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Biomedical subjects

L J Wallace

Publications and source records attributed to L J Wallace.

At least 19 recordsLinked to original sources

Chronic bicipital tenosynovitis in dogs: 29 cases (1985-1992).

Medical records of 23 dogs with unilateral and 3 dogs with bilateral chronic bicipital tenosynovitis were reviewed. Mean age of affected dogs was 4.6 years (SD, 2.0 years), and mean body weight was 32.6 kg (SD, 14.5 kg). Neither a breed nor a gender predilection was detected. All dogs had a history of intermittent or progressive weight-bearing lameness that became worse after exercise. Mean duration of lameness prior to medical or surgical treatment was 6.5 months (range, 0.25 to 24 months). In all dogs, signs of pain were evident during palpation of the biceps tendon within the intertubercular groove. Radiography revealed sclerosis or osteophytosis of the intertubercular groove in all 29 shoulder joints. Mild degenerative joint disease was evident radiographically in 17. Arthrography was performed in 12 joints, and in 11 there were irregularities of or filling defects along the biceps tendon. Arthrocentesis was performed on 17 joints; 14 synovial fluid samples had cytologic abnormalities consistent with degenerative joint disease. Medical treatment, consisting of injection of methylprednisolone acetate into the biceps tendon and its synovial sheath, was attempted in 21 of the 29 affected shoulder joints. Surgery, which consisted of tenodesis of the biceps tendon, was attempted in 14 joints; 8 of these had not been treated medically; the remaining 6 had poor results following medical treatment. Gross and histologic findings consistent with chronic bicipital tenosynovitis were observed in all 14 joints in which surgery was performed. Seventeen of the medically treated shoulders were available for clinical evaluation, and results were excellent or good in 7.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Biomechanical properties of canine corticocancellous bone frozen in normal saline solution.

Eleven pairs of canine metacarpal bones, 10 pairs of metatarsal bones, and 7 pairs of ribs were harvested cleanly and prepared for banking at -20 C for 1 year. One bone of each pair was randomly assigned to 1 type of storage: plastic pack vs immersion in a normal solution of sodium chloride. The contralateral bone was assigned to the opposite treatment. Six pairs of metacarpal bones and 5 pairs of metatarsal bones were tested in torsion to failure. No significant difference was found within pairs. All ribs, 5 pairs of metacarpal bones, and 5 pairs of metatarsal bones were loaded in 4-point bending to failure. The energy absorbed at failure and the ultimate displacement of ribs and metacarpal and metatarsal bones were increased by 25 to 30% and 18 to 24%, respectively, when the bones were frozen in isotonic saline solution. Corticocancellous grafts frozen in normal saline solution are biomechanically less fragile and brittle than grafts stored in plastic without saline solution.

Animals

Comparison of in vivo and in vitro adjacent segment motion after lumbar fusion.

STUDY DESIGN: For in vitro studies, there is no basis for choosing a "load control study" over a "displacement control" study. This study qualitatively compared results from in vitro and in vivo tests, allowing the authors to address the experimental assumptions that in vitro testing contributes to the understanding of the in vivo condition. OBJECTIVES: To compare motion changes at segments adjacent to fusions for in vitro and in vivo tests. SUMMARY OF BACKGROUND DATA: Investigators have measured the effects of spinal fusions on the adjacent segment in a human cadaver model and found greater adjacent facet joint load after fusions. Others have found significant increases in motion and facet loads at segments adjacent to in vitro lumbosacral and long fusions, when the same range of motion was repeated before and after immobilization of lumbar segments. METHODS: L2-L3 motion was measured in vitro by an instrumented spatial linkage under load and displacement control before and after immobilization of segments (L3-L7). In vivo, L2-L3 motion was measured while animals walked on a treadmill. L3-L7 was fused and the L2-L3 motion testing was repeated. The change in in vivo adjacent segment motion was qualitatively compared with the in vitro change under "load" and "displacement" control. RESULTS: Under "load" control, in vitro facet motion did not significantly change after immobilization, whereas under "displacement" control, the facet motion significantly increased from 2.2 +/- 0.4 mm to 4.1 +/- 0.6 mm. Post-instrumentation, in vivo L2-L3 facet motion increased significantly. This change in vivo related better to the changes seen in the in vitro "displacement" control test than to the in vitro "load" control test.

