An Inter-Institutional Collaboration to "Make Teaching Matter": The Teaching Academy of the Consortium of West Region Colleges of Veterinary Medicine.

Veterinary medical education is a relatively small community with limited numbers of institutions, people, and resources widely dispersed geographically. The problems faced, however, are large-and not very different from the problems faced by (human) medical education. As part of an effort to share resources and build a community of practice around common issues, five colleges in the westernmost region of the United States came together to form a regional inter-institutional consortium. This article describes the processes by which the consortium was formed and the initiation of its first collaborative endeavor, an inter-institutional medical/biomedical teaching academy (the Regional Teaching Academy, or RTA). We report outcomes, including the successful launch of three RTA initiatives, and the strategies that have been considered key to the academy's success. These include strong support from the consortium deans, including an ongoing financial commitment, a dedicated part-time Executive Coordinator, regular face-to-face meetings that supplement virtual meetings, an organization-wide biennial conference, an effective organizational structure, and a core group of dedicated leaders and RTA Fellows. The western consortium and RTA share these processes, insights, and outcomes to provide a model upon which other colleges of veterinary medicine can build to further leverage inter-institutional collaboration.

Survey of colleges and schools of veterinary medicine regarding education in complementary and alternative veterinary medicine.

OBJECTIVE: To obtain information on educational programs offered in complementary and alternative veterinary medicine (CAVM) among AVMA Council on Education (COE)-accredited colleges and schools of veterinary medicine. DESIGN: Survey. SAMPLE: 41 COE-accredited colleges and schools of veterinary medicine. PROCEDURE: A questionnaire was e-mailed to academic deans at all COE-accredited colleges and schools of veterinary medicine. RESULTS: Responses were received from 34 of 41 schools: 26 in the United States, 2 in Canada, 3 in Australia and New Zealand, and 3 in Europe. Sixteen schools indicated that they offered a CAVM course. Nutritional therapy, acupuncture, and rehabilitation or physical therapy were topics most commonly included in the curriculum. One school required a course in CAVM; all other courses were elective, most of which were 1 to 2 credit hours. Courses were usually a combination of lecture and laboratory; 2 were lecture only, and 1 was laboratory only. Of the 18 schools that reported no courses in CAVM, many addressed some CAVM topics in other courses and 4 indicated plans to offer some type of CAVM course within the next 5 years. CONCLUSIONS AND CLINICAL RELEVANCE: The consensus among survey respondents was that CAVM is an important topic that should be addressed in veterinary medical education, but opinions varied as to the appropriate framework. The most common comment reflected strong opinions that inclusion of CAVM in veterinary medical curricula must be evidence-based. Respondents indicated that students should be aware of CAVM modalities because of strong public interest in CAVM and because practitioners should be able to address client questions from a position of knowledge.

Neural proliferation and restoration of neurochemical phenotypes and compromised functions following capsaicin-induced neuronal damage in the nodose ganglion of the adult rat.

We previously reported that neuronal numbers within adult nodose ganglia (NG) were restored to normal levels 60 days following the capsaicin-induced destruction of nearly half of the neuronal population. However, the nature of this neuronal replacement is not known. Therefore, we aimed to characterize neural proliferation, neurochemical phenotypes, and functional recovery within adult rat NG neurons following capsaicin-induced damage. Sprague-Dawley rats received intraperitoneal injections of capsaicin or vehicle solution, followed by 5-bromo-2-deoxyuridine (BrdU) injections to reveal cellular proliferation. NG were collected at multiple times post-treatment (up to 300 days) and processed for immunofluorescence, RT-PCR, and dispersed cell cultures. Capsaicin-induced cellular proliferation, indicated by BrdU/Ki-67-labeled cells, suggests that lost neurons were replaced through cell division. NG cells expressed the stem cell marker, nestin, indicating that these ganglia have the capacity to generate new neurons. BrdU-incorporation within ß-III tubulin-positive neuronal profiles following capsaicin suggests that proliferating cells matured to become neurons. NG neurons displayed decreased NMDAR expression up to 180-days post-capsaicin. However, both NMDAR expression within the NG and synaptophysin expression within the central target of NG neurons, the NTS, were restored to pre-injury levels by 300 days. NG cultures from capsaicin-treated rats contained bipolar neurons, normally found only during development. To test the functional recovery of NG neurons, we injected the satiety molecule, CCK. The effect of CCK on food intake was restored by 300-days post-capsaicin. This restoration may be due to the regeneration of damaged NG neurons or generation of functional neurons that replaced lost connections.

