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Gilbert A Burns

Publications and source records attributed to Gilbert A Burns.

8 recordsLinked to original sources
PubMed2006

N-methyl-D-aspartate receptor subunit phenotypes of vagal afferent neurons in nodose ganglia of the rat.

Most vagal afferent neurons in rat nodose ganglia express mRNA coding for the NR1 subunit of the heteromeric N-methyl-D-aspartate (NMDA) receptor ion channel. NMDA receptor subunit immunoreactivity has been detected on axon terminals of vagal afferents in the dorsal hindbrain, suggesting a role for presynaptic NMDA receptors in viscerosensory function. Although NMDA receptor subunits (NR1, NR2B, NR2C, and NR2D) have been linked to distinct neuronal populations in the brain, the NMDA receptor subunit phenotype of vagal afferent neurons has not been determined. Therefore, we examined NMDA receptor subunit (NR1, NR2B, NR2C, and NR2D) immunoreactivity in vagal afferent neurons. We found that, although the left nodose contained significantly more neurons (7,603), than the right (5,978), the proportions of NMDA subunits expressed in the left and right nodose ganglia were not significantly different. Immunoreactivity for NMDA NR1 subunit was present in 92.3% of all nodose neurons. NR2B immunoreactivity was present in 56.7% of neurons; NR2C-expressing nodose neurons made up 49.4% of the total population; NR2D subunit immunoreactivity was observed in just 13.5% of all nodose neurons. Double labeling revealed that 30.2% of nodose neurons expressed immunoreactivity to both NR2B and NR2C, whereas NR2B and NR2D immunoreactivities were colocalized in 11.5% of nodose neurons. NR2C immunoreactivity colocalized with NR2D in 13.1% of nodose neurons. Our results indicate that most vagal afferent neurons express NMDA receptor ion channels composed of NR1, NR2B, and NR2C subunits and that a minority phenotype that expresses NR2D also expresses NR1, NR2B, and NR2C.

Animals↗
PubMed2006

Teaching non-technical (professional) competence in a veterinary school curriculum.

Data from focused studies and comprehensive surveys suggest that developing or enhancing non-technical (professional) skills will result in a more satisfied and successful veterinary student or veterinary graduate. The College of Veterinary Medicine at Washington State University has devoted considerable time, effort, and resources to augmenting the non-technical aspects of its curriculum while maintaining the traditional strengths of its DVM program. Here we summarize pertinent research and best-practice recommendations from a variety of sources and outline the steps that have been taken, with the underlying rationales, to integrate the teaching and modeling of non-technical (professional) competence throughout a four-year course of veterinary study.

Curriculum↗
PubMed2005

Veterinary students as elite performers: preliminary insights.

The KPMG ''Mega Study'' (Brown JP, Silverman JD. The current and future market for veterinarians and veterinary medical services in the United States. J Am Vet Med Assoc 215:161-183, 1999) and other studies (Cron WL, Slocum JV, Goodnight DB, Volk JO. Impact of management practices and business behaviors on small animal veterinarians' incomes. J Am Vet Med Assoc 217:332-338, 1999; Lewis RE. Non-technical Competencies Underlying Career Success as a Veterinarian: A New Model for Selecting and Training Veterinary Students. Minneapolis: Personnel Decisions, 2002) concur that improvement in veterinary practitioner performance is necessary. Improvement in practitioners' non-technical competencies is considered most vital. Little research exists that identifies underlying psychological factors harbored by veterinary students that inhibit ability to achieve sustained maximum professional performance. Left unaddressed, these same characteristics may lead to coping behaviors that disrupt or, in the worst cases, lead to voluntary or involuntary termination of professional careers. Several performance-related characteristics and interpersonal dynamics are investigated in this study that provide preliminary evidence for the long-term shortcomings addressed in previous veterinary practice management literature. Pedagogical recommendations for addressing these student psychological characteristics are submitted for consideration.

Adult↗
PubMed2004

NMDA receptor blockade attenuates CCK-induced reduction of real feeding but not sham feeding.