Animals

Interaction of permanently charged metoclopramide analogs with D-2 dopamine receptors.

1. The binding of permanently charged benzamides to the D-2 dopamine receptor of striatal membranes was compared with that of tertiary amine benzamides. 2. The permanently charged benzamides were able to inhibit the binding of [3H]-spiperone to striatal membranes but were less potent than the corresponding tertiary amines. 3. Removal of sodium or decreasing the pH from 7.8 to 6.2 decreased the binding of all benzamides tested, but the permanently charged analogs were affected less by these changes than the tertiary amines. 4. These results suggest that while the binding properties of the permanently charged benzamides are similar to those of the tertiary amine benzamides, there are differences in the manner in which these compounds interact with the D-2 receptor.

Animals

The role of dopamine and AMPA/kainate receptors in the nucleus accumbens in the hypermotility response to MK801.

The purpose of this study was to evaluate the role of endogenous dopamine in the hypermotility response to MK801. The administration of MK801 (0.1 mg/kg, SC) to rats produced an intense stimulation of coordinated locomotor activity, which was not associated with stereotyped behavior. This stimulatory response was inhibited by pretreatment with either reserpine (5 mg/kg, IP) or alpha-methyl-p-tyrosine (2 doses of 250 mg/kg, IP). Similarly, pretreatment with the D2 antagonist eticlopride (0.03 mg/kg, SC) or the D1 antagonist SCH23390 (0.1 mg/kg, SC) produced a marked inhibition of MK801-stimulated hypermotility, and the combination of eticlopride (0.03 mg/kg, SC) and SCH23390 (0.03 mg/kg, SC) produced a greater inhibition of MK801-stimulated locomotion than either agent alone. The administration of SCH23390 or eticlopride directly into the nucleus accumbens inhibited the locomotor response to MK801, with the combination of both drugs producing a greater inhibition than either agent alone. The intra-accumbens administration of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptor antagonists DNQX or GAMS also inhibited the locomotor response produced by MK801. These data suggest that the activation of D1 and D2 dopaminergic receptors and AMPA/kainate excitatory amino acid receptors in the nucleus accumbens is required for the stimulation of locomotor activity produced by MK801.

Animals

AMPA/kainate antagonists in the nucleus accumbens inhibit locomotor stimulatory response to cocaine and dopamine agonists.

The purpose of this study was to determine whether AMPA/kainate excitatory amino acid receptors in the nucleus accumbens (NAc) play a role in the locomotor stimulation produced by cocaine and dopamine receptor agonists. The stimulation of locomotor activity produced by the systemic administration of cocaine was markedly attenuated by either the D1 receptor antagonist SCH23390 or the D2 receptor antagonist eticlopride administered directly into the NAc. This indicates that both dopaminergic receptor subtypes in the NAc are involved in the motor stimulant response to cocaine. The intra-accumbens administration of DNOX or GAMS, which have been shown to inhibit the locomotor stimulation produced by the excitatory amino acid agonist AMPA, antagonized the locomotor stimulant response to cocaine administered either systemically or directly into the NAc. DNOX and GAMS also inhibited the stimulation of locomotor activity produced by the coinjection of the D1 agonist SKF38393 and the D2 agonist quinpirole injected into the NAc of normal animals and of animals pretreated with reserpine. These results suggest that the activation of AMPA/kainate receptors in the NAc plays an important role in the locomotor stimulation produced by cocaine and directly acting dopaminergic receptor agonists. The effects produced by the activation of these receptors is independent of endogenous dopamine stores, suggesting that these receptors are located postsynaptic to the dopaminergic nerve terminals.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben

AMPA glutamate receptor activation in the posterior zona incerta inhibits amphetamine- and apomorphine-induced stereotypy.