Recovery of viscerosensory innervation from the dorsal root ganglia of the adult rat following capsaicin-induced injury.

Capsaicin is a neurotoxin selective for C- and Adelta-type neurons. Systemic treatment with capsaicin is known to reduce this subpopulation in the dorsal root ganglia (DRG) of neonatal rats. To better understand the effects of capsaicin on adult afferent fibers, we examined DRG neurons retrogradely labeled by an i.p. injection of Fast Blue (FB) administered 3, 30, or 60 days after systemic capsaicin treatment (125 mg/kg i.p.). FB labeling in the 12th and 13th thoracic DRG was dramatically reduced 3 and 30 days post capsaicin (50% and 35% of control, respectively). However, the number of retrogradely labeled neurons rose to 65% of control by 60 days post capsaicin. In addition to FB labeling, we quantified the immunoreactivity of NR1, the obligatory N-methyl-D-aspartate receptor subunit, and Na(v)1.8, a DRG-specific sodium channel, in FB-labeled neurons as well as mRNA levels for both proteins in the 5th and 6th lumbar DRG. NR1 immunoreactivity and mRNA expression followed a pattern of early reduction and subsequent partial restoration similar to FB labeling. Na(v)1.8 immunoreactivity and mRNA expression dropped to approximately 50% of control at 3 days post capsaicin but completely recovered by 60 days. These data strongly support the conclusion that restoration of spinal afferent projections and signaling occurs in adult rats following capsaicin-induced damage.

Expression of transient receptor potential channels and two-pore potassium channels in subtypes of vagal afferent neurons in rat.

Vagal afferent neurons relay important information regarding the control of the gastrointestinal system. However, the ionic mechanisms that underlie vagal activation induced by sensory inputs are not completely understood. We postulate that transient receptor potential (TRP) channels and/or two-pore potassium (K2p) channels are targets for activating vagal afferents. In this study we explored the distribution of these channels in vagal afferents by quantitative PCR after a capsaicin treatment to eliminate capsaicin-sensitive neurons, and by single-cell PCR measurements in vagal afferent neurons cultured after retrograde labeling from the stomach or duodenum. We found that TRPC1/3/5/6, TRPV1-4, TRPM8, TRPA1, TWIK2, TRAAK, TREK1, and TASK1/2 were all present in rat nodose ganglia. Both lesion results and single-cell PCR results suggested that TRPA1 and TRPC1 were preferentially expressed in neurons that were either capsaicin sensitive or TRPV1 positive. Expression of TRPM8 varied dynamically after various manipulations, which perhaps explains the disparate results obtained by different investigators. Last, we also examined ion channel distribution with the A-type CCK receptor (CCK-R(A)) and found there was a significant preference for neurons that express TRAAK to also express CCK-R(A), especially in gut-innervating neurons. These findings, combined with findings from prior studies, demonstrated that background conductances such as TRPC1, TRPA1, and TRAAK are indeed differentially distributed in the nodose ganglia, and not only do they segregate with specific markers, but the degree of overlap is also dependent on the innervation target.

Facilitating appreciation of anatomical variation and development of teamwork skills in the gross anatomy laboratory using a cadaver reassignment system.

Developing a mental map of the body in three dimensions incorporating normal anatomical variations is a challenge for students of gross anatomy. Acquisition of this ability is facilitated by frequently reassigning students to work on different specimens in gross anatomy laboratories, a significant departure from traditional teaching strategies. This article analyzes student and faculty experiences with a reassignment system over a six-year period, including effects on early professional development and students' attitudes toward the cadavers. Students were strongly supportive of the method, noting that specimen reassignments facilitated learning, encouraged dissection skill building, and fostered collaborative interactions. Students' perception of the value of the contribution of each cadaver to their education was preserved and, for many, enhanced. Frequent specimen reassignments offer an opportunity to model public accountability for work and some aspects of the relationships between multiple health care teams caring for a patient.

A low-cost telemetry system suitable for measuring mouse biopotentials.

The ability to generate specific genetic mutations in mice is a powerful tool to study normal and pathophysiological function. In order to determine the effects of a mutation, measurement of physiological variables, such as biopotentials, is often necessary. However, such measurements can be particularly challenging to obtain from an awake, unrestrained mouse. The goal of this study was to design and implement a telemetry system suitable for recording biopotentials from a mouse. A battery-powered system was fabricated from commercially available electronic components mounted on a small circuit board. The frequency response of the system was measured over a range of frequencies and found suitable for recording biopotentials in mice and larger animals. We affixed the circuit board externally to a mouse and connected surface electrodes to measure electrocardiograms (ECG). The size and weight of the board did not disturb normal behavior over 30-60 min. Recorded ECGs had easily identifiable components relevant to physiological parameters and had a similar frequency spectrum compared to recordings obtained from a commercially available measurement system. In conclusion, the telemetry system was low-cost due to the availability of the components, straightforward to implement, and provided biopotential recordings suitable for measuring physiological parameters in an awake mouse.

Comparison of gamma-aminobutyrate receptors in the medial vestibular nucleus of control and Scn8a mutant mice.

The Purkinje cells of the cerebellum provide inhibitory input to vestibular nucleus neurons, with gamma-aminobutyrate (GABA) as neurotransmitter. Using extracellular recordings and bath application of agonists and antagonists, we compared GABA receptors in the medial vestibular nucleus of brain slices from Scn8a mutant mice of med(J) type, in which there is greatly reduced spontaneous and evoked activity of Purkinje cells, to those in slices from control mice. Muscimol, an agonist at GABA(A) receptors, produced a larger reduction of firing rate in neurons of mutant mice than in neurons of control mice, whereas there was no difference for baclofen, an agonist at GABA(B) receptors. In most cases tested, the effects of muscimol and baclofen remained similar when synaptic transmission was blocked, suggesting that the effects were predominantly directly upon GABA receptors of the neurons being recorded from. The up-regulation of GABA(A) receptors was similar in magnitude to that previously found for rats with bilateral transection of the inferior cerebellar peduncle. It may relate in both cases to reduced Purkinje cell input to medial vestibular nucleus neurons. The lack of effect on GABA(B) receptors suggests that the changes found with peduncle transection may have resulted from something more than reduced Purkinje cell activity, such as reduced concentrations of GABA, or that reduction of Purkinje cell activity in Scn8a mutant mice was insufficient to affect GABA(B) receptors. Other possible explanations of the results cannot be excluded since the Scn8a mutation affects other neuron types besides Purkinje cells.

Reorganizing small animal gross anatomy: improving the faculty and student experience and incorporating non-technical competency development.

The organization of the small animal gross anatomy course at Washington State University's College of Veterinary Medicine was modified in several ways over a two-year period. These modifications were motivated in part by the need to accommodate a larger number of students, but also by our desire to make more efficient use of faculty and student time as well as physical resources and to give our students opportunities to develop non-technical competencies such as communication and teamwork skills. The four major changes were (1) increasing dissection group size, (2) assigning specimens to dissection groups on a rotating basis, (3) reducing the amount of dissection time relative to time spent studying prepared specimens, and (4) introducing ''transition reviews,'' a limited form of peer teaching meant to emphasize peer interaction and communication skills rather than conveyance of specific and detailed subject matter. This article describes the details of these changes and evaluates their effectiveness based on faculty assessments, results from surveys of participating students, and comparison of examination performance and formal end-of-course student evaluations before and after reorganization of the course. Increasing the dissection group size and reducing per-student dissection time did not adversely affect student performance and were viewed at least neutrally or favorably by most students. Notably, the rotation of specimens and the transition reviews elicited strongly favorable responses from a large majority of students and had several beneficial effects of which students may not have been aware but which were apparent to participating faculty. Overall, the changes were well received by both faculty and students and were, in our view, of sufficient value that this course organization plan would be used regardless of class size.

Expression and distribution of TTX-sensitive sodium channel alpha subunits in the enteric nervous system.

The expression and distribution of TTX-sensitive voltage-gated sodium channel (VGSC) alpha subunits in the enteric nervous system (ENS) has not been described. Using RT-PCR, expression of Na(v)1.2, Na(v)1.3, Na(v)1.6, and Na(v)1.7 mRNA was detected in small and large intestinal preparations from guinea pigs. Expression of Na(v)1.1 mRNA as well as Na(v)1.1-like immunoreactivity (-li) were not observed in any intestinal region investigated. Na(v)1.2-li was primarily observed within the soma of the majority of myenteric and submucosal neurons, although faint immunoreactivity was occasionally observed in ganglionic and internodal fibers. Na(v)1.3-li was observed in dendrites, soma, and axons in a small group of myenteric neurons, as well as in numerous myenteric internodal fibers; immunoreactivity was rarely observed in the submucosal plexus. Na(v)1.6-li was primarily observed in the initial axonal segment of colonic myenteric neurons. Na(v)1.7-li was observed in dorsal root ganglia neurons but not in the myenteric plexus of the small and large intestine. In the ileum, 37% of Na(v)1.2-li cell bodies colocalized with calbindin-li while colocalization with calretinin-li was rare. In contrast, 22% of Na(v)1.3-li cell bodies colocalized with calretinin-li but colocalization with calbindin-li was not observed. In the colon, both Na(v)1.2-li and Na(v)1.3-li cell bodies frequently colocalized with either calretinin-li or calbindin-li. Na(v)1.2-li cell bodies also colocalized with the majority of NeuN-li cells in the small and large intestine. These data suggest that Na(v)1.1 may not be highly expressed in the ENS, but that Na(v)1.2, Na(v)1.3, and Na(v)1.6, and possibly Na(v)1.7, have broadly important and distinct functions in the ENS.

Allelic mutations of the sodium channel SCN8A reveal multiple cellular and physiological functions.

Allelic mutations of Scn8a in the mouse have revealed the range of neurological disorders that can result from alternations of one neuronal sodium channel. Null mutations produce the most severe phenotype, with motor neuron failure leading to paralysis and juvenile lethality. Two less severe mutations cause ataxia, tremor, muscle weakness, and dystonia. The electrophysiological effects have been studied at the cellular level by recording from neurons from the mutant mice. The data demonstrate that Scn8a is required for the complex spiking of cerebellar Purkinje cells and for persistent sodium current in several classes of neurons, including some with pacemaker roles. The mouse mutations of Scn8a have also provided insight into the mode of inheritance of channelopathies, and led to the identification of a modifier gene that affects transcript splicing. These mutations demonstrate the value of mouse models to elucidate the pathophysiology of human disease.

High-resolution mapping of the sodium channel modifier Scnm1 on mouse chromosome 3 and identification of a 1.3-kb recombination hot spot.

Variation between inbred strains of mice can be used to identify modifier genes affecting the susceptibility to inherited disease. The medJ allele of the sodium channel Scn8a contains a splice site mutation that results in sodium channel deficiency. The severity of the neurological disorder is determined by the modifier locus Scnm1. The wild-type allele of the modifier results in correct splicing of 10% of Scn8amedJ pre-mRNA and a dystonic phenotype. The susceptible allele of the modifier in strain C57BL/6J results in 5% correctly spliced transcripts and a lethal phenotype. A mapping cross with C3H using 26 new markers and 2304 affected F2 animals localized the modifier gene to a 950-kb interval on mouse chromosome 3. Fine mapping of recombination breakpoints revealed a recombination hot spot of 1.3 kb. The ratio of genetic to physical distance in the hot spot is 85 cM/Mb, two orders of magnitude higher than the mouse genome average of 0.5 cM/Mb. The role of the modifier in other disorders in human and mouse can be tested with linked markers described here.

Molecular and pathological effects of a modifier gene on deficiency of the sodium channel Scn8a (Na(v)1.6).

Scn8a encodes an abundant, widely distributed voltage-gated sodium channel found throughout the central and peripheral nervous systems. Mice with different mutant alleles of Scn8a provide models of the movement disorders ataxia, dystonia, tremor and progressive paralysis. We previously reported that the phenotype of the hypomorphic allele of Scn8a, medJ, is dependent upon an unlinked modifier locus, Scnm1. Strain C57BL/6J carries a sensitive allele of the modifier locus that results in juvenile lethality. We now provide evidence that the modifier acts on the splicing efficiency of the mutant splice donor site. Mutant mice display either 90% or 95% reduction in the proportion of correctly spliced mRNA, depending on modifier genotype. The abundance of the channel protein, Na(v)1.6, is also reduced by an order of magnitude in medJ mice, resulting in delayed maturation of nodes of Ranvier, slowed nerve conduction velocity, reduced muscle mass and reduction of brain metabolic activity. medJ mice provide a model for the physiological effects of sodium channel deficiency and the molecular mechanism of bigenic disease.

Mutations of voltage-gated sodium channels in movement disorders and epilepsy.

Spontaneous and induced mutations of neuronal Na+ channels in human patients and mutant mice result in a broad range of neurological-disease. Epilepsy, a disorder of neuronal hyperexcitability, has been associated with delayed inactivation of SCN2A in mice, and with altered kinetics of SCN1A in human patients. Movement disorders including tremor, ataxia, dystonia and paralysis have been observed in mice with mutations of SCN8A. Electrophysiological recordings from neurons isolated from mice with mutations in individual channels reveal the contributions of each channel to in vivo firing patterns. In addition to monogenic disease, Na+ channel mutations are likely to contribute to polygenic disease susceptibility and to normal variation in neuronal function. Advances in molecular methods coupled with genomic sequences from the Human Genome Project will permit identification of many new patient mutations and generation of animal models to dissect their physiological and cellular consequences.