Systemic injection of MK-801, a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) receptor ion channels, increases meal size and delays satiation. We examined whether MK-801 increases food intake by directly interfering with actions of cholecystokinin (CCK). Prior administration of MK-801 (100 microg/kg ip) reversed the inhibitory effects of CCK-8 (2 and 4 microg/kg ip) on real feeding of both liquid and solid foods. MK-801 alone did not alter 30-min sham intake of 15% sucrose compared with intake after saline. Furthermore, while CCK-8 (2 or 4 microg/kg ip) reduced sham intake, this reduction was not attenuated by MK-801 pretreatment. To ascertain whether MK-801 attenuation of CCK-induced reduction of real feeding was associated with attenuated inhibition of gastric emptying, we tested the effect of MK-801 pretreatment on CCK-induced inhibition of gastric emptying of 5-ml saline loads. Ten-minute gastric emptying was accelerated after MK-801 (3.9 +/- 0.2 ml) compared with saline vehicle (2.72 +/- 0.2 ml). CCK-8 (0.5 microg/kg ip) reduced 10-min emptying to 1.36 +/- 0.3 ml. Pretreatment with MK-801 did not significantly attenuate CCK-8-induced reduction of gastric emptying (0.9 +/- 0.4 ml). This series of experiments demonstrates that blockade of NMDA ion channels reverses inhibition of real feeding by CCK. However, neither inhibition of sham feeding nor inhibition of gastric emptying by CCK is attenuated by MK-801. Therefore, increased food intake after NMDA receptor blockade is not caused by a direct interference with CCK-induced satiation. Rather, increased real feeding, either in the presence or absence of CCK, depends on blockade of NMDA receptor participation in other post-oral feedback signals such as gastric sensation or gastric tone.

Animal Feed↗
PubMed2004

AT4 receptor binding in the developing rabbit.

The binding of the AT(4)-specific analog, divalinal-AngIV (Dival), was studied in rabbit fetuses of various gestational ages. Saturation isotherm and competition data from selected tissues indicate that fetal Dival binding sites are saturable and specific for AT(4) ligands. Autoradiographs revealed that binding was present in all the specimens examined. The peripheral nerves, kidneys, and heart were particularly heavily labeled. Labeling of some tissues, such as forming bones, was not constant as gestational age increased. Other tissues, including multilocular fat, sinus hairs, and enamel organs of nascent teeth, exhibited substantial binding as these tissues developed.

Angiotensin II↗
PubMed2003

Cholinergic neurotransmission participates in increased food intake induced by NMDA receptor blockade.

MK-801, a noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist, enhances gastric emptying while increasing food intake. Although our previously reported results implicate the vagus in MK-801's effect on feeding, it is not clear whether vagal motor fibers participate in the feeding response. Control of gastric emptying is exerted, in part, by cholinergic vagal motor neurons. Therefore, we examined the ability of MK-801 to increase meal size in the presence or absence of the muscarinic receptor antagonist atropine methyl nitrate. Both central and systemic administration of MK-801 significantly increased intake of 15% sucrose. Intraperitoneal injection of atropine abolished MK-801-induced increase in sucrose intake, whereas administration into the fourth ventricle had no effect. To determine whether augmentation of cholinergic tone produces an enhancement of food intake in the absence of MK-801, we tested the ability of cisapride, a gastric prokinetic agent that promotes acetylcholine release through an action on presynaptic serotonin (5-HT4) receptors, to increase sucrose consumption. Cisapride (500 microg/kg ip) induced a small but significant increase in 15% sucrose intake (15.5 +/- 0.5 ml) compared with NaCl (13.0 +/- 0.6 ml). Furthermore, when MK-801 (100 microg/kg ip) was given in combination with cisapride, intake was significantly higher (19.8 +/- 0.9 ml) than following either agent given alone. Pretreatment with atropine abolished the cisapride-induced increase in intake (12.1 +/- 0.9 ml) as well as the increased intake induced by combining MK-801 and cisapride. These results suggest that blockade of NMDA-gated ion channels in the hindbrain increases food intake, in part, via a peripheral muscarinic cholinergic mechanism.

Acetylcholine↗