Previous work demonstrated that alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) glutamate receptor antagonism in the zona incerta (ZI) dorsal to the subthalamic nucleus inhibits stereotypy in rats. The current investigation was undertaken to determine if AMPA receptors in a more caudal portion of the ZI have a role in the expression of stereotyped behavior. Rats were injected bilaterally with AMPA into the posterior ZI dorsal to the substantia nigra, and immediately given a systemic injection of d-amphetamine (10 mg/kg, s.c.) or apomorphine (1 mg/kg s.c.). AMPA produced a dose-dependent inhibition of stereotypy induced by both drugs which was prevented by the coadministration of the AMPA/kainic acid antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX) (0.5 microgram/0.5 microliter). A dose of AMPA as low as 62.5 ng completely abolished the oral component of stereotypy induced by both apomorphine and amphetamine. This dose of AMPA alone had no significant effect on spontaneous locomotor activity but enhanced the locomotor response stimulated by amphetamine (10 mg/kg, s.c.) due to an inhibition of stereotypy. The finding that activation of AMPA receptors in the posterior ZI inhibits stereotypy shows a contrast to results in the neighboring medial ZI dorsal to the subthalamic nucleus, where blockade of AMPA/kainic acid glutamate receptors with DNQX inhibits stereotypy.

Animals

Stimulation of locomotor activity by intra-accumbens AMPA is not inhibited by neonatal 6-hydroxydopamine-induced lesions.

The involvement of dopamine in the hypermotility responses to amphetamine s.c. or AMPA injected into the nucleus accumbens was evaluated in adult rats depleted of dopamine as neonates with 6-hydroxydopamine. The hypermotility response to amphetamine was markedly inhibited in the lesioned animals, while that to AMPA was enhanced. In addition, the hypermotility produced by AMPA in these rats was not inhibited by sulpiride+SCH-23390; however, it was inhibited completely by alpha-methyl-p-tyrosine. These results suggest that the hypermotility produced by AMPA requires endogenous dopamine, but is mediated by a different mechanism than that produced by amphetamine.

Amphetamine

AMPA/kainic acid glutamate receptor antagonism in the zona incerta dorsal to the subthalamic nucleus inhibits amphetamine-induced stereotypy bur not locomotor activity.

The effect of 6,7-dinitroquinoxaline-2,3-dione (DNQX), an alpha-amino-3- hydroxy-5-methyl-4-isoxazole-propionate (AMPA)/kainic acid glutamate receptor antagonist, injected into the zona incerta (ZI) was investigated to determine whether the behavioral responses to systemic amphetamine involve AMPA/kainic acid receptors in this brain region. Rats were injected bilaterally in the ZI with either vehicle or DNQX (1 microgram/0.5 microliter) and immediately given a systemic injection of D-amphetamine (0.5, 1.0 or 10.0 mg/kg, s.c.). Locomotor activity was recorded for 1 h. DNQX did not significantly affect hypermotility stimulated with 0.5 and 1.0 mg/kg amphetamine, but markedly increased the level of locomotor activity elicited by the higher dose, 10 mg/kg. To test the hypothesis that the enhanced locomotor response to high dose amphetamine was due to an inhibition of stereotyped behavior, the effect of DNQX in the ZI on amphetamine and apomorphine-induced stereotypy was investigated. DNQX significantly inhibited stereotypy induced by amphetamine (10 mg/kg) and apomorphine (1 mg/kg), with the onset of inhibition of amphetamine-induced stereotypy corresponding to the onset of enhanced locomotor activity. Ibotenic acid lesions of the ZI produced similar results, having an insignificant effect on locomotor activity stimulated by low dose amphetamine (1 mg/kg) and an attenuation of apomorphine-induced stereotypy which was of a magnitude comparable to that produced by DNQX. Thus, the AMPA/kainic acid subtypes of glutamate receptors in the ZI may be involved in the regulation of motor function mediated via striatal output but not mesolimbically generated locomotor activity.

Animals

Effect of serotonergic agonists in the nucleus accumbens on d-amphetamine-stimulated locomotion.

Serotonergic projections from the raphe nuclei are thought to modulate locomotor activity in the rat, and serotonin injection into the nucleus accumbens attenuates the hypermotility elicited by amphetamine. The purpose of the present study was to characterize the effects of various classes of serotonergic agonists administered into the nucleus accumbens on d-amphetamine-stimulated locomotor activity in order to determine which serotonin receptor subtypes are involved. Administration of the nonselective 5-HT agonist quipazine, the 5-HT-1 agonist mCPP, the 5-HT-1a agonist 8-OH-DPAT, the 5-HT-1b agonist CGS-12066B, and the 5HT-1c/2 agonist DOI did not inhibit d-amphetamine-stimulated locomotor activity. Pronounced lateral head weaving was noted after 8-OH-DPAT administration. The combination of the 5-HT-1a agonist 8-OH-DPAT and the 5-HT-1b agonist CGS-12066B, however, did inhibit d-amphetamine-stimulated locomotor activity. In contrast, the 5-HT-3 agonist 1-phenylbiguanide enhanced the locomotor effect of d-amphetamine. This effect was partially reversed by the 5-HT-3 antagonist MDL-7222. These studies suggest that serotonin has complex and multiple effects on the regulation of locomotor activity within the nucleus accumbens.

