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Article: Effects of assisted feeding on Wobbler mouse motoneuron disease and on serotonergic and peptidergic sprouting in the cervical spinal ventral horn

TitleEffects of assisted feeding on Wobbler mouse motoneuron disease and on serotonergic and peptidergic sprouting in the cervical spinal ventral horn
Authors
Issue Date1999
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/brainresbull
Citation
Brain Research Bulletin, 1999, v. 48 n. 4, p. 429-439 How to Cite?
AbstractThe Wobbler mouse is used as a model of human motoneuron disease (MND). During the disease progress, the significant loss of motoneurons in cervical spinal cord and cranial motor nuclei leads to the progressive loss of motor function in the forelimb, head, and neck regions. The loss of cutting and chewing ability that results in the inability to feed properly might lead to a lower mean body weight (b. wt.) that is generally one-half that of the normal phenotype littermate controls. Nutritional deficit might also influence neuronal processes sprouting in the cervical spinal ventral horn. To determine whether nutritional deficits contribute to the wt. loss, and influence the progress of MND as well as its sprouting phenomenon, Wobbler and normal phenotype control littermates were dropper-fed three times daily on a regular laboratory diet of Rat Chow. Weight measurements and behavioral tests were taken to monitor the disease. Immunocytochemistry of serotonin, substance P, and leucine enkephalin were conducted in the cervical spinal cord to investigate if any alteration occurred on the previously reported values in ad lib-fed animals. Organ wts. were measured to determine where nutritional benefit was incurred. Although mean wt. loss in Wobblers was reduced, wt. differed significantly from the control values after dropper feeding. However, the progress of the disease or alteration of neurotransmitters containing neuronal processes were not affected by nutritional factors. Therefore, nutritional intake affects wt. gain, but is not a primary consideration in the progress of MND. Behavioral deficits and neurotransmitter alterations are probably directly caused by motoneuron losses.
Persistent Identifierhttp://hdl.handle.net/10722/151541
ISSN
2015 Impact Factor: 2.572
2015 SCImago Journal Rankings: 1.410
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBose, Pen_US
dc.contributor.authorFielding, Ren_