midbrain of the rat.

Induction of c-fos gene is an immediate and early response in the cascade of molecular events that ultimately lead to long-term alterations in gene expression in neurons. The psychomotor stimulant and positive reinforcing effects of nicotine have been speculated to be mediated by the dopaminergic neurons of the ventral tegmental area (VTA). To identify the precise subsets of VTA neurons of the rat that mediate the acute nicotinergic effects, the pattern of expression of c-fos gene was mapped using immunocytochemical methods. Acute nicotine injections resulted in prominent Fos-like immunoreactivity (-LI) in the medial terminal nucleus of the accessory optic system, the interpeduncular nucleus, and in the caudal linear subnucleus of VTA. The neurons of other VTA subnuclei, viz., the rostral linear, paranigralis, nucleus parabrachialis pigmentosus, and nucleus interfascicularis or the substantia nigra pars compacta did not contain any cells with Fos-LI. Mecamylamine abolished Fos-LI in most of the VTA neurons. These results suggest that acute nicotine injections induce c-fos expression mostly in non-dopaminergic neurons of the ventral tegmental area of the rat and that nicotine induces c-fos most intensely in the interpeduncular nucleus, the superior colliculus, and several other subnuclei of the accessory optic system.

Dental bur fragments causing metal artifacts on MR images.

PURPOSE: Our purpose was to define the role of dental bur fragments in producing metal artifacts on MR images. METHODS: Dental prosthetic reconstructions were made for two dogs. The two lower second premolars were prepared for full-cast crowns by using a diamond bur. The crown margin was placed subgingivally on the right side (1 mm below the free gingival margin) and at the same level as the free gingival margin on the left side. After 1 week, full-cast crowns were cemented in place. MR imaging was performed 7 days later. RESULTS: Metal artifacts appeared in both second premolar regions of the mandible on MR images, with the right side, in which the crown margin was positioned subgingivally, displaying a larger signal distortion than the left side. After removal of the crown, the artifact remained on the right. On histopathologic examination, bur fragments were detected in the gingiva, more on the right than on the left. X-ray fluorescent element analysis showed iron in the gingival tissue containing bur fragments. CONCLUSION: Distortion of MR images was considered to be attributable in part to the damage of the gingiva and in part to the presence of dental bur fragments.

Contact microradiographic analysis of feline tooth resorptive lesions.

Feline tooth resorptive lesions were studied using contact microradiographic analysis of ground sections. Contact microdiagram films were developed with a PIAS-imaging device, and decalcification patterns were evaluated, revealing a clear boundary between normal tissue and the resorptive area, which was different from the image of dental caries in humans. By contrasting analysis, decalcification signs appearing in human caries were not observed in feline resorptive lesions.

Pulpal reactions to two experimental bonding systems for pulp capping procedures.

This study evaluated the pulpal responses induced by application of two types of bonding system to the exposed dental pulp. One consisted of the following steps: etching with neutralized EDTA, application of an experimental water-based photocuring bonding agent, and restoration with a commercially available photocuring resin composite (EDTA etching system). The other was treatment with an experimental water-based self-etching primer, application of a commercially available bonding agent, and restoration with a commercially available photocuring resin composite (self-etching system). These two systems of treatment were applied to the exposed pulp. Calcium hydroxide was used as a control for the direct pulp-capping material. The pulps in class V cavities in the anterior teeth of beagles were mechanically exposed and then filled using the etching, the self-etching, or the Ca(OH)2 system. The beagles were sacrificed on the 7th, 30th or 90th postoperative day, and pulpal responses were investigated histopathologically using light microscopy. The EDTA etching system induced severe pulp reactions at 7 days after the operation. These reactions did not completely diminish after 90 days. Reparative dentin formation was observed at day 90. The self-etching system showed moderate pulp reactions, which gradually decreased over the experimental period. Reparative dentin bridge formation was observed at day 90. No necrosis of the pulp was observed at any time. Calcium hydroxide induced both moderate and severe initial pulp reactions, with reparative dentin formation evident at day 30. Necrosis was observed in the superficial pulp. It is suggested that the EDTA etching agent caused not only pulpal damage but also re-bleeding because of rinsing and drying. The self-etching system is a promising system for direct pulp capping.

Patho-morphological study of the supplemental groove.

The following results have been obtained in consequence of patho-morphological examination regarding the supplemental groove. 1. Light microscopic observation of cross-sectioned supplemental grooves revealed that most of them were shallow in the form of plate or bowl. Some of the supplemental grooves had contents not described in the past and the structure of the contents was not clear under a light microscope. The contents were found in 22% of the supplemental grooves examined. 2. The contents in supplemental grooves which were confirmed under a light microscope were found to consist of enamel itself when examined by means of an electron microscope. Microhardness measurements of this enamel showed less than one third the values of normal enamel. By means of microradiography, it was established that radiolucency of this enamel was, for the most part, much higher than normal enamel. 3. It was ascertained that enamel with low hardness and high radiolucency constitutes the contents of supplemental grooves. Judging from its tissue properties, the contents were believed to be susceptible to attack by caries. This view was supported by the results of an investigation of caries sites in supplemental grooves.