Comparison of trace elements in tissue of beaver (Castor canadensis) and local vegetation from a rural region of southern Ontario, Canada.

Beavers have been analyzed in several studies examining trace elements (TEs) in wildlife; however, most of these studies were undertaken in areas with known environmental pollutants. To understand and quantify natural enrichments of TEs in beaver tissue, samples of kidney, liver, muscle from 28 animals were compared with bark from 40 species of trees and shrubs, from the same, uncontaminated watershed. Pearson correlation and factor analysis show that conservative, lithophile elements such as Al, Ga, Th, and Y, all surrogates for mineral dust particles, explain 61% of the variation in the bark data. In contrast, Cd, Co, Cu, Mn, Mo, Ni, Rb, Se, Sr, and Tl in bark are independent of Al, and therefore most likely occur in non-mineral forms. Comparing tissue concentrations of beaver and bark, the organs are enriched in micronutrients such as Cu, Fe, Mo, Se, and Zn, but also non-essential, benign elements such as Cs and Rb, and potentially toxic elements such as Cd and Tl. Thus, the elements most enriched in beaver organs are those that apparently occur in biological form in the plant tissue. The elements enriched in these animals, relative to bark, appear to offer the most promise for monitoring environmental contamination by TEs using beavers. The majority of TEs of environmental relevance are most abundant in beaver kidney. However, monitoring studies must consider the variation in TE concentrations in beaver tissue, including those due to sex and age. Also, due consideration must be given to background concentrations of TEs in the vegetation composing the diet of the animals. The natural enrichment in the case of elements such as Cd, in beaver tissue relative to bark, is profound. These data establish critical baseline values for TEs in beavers in an unpolluted environment, thereby allowing for their use as model organisms in tracking how heavy metal pollutants may affect wildlife.

Vesicle-released glutamate is necessary to maintain muscle spindle afferent excitability but not dynamic sensitivity in adult mice.

KEY POINTS: Muscle spindle afferents are slowly adapting low threshold mechanoreceptors that report muscle length and movement information critical for motor control and proprioception. The rapidly adapting cation channel PIEZO2 has been identified as necessary for muscle spindle afferent stretch sensitivity, although the properties of this channel suggest that additional molecular elements are necessary for mediating the complex slowly adapting response of muscle spindle afferents. We report that glutamate increases muscle spindle afferent static sensitivity in an ex vivo mouse muscle nerve preparation, although blocking glutamate packaging into vesicles by the sole vesicular glutamate transporter, VGLUT1, either pharmacologically or by transgenic knockout of one allele of VGLUT1 decreases muscle spindle afferent static but not dynamic sensitivity. Our results confirm that vesicle-released glutamate is an important contributor to maintained muscle spindle afferent excitability and may suggest a therapeutic target for normalizing muscle spindle afferent function. ABSTRACT: Muscle spindle afferents are slowly adapting low threshold mechanoreceptors that have both dynamic and static sensitivity to muscle stretch. The exact mechanism by which these neurons translate muscle movement into action potentials is not well understood, although the PIEZO2 mechanically sensitive cation channel is essential for stretch sensitivity. PIEZO2 is rapidly adapting, suggesting the requirement for additional molecular elements to maintain firing during stretch. Spindle afferent sensory endings contain glutamate-filled synaptic-like vesicles that are released in a stretch- and calcium-dependent manner. Previous work has shown that glutamate can increase and a phospholipase-D coupled metabotropic glutamate antagonist can abolish firing during static stretch. Here, we test the hypothesis that vesicle-released glutamate is necessary for maintaining muscle spindle afferent excitability during static but not dynamic stretch. To test this hypothesis, we used a mouse muscle-nerve ex vivo preparation to measure identified muscle spindle afferent responses to stretch and vibration. In C57BL/6 adult mice, bath applied glutamate significantly increased the firing rate during the plateau phase of stretch but not during the dynamic phase of stretch. Blocking the packaging of glutamate into vesicles by the sole vesicular glutamate transporter, VGLUT1, either with xanthurenic acid or by using a transgenic mouse with only one copy of the VGLUT1 gene (VGLUT1+/- ), decreased muscle spindle afferent firing during sustained stretch but not during vibration. Our results suggest a model of mechanotransduction where calcium entering the PIEZO2 channel can cause the release of glutamate from synaptic-like vesicles, which then helps to maintain afferent depolarization and firing.