Animals

Pectineus tendon surgery for the management of canine hip dysplasia.

Pectineus tendonectomy is a useful procedure for relieving pain and rehabilitating the dysplastic dog in select cases. Relief of pain is believed to come from a combination of releasing tension on the hip joint capsule and providing a better loading contact surface on the articular cartilage owing to the increased abduction of the hind legs after surgery. Some pain relief also may come from the release of tension on the pectineus muscle. The modified procedure described in this article results in less seroma formation and less reattachment of the severed ends of the pectineus tendon of origin than the procedure originally described by the author.

Animals

alpha-Amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptor antagonists in the nucleus accumbens and ventral pallidum decrease the hypermotility response to psychostimulant drugs.

The purpose of this study was to determine the role of alpha-amino-3-hydroxy- 5-methylisoxazole-4-propionate (AMPA)/kainate excitatory amino acid receptors in the nucleus accumbens and the ventral pallidum in the hypermotility responses to amphetamine, caffeine and scopolamine. To accomplish this, we determined the effects of intracranial injections of 6,7-dinitroquinoxaline-2,3-dione (DNQX) and gamma-D-glutamylaminomethyl-sulfonate (GAMS), which inhibit the responses to AMPA, quisqualate and kainate in electrophysiological and behavioral studies. The bilateral administration of either DNQX (1 micrograms/0.5 microliters) or GAMS (5 micrograms/0.5 microliters) into the nucleus accumbens inhibited the locomotor stimulation produced by amphetamine (0.5 mg/kg s.c.) but not by caffeine (20 mg/kg s.c.) or scopolamine (0.5 mg/kg s.c.). However, the bilateral administration of either of the two antagonists into the ventral pallidum inhibited the response to all three stimulants. The administration of 6-amino-7-fluroquinoxaline-2,3-dione, a chemical analog of DNQX that does not bind to AMPA receptors, into either the nucleus accumbens or the ventral pallidum did not inhibit the locomotor stimulation produced by amphetamine. Neither DNQX nor GAMS injected into either the nucleus accumbens or the ventral pallidum produced significant changes in the locomotor activity of animals not injected with the stimulants. These results suggest that activation of AMPA/kainate receptors in the nucleus accumbens is important in the stimulation of locomotion produced by amphetamine, whereas activation of these receptors in the ventral pallidum is involved in the hypermotility response to all three central nervous system stimulants.

Animals

Activation of AMPA/kainic acid glutamate receptors in the zona incerta stimulates locomotor activity.

Direct injections of DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), an AMPA/quisqualic acid receptor agonist, into the medial or posterior zona incerta (ZI) produced a marked stimulation of locomotor activity accompanied by a postural change. Similar responses were obtained by injection of kainic acid (KA) into the same areas. The behavioral effects of AMPA and KA were antagonized by coinjection of 6,7-dinitroquinoxaline-2,3-dione (DNQX), and non-N-methyl-D-aspartate (NMDA) glutamate receptor antagonist. In contrast, injections of NMDA or ibotenic acid failed to significantly stimulate locomotor activity. These results suggest that the AMPA/kainate glutamate receptor subtypes in the zona incerta may have a functional role in regulating locomotor activity.

Animals

Stimulation of mono- and diacylglycerol lipase activities in ibotenate-induced lesions of nucleus basalis magnocellularis.

Ibotenic acid was injected into the nucleus basalis magnocellularis region of rat brain in order to study whether an elevation of lipase activities was associated with the degeneration of cholinergic neurons in this potential animal model of Alzheimer's disease. Two plasma membrane fractions were prepared from different regions of ibotenate injected (right hemisphere) and non-injected (left hemisphere) rat brain. One plasma membrane fraction was from synaptosomes (SPM) and the other from glial and neuronal cell bodies (PM). Activities of mono- and diacylglycerol lipases in these plasma membrane fractions were markedly increased (3- to 5-fold) in hippocampus, midbrain and frontal cortical regions of rat brain at 10 days after the injection of ibotenate. The activity of choline acetyltransferase was decreased in frontal cortex but unchanged in hippocampus and midbrain. Our results suggest that the increase in lipase activity is much more widespread and non-specific than is the decrease in cholinergic function.

Alzheimer Disease

The role of endogenous dopamine in the hypermotility response to intra-accumbens AMPA.

The present study was designed to investigate the role of dopamine in the locomotor stimulant response produced by the bilateral administration of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) into the nucleus accumbens. The hypermotility produced by lower doses of AMPA (up to 0.25 microgram) was inhibited by either SCH23390 or sulpiride, a D1 and D2 receptor antagonist, respectively. The locomotor response to a higher dose of AMPA (0.5 microgram) was greater than the maximum response to intra-accumbal injection of amphetamine and was significantly inhibited only when both the D1 and D2 antagonists were administered together. Alpha-Methyl-p-tyrosine inhibited the locomotor response to AMPA (0.5 microgram), and this inhibition was reversed by the co-injection of AMPA with either SKF38393, a D1 agonist, or quinpirole, a D2 agonist, at doses which were ineffective in the absence of AMPA. AMPA when infused into the nucleus accumbens produced an increase in extracellular dopamine, suggesting that AMPA can enhance dopamine efflux. The injection of AMPA into the nucleus accumbens significantly increased the DOPAC/dopamine ratio, which is different from the decrease in ratio reported for amphetamine. These data suggest that the stimulation of locomotor activity by intra-accumbal AMPA may be the result of an enhancement in dopamine efflux as well as a change in the response to dopaminergic receptor activation.

Amphetamine

Effects of morphine in the nucleus accumbens on stimulant-induced locomotion.

This study assessed the effects of morphine in the nucleus accumbens on motility elicited by dopaminergic and other classes of drugs, using locomotor activity as the measured response. Dopaminergic stimulants, d-amphetamine (10 micrograms) or dopamine (20 micrograms, 2 hours after nialamide, 200 mg/kg, IP) induced large increases in locomotor activity when injected into the nucleus accumbens. This response was blocked by coadministration of morphine (5 micrograms). The hypermotility response elicited by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA; 0.5 micrograms), an excitatory amino acid agonist, was also abolished by coadministration of morphine. Increasing the dose of AMPA to 1.5 micrograms partially overcame the morphine block, while increasing the dose of amphetamine to 50 micrograms did not. In other experiments, morphine (5 micrograms) injected into the nucleus accumbens blocked the hypermotility elicited by systemic caffeine (10 mg/kg, SC) or scopolamine (0.5 mg/kg, SC) or intra-accumbal MK-801 (5 micrograms). However, picrotoxin (0.15 or 0.5 microgram) injected into the nucleus accumbens elicited a hypermotility that was not attenuated by coinjection of morphine (5 or 10 micrograms). These data demonstrate that opiate and dopaminergic pathways have competing actions on the regulation of locomotion in the nucleus accumbens. Furthermore, the results with combinations of picrotoxin and morphine suggest the presence of two distinct locomotor pathways or a GABA receptor site "downstream" from the morphine site in a single pathway.

Amphetamine

Characterization of muscarinic receptors of bovine adrenal chromaffin cells: binding, secretion and anti-microtubule drug effects.

1. Binding of [3H]QNB to adrenal membranes is saturable, specific and to a single class of receptors. 2. Tubulozole, and not other microtubule drugs, inhibits [3H]QNB binding. 3. Pretreating cultured chromaffin cells with oxotremorine, a muscarinic receptor agonist, has no effect on either basal, nicotine (10 microM) or K(+)-stimulated catecholamine release and failed to enhance secretion of submaximal concentrations of nicotine (3-5 microM). 4. These results confirm that binding of [3H]QNB is associated with muscarinic receptors on bovine adrenal medullary tissue. 5. These studies also demonstrate that although bovine adrenal chromaffin cells possess muscarinic receptors, these receptors do not appear to be coupled to secretory processes.

Adrenal Glands