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Human fetal ethanol exposure is strongly associated with ethanol avidity during adolescence. Evidence that intrauterine olfactory experience influences chemosensory-guided postnatal behaviors suggests that an altered response to ethanol odor resulting from fetal exposure may contribute to later abuse risk. Using behavioral and neurophysiological methods, the authors tested whether ethanol exposure via the dam's diet resulted in an altered responsiveness to ethanol odor in infant and adult rats. Compared with controls, (a) fetal exposure tuned the neurophysiologic response of the olfactory epithelium to ethanol odor at some expense to its responsiveness to other odorants in infantile rats-this effect was absent in adults; (b) the neural effect in infantile rats was paralleled by an altered behavioral response to ethanol odor that was specific to this odorant-this effect was also absent in adults; and (c) a significant component of the infantile behavioral effect was attributable to ethanol's effect on the olfactory neural modality. These data provide evidence for an important relationship between prenatal ethanol experience and postnatal behavioral responsiveness to the drug that is modulated or determined by olfactory function. Keywords NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptThe chemical senses are among the earliest systems to develop (Gottlieb, 1971;Schaal & Orgeur, 1992;Smotherman & Robinson, 1990), and in the chemosensory world of the uterus, they may have a unique salience. This statement is of potential significance to the field of ethanol research given that clinical and epidemiological studies provide strong data for a predictive relationship between prenatal ethanol exposure and the risk for ethanol abuse in adolescent and young adults (Alati et al., 2006;Baer, Bar, Bookstein, Sampson, & Streissguth, 1998;Streissguth, 1998;Yates, Cadoret, Troughton, Steward, & Giunta, 1998).It is well documented that olfactory function is fundamental to regulating a variety of biological processes, such as reproduction, food intake, and different social behaviors. Even communication between conspecific and heterospecific animals relies heavily on the reception and processing of odors produced by body glands and even feces and urine. Given this profound level of functional importance, not surprisingly, experience-induced plasticity in response to odorants is a means by which the olfactory system can be tuned to emphasize the transduction of stimuli that are deemed relevant within the animal's environment (Hudson, 1993(Hudson, , 1999. A variety of data indicate that the olfactory system is plastic in response to the odorant environment and have been gathered using different experimental manipulations, such as selective odorant exposure in neonates (Coopersmith & Leon, 1984;Johnson, Woo, Duong, Nguyen, & Leon, 1995;McCollum, Woo, & Leon, 1997;McLean & Harley, 2004;Sullivan & Leon, 1986;Sullivan, McGaugh, & Leon, 1991;Sullivan, Wilson, & Leon, 1989;Woo, Coopersmith, & Leon, 1987;Wo...

Olfactory epithelium retains the capacity to recover anatomically after damage well into adult life and perhaps throughout its duration. None the less, olfactory dysfunctions have been reported widely for elderly humans. The present study investigates the effects of aging on the neurophysiological and anatomical status of the olfactory epithelium in barrier-raised Fischer 344X Brown Norway F1 hybrid rats at 7, 10, 25 and 32/35 months old. The posterior part of the olfactory epithelium in 32/35-month-old rats is well preserved. Globose basal cells are dividing, and new neurons are being born even at this advanced age. None the less, the numbers of proliferating basal cells and immature, GAP-43 (+) neurons are significantly decreased. Neurophysiological status was evaluated using voltage-sensitive dye techniques to assess inherent patterns of odorant-induced activity in the epithelium lining the septum and the medial surface of the turbinates. In middle and posterior zones of the epithelium, there were neither age-related changes in overall responsivity of this part of the olfactory epithelium to any of five odorants, nor shifts in the location of the odorant-induced hotspots. The inherent activity patterns elicited by the different odorants do become more distinct as a function of age, which probably reflects the decline in immature neurons and a slight, but not statistically significant, increase in mature neurons as a function of age. In contrast with the excellent preservation of posterior epithelium, the epithelium lining the anterodorsal septum and the corresponding face of the turbinates is damaged in the 32/35-month-old animals: in this part, horizontal basal cells are reactive, more basal cells and sustentacular cells are proliferating than in younger animals or in posterior epithelium of the same animals, and the neuronal population is less mature on average. Our findings indicate that degeneration of the olfactory epithelium is not an inevitable or pre-programmed consequence of the aging process, since the posterior zone of the epithelium is very well preserved in these barrier-protected animals. However, the deterioration in the anterior epithelium suggests that environmental insults can accumulate or become more severe with age and overwhelm the regenerative capacity of the epithelium. Alternatively, the regenerative capacity of the epithelium may wane somewhat with age. Either of these mechanisms or some combination of them can account for the functional and anatomical deterioration of the sense of smell associated with senescence in humans.

We report a severe acute headache that occurred in conjunction with a solitary fresh lesion of multiple sclerosis in the periaqueductal gray region of a 16-year-old girl. This unique natural event supports the recent proposition, based on observations of patients with implanted electrodes, that perturbations of the periaqueductal gray region can produce headache. It also suggests that headaches accompanying attacks of multiple sclerosis are due to disturbances in particular regions of the brain.

From amphibian data, two mechanisms that could underlie the encoding of odorants by the mucosal activity patterns they engender are as follows (1) receptors with similar odorant selectivities could be aggregated spatially on the mucosa (inherent patterns); (2) in analogy to gas chromatography, as odorants are drawn along the surface of the mucosa the strongly sorbed ones could be deposited preferentially upstream, whereas the weakly sorbed ones could be distributed more evenly (imposed patterns). Do both of these possible coding mechanisms operate in mammals and, if so, how do they interact in giving composite patterns (imposed + inherent)? Fluorescence changes in di-4-ANEPPS applied to rat mucosas were monitored by a 10 x 10 pixel photodiode array. To observe the inherent patterns, three odorants of varying sorbabilities first were puffed uniformly onto the entire mucosa mounted in a Delrin chamber. To bring out the imposed patterns, the chamber was then sealed to replicate anatomically the rat's nasal cavity, and these same odorants were drawn at three flow rates along the mucosal flow path. The results demonstrated for the first time the existence of imposed patterns in a mammal. The strongly sorbed odorants, unlike the weakly sorbed one, showed marked imposed patterns. Within physiological limits, increasing the flow rate decreased the magnitude of the imposed patterns. One might consider strategies that the olfactory process could use either to negate or to take advantage of the chromatographic effect, because the lability of the composite patterns with changing stimulus conditions raises questions about their role in odorant encoding.