A novel procedure for initiation of voluntary ethanol consumption in the rat was evaluated in terms of ease of initiation, consistency, and resulting brain ethanol levels. The "jello shot" consists of 10% ethanol in gelatin along with a caloric source (Polycose). Initiation of "jello shot" consumption in Sprague-Dawley rats required no food or water restriction and resulted in initial daily (8.4±0.6 g/kg body weight) and eventual hourly (1.1±0.1 g/kg body weight) intake of ethanol comparable to other procedures using either alcohol-preferring or non-genetically selected rats. Rat intake of ethanol via "jello shots" recovered quickly from environmental alterations and surgical implantation of a guide cannula. During 1-hr free access sessions, consumption of the "jello shot" occurred during the initial 10 minutes and resulted in a dose-related increase in ethanol levels in nucleus accumbens measured using microdialysis. These brain ethanol levels were comparable to those achieved using other selfadministration methods. However, when 0.5 g/kg ethanol was gavaged either in "jello shot" or saline, there was about a 20% decrease in brain ethanol concentrations after gavage of the "jello shot" compared to saline. Even so, lack of a need for initial food or water deprivation and the rapidity with which stable self-administration can be achieved both suggest utility of the "jello shot" as a completely voluntary ethanol procedure. Keywordsethanol self-administration; water deprivation; nucleus accumbens; gelatin; Polycose Alcohol ranks second only to tobacco in terms of the magnitude of adverse public health consequences of its abuse. It is important to develop animal models that emulate conditions of human abuse in order to study neural mechanisms implicated in the etiology of alcoholism. Animal models of alcoholism usually induce animals to drink sufficient quantities of ethanol by initial temporary food or water restriction to encourage rats to partake of unfamiliar tastes. For example, Czachowski et al. (1999) initiates ethanol consumption by providing the 10% ethanol solution as the only available fluid for three days before operant training. Additionally, the fluid received as a result of barpressing is the only fluid available during the first 5-7 days of operant training. Even when sucrose or saccharin is added to the ethanol solution to provide additional reinforcement, rats still need to be initially water deprived in order to encourage them to consume the novel sweet taste (reviewed in Samson & Czachowski 2004). Another 1 Mail proofs to:Joanna Peris, Ph.D. Department of Pharmacodynamics, Box 100487, University of Florida, Gainesville FL 32610, Phone: 352-392-9768, Fax: 352-392-9187, Email: peris@cop.ufl.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is pub...

The age-related induction of inducible nitric synthase (iNOS) and apoptotic cell death in spiral ganglion cells (SGCs) of ddy strain mice were studied with immunohistochemical method and TdT-mediated dUTP-biotin nick end labeling (TUNEL), respectively. A large amount of iNOS was expressed in SGCs of 18- to 24-month-old mice, but not in those of the mice less than 12 months of age. Moreover, these mice were accompanied by a great rise in auditory brainstem response threshold as well as a great decrease in the number of SGCs that seemed to be due to preceding cell death of the cells. However, we were unable to find apoptotic TUNEL-positive cells in the spiral ganglions. This was assumed to be due to a very short clearance time of the dead cell bodies of less than one hour. As has been known, NO produced by iNOS can implicate in causes for either protection of cells from peroxidation and cell death. In the present study, therefore, the steep augmentation of iNOS in the SGCs of senescent mice implies that the iNOS initially induced to protect SGCs from the cytotoxicity of cellular peroxidation eventually contribute to the cell death of SGCs themselves.

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Summary: Since the localization of nitric oxide synthase (NOS) can be identified by enzyme histochemistry for NADPH-diaphorse (NADPH-d), this method has been used widely for mapping NOS-containing (presumablyThe NADPH-d positive neurons were predominantly found in two main subdivisions of the IC: the external cortex (ECIC) and the dorsal cortex (DCIC). The large numbers of these NADPH-d positive neurons appeared immunostained for GLU while only a small number, seemed to belong to the small cells (somatic area < 100 μm 2 ) similarity to stellate cells group was positive for GABA throughout the cortex of the IC. Owing to no coexistence between GABA and GLU in the same NADPH-d positive neuron in the pairs of adjacent sections of the IC by the mirror-image technique, the present results consequently support that NOergic neurons could be subdivided into at least three distinct populations with a large proportion of about 77% being GLUergic, much lower frequency of about 11% being GABAergic and the remaining 12% expressing non-GABA and non-GLU.In summary, the existence of two functionally distinct populations of NO/GABAergic and NO/GLUergic neurons in the NOergic neurons of IC suggest that at least two differential pattern of GLU-mediated excitatory NO transmission and GABA-mediated inhibitory NO transmission are involved in the networking of auditory communication in the cortex of IC.

We previously reported that a loss of contraction in the mucosal tissue of the palate arch is effectively induced by ethanol injections of moderate concentration and dosage. The present study was performed to obtain more information on how such ethanol injections induce contraction loss in mucosa tissue. Guinea pigs of both sexes were used in this study. The left arch of the palate mucosa was injected with 2 microliters of 70% ethanol and used as the experimental group. The right arch of the palate mucosa of the same animal was injected with saline and used as a control. One, three, five, eight, 10, 30, 50, and 90 days after injection, the mucosal tissues that received the injection were resected under anesthesia and processed for light microscopy using standard procedures. One day after the ethanol injection, severe coagulative degeneration of the mucosal tissue of the palate was seen. However, the damaged area was strictly restricted to the arch of the palate. Coagulative degeneration of the tissue peaked three days after the injection. Thereafter, the mucosal epithelial and mucosal connective tissues regenerated, and the damaged mucosal tissue quickly began to repair. An apparent cicatricial contraction loss was observed 10 days after the ethanol injection, along with the progression of fibrotic changes in the submucosal connective tissue of the arch of the palate. The regenerative action of the mucosal arch of the palate abated 30 days after the ethanol injection, and the reduced mucosal tissue appeared to have become denser as a result of an increase in dense fibrous connective tissue in the submucosal layer. No cell malignancies were seen throughout the entire 90-day observation period. In conclusion, cicatricial contraction loss of the mucosal arch of the palate resulting from the injection of an appropriate concentration and dosage of ethanol leads to the regeneration of the mucosal epithelium and fibrotic changes in the submucosa. The ethanol injection described here seems to be extremely safe, since it exerted no malignant effects on the cells and tissues either morphologically or functionally.