The olfactory system is of great interest in research due to the olfactory epithelium’s regenerative capability and as a potential as a source of neural stem cells. The olfactory sensory neurons are constantly being replaced by the stem cells that lie at the base of the olfactory epithelium. These stem cells also remain intact after an injury to the epithelium and lead to the regeneration of the olfactory epithelium. We have developed a fate mapping technique to trace axonal regrowth from newly born olfactory sensory neurons using an inducible Cre-ERT2 model after chemical ablation by the drug methimazole. Our data shows that newly generated olfactory sensory neurons labeled 1 day after chemical ablation by injection of 4-HO-tamoxifen extend an axon that reaches the olfactory bulb and extend to the glomeruli in a timeline that is consistent with control mice that received 4-HO-tamoxifen but were injected with saline 1 day prior. In addition, we assessed the functional recovery of the olfactory epithelium by testing the ability of mice to find a hidden cookie after methimazole injection. Mice were tested at 3 and 14 days post methimazole. There was a severe impairment in the ability to find a hidden cookie at 3 days post methimazole. The mice tested at 14 days post methimazole showed an improvement in the ability to find the cookie but the latency to find the cookie was still significantly higher than controls. In conclusion, while we demonstrate that axons extend to the olfactory bulb and the glomeruli earlier than 14 days, our behavioral data suggest that there must be a critical number of axons that must reach each specific glomerulus to regain function of the olfactory system.

Soccer players change direction repeatedly throughout a game, making agility an important component of their performance. The purpose of this project was to identify how anatomical and physical characteristics influence agility performance among soccer players. The influences of anthropometry, strength, and power on agility performance in soccer players were investigated. The participants were NCAA Division I soccer players (N = 65). Anthropometric measures included height, body mass, percent body fat, lean body mass. Strength was evaluated using an isometric mid-thigh pull, and power was measured by vertical jumps. In correlation analysis, agility performance showed a statistically significant correlation (p<0.05) with peak power (PP) from 0kg and 20kg counter-movement jumps (r=-.379 & r=-.364 respectively) for the male players. Also for the males, percent body fat showed significant correlations (p<0.05) with Average 2 (r=-.438), 3 (r=-.411), and All (r=-.436). I conclude that the anthropometric measures evaluated have little influence on agility performance.

Repetitive stimulation of motor nerves causes an increase in the number of packets of transmitter ("quanta") that can be released in the ensuing period. This represents a type of conditioning, in which synaptic transmission may be enhanced by prior activity. Despite many studies of this phenomenon, there have been no investigations of the quantal mechanisms underlying these events, due to the rapid changes in transmitter output and the short time periods involved. To examine this problem, a method was developed in which estimates of the quantal release parameters could be obtained over very brief periods (3 s). Conventional microelectrode techniques were used to record miniature endplate potentials (MEPPs) from isolated frog (Rana pipiens) cutaneous pectoris muscles, before and after repetitive (40 sec at 80 Hz) nerve stimulation. Estimates were obtained of m (number of quanta released), n (number of functional release sites), p (mean probability of release) and var$\rm\sb{s}$p (spatial variance in p) using a method that employs counts of MEPPs per unit time. Fluctuations in the estimates were reduced using a moving bin technique (bin size = 3 s, $\Delta$bin = 1 s). Muscle contraction was prevented using low Ca$\sp{2+},$ high Mg$\sp{2+}$ Ringer or normal Ringer to which $\mu$-conotoxin GIIIA was added. These studies showed that: (1) the post-stimulation increase in transmitter release was dependent on stimulation frequency and not on the total number of stimulus impulses. When the total number of pulses was kept constant, the high frequency pattern produced a higher level of transmitter release than did the lower frequency patterns; (2) augmentation and potentiation were present in both low Ca$\sp{2+},$ high Mg$\sp{2+}$ and normal Ringer solutions, but potentiation, m, n, p and var$\rm\sb{s}$p were greater in normal Ringer solution than in low Ca$\sp{2+},$ high Mg$\sp{2+}$ solution. In low Ca$\sp{2+},$ high Mg$\sp{2+}$ solution, there was a larger decrease in n compared to p; (3) hypertonicity (addition of 100 mM sucrose) produced a marked increase in both basal and stimulation-induced values of m, n, and p. By contrast, there was a marked increase in the stimulation-induced but not the basal values of var$\rm\sb{s}$p; (4) hypertonicity produced a decrease in augmentation but had no effect on potentiation; (5) augmentation and potentiation appeared to involve mitochondrial uptake and efflux of cytoplasmic Ca$\sp{2+}.$ Tetraphenylphosphonium (which blocks mitochondrial Ca$\sp{2+}$ efflux and uptake) decreased augmentation and potentiation in low Ca$\sp{2+},$ high Mg$\sp{2+}$ solutions but increased potentiation in the same solution made hypertonic with 100 mM sucrose; (6) the overall findings suggest that this new method may be useful for investigating the subcellular dynamics of transmitter release following nerve stimulation.

An in vitro model was used to assess the effect of cocaine and its metabolites on the umbilical artery. Objectives were to pharmacologically confirm the presence of adrenergic innervation using tyramine, evaluate the ability of cocaine, benzoylecgonine, norcocaine and cocaethylene to potentiate vasoconstriction by serotonin and norepinephrine, examine the ability of ketanserin to block the enhanced vasoconstriction produced by cocaine, and determine displacement of 3 H-ketanserin by serotonin, norepinephrine, tyramine and mianserin. The vasoconstrictive effect of tyramine (100 μM) was enhanced in the presence of cocaine by 257%. Vasoconstrictive effects of serotonin and norepinephrine were significantly enhanced by cocaine by 28%, and 64% respectively; producing significant increases in the cumulative response. Norcocaine significantly augmented the maximum response to norepinephrine by 54%. Benzoylecgonine significantly decreased the maximum response to serotonin by 36% as well as the cumulative response. Ketanserin (0.03 μM) completely attenuated the vasoconstrictive potentiation of serotonin and norepinephrine by cocaine; shifting the EC50 for serotonin to the right 10-fold in the presence of ketanserin and cocaine. Ketanserin shifted the EC15 for norepinephrine with cocaine to the right 205-fold. Maximum response to norepinephrine with cocaine was depressed 54% by ketanserin. Serotonin, tyramine, and mianserin were able to displace 3 H-ketanserin (3 nM) from the membrane fraction of the human umbilical artery. Indicating that serotonin2 receptors are involved in vasoconstrictive responses to serotonin and tyramine. Norepinephrine did not displace 3 H-ketanserin in the membrane fraction of the umbilical artery. These data suggest that enhanced vasoconstriction of norepinephrine and serotonin by cocaine and potentiation of the maximum response to norepinephrine by norcocaine in the human umbilical artery may be important components of perinatal cocaine toxicity. Ketanserin was able to suppress the umbilical artery constriction produced by cocaine, demonstrating its antidotal potential. The potentiation of the tyramine response by cocaine and the displacement of 3 H-ketanserin by tyramine indicate that tyramine may be producing its vasoconstrictive effect through serotonin2 in the umbilical artery.

Dwarfism is considered one of the most recognized congenital defects of animals and humans and can be hereditary or sporadic in cause and expression. There are two general morphologic categories within this vastly diverse disease. These categories are disproportionate and proportionate dwarfism and within each of these there are numerous phenotypes which have been extensively described in humans, and to a lesser extent in dogs, cattle, mice, chickens, and other domestic species. Ponies and Miniature horses largely differ from full size horses only by their stature. Ponies are often defined as those whose height is not greater than 14.2 hands; however the maximum height for Miniature horses is constitutionally defined as 8.2 hands. Dwarfism is not considered a desirable genetic trait for Miniature horses. A majority of these conformationally inferior horses showed consistent physical abnormalities typical of disproportionate dwarfisms as seen in other mammal species. A whole genome scan with the Illumina Equine SNP50 chip clearly implicated a region on ECA1 as being associated with dwarfism of horses. The region implicated on the horse chromosome 1 (Equus Caballus; ECA1) contained a candidate gene for dwarfism, aggrecan (ACAN). Mutations were found in Exons 2, 6, 11 and 15 with each mutation associated with a distinct type of dwarfism. These mutations are independently transmitted throughout the population. Absence of normal homozygotes for these mutations and absence of normal horses which were heterozygous for these mutations indicated that these alleles caused dwarfism in those genotypes. These genotypes did not explain all observed dwarves in this population.

Chronic kidney disease (CKD) progresses faster in males than females; however, the underlying mechanisms remain poorly understood. Sex differences in glomerular capillary morphology has been hypothesized to contribute, in part, to the increased susceptibility to hypertension-induced renal injury and CKD progression in males, but this has not been investigated. The goal of the present study was to assess glomerular capillary morphology in male vs. female rats with intact kidneys and after uninephrectomy (UNX). We hypothesized that glomerular capillary radii (RCAP) and length (LCAP) would be greater in male rats. Male (n=4) and female (n=4) with intact kidneys and UNX (n=4 males, n=4 females) provided a 0.4% NaCl diet and water ad libitum. Kidneys were perfusion-fixed, the left kidney was excised, and a 3 mm transverse section through the midline of the kidney was selected for further processing. Multiple 1 mm3 cubes were randomly excised from the left, middle, and right regions of the outer cortex, embedded in EPONTM, sectioned (1 μm), and stained with toluidine blue. Four glomeruli from each region were randomly selected for stereological analysis. Glomerular tuft volume (VG), RCAP, and LCAP were assessed. In rats with intact kidneys, no significant sex differences were observed in VG, RCAP, or LCAP. VG, RCAP, and LCAP were significant greater in both male and female rats with UNX vs. respective rats with intact kidneys. In rats with UNX, males exhibited a significantly greater VG and LCAP, but not RCAP, as compared to females despite no significant differences in relative kidney weight. These data indicate that males exhibit greater compensatory increases in LCAP following UNX. The greater capillary length may lead to reduced podocyte density, a well-known mechanism that increases the susceptibility to CKD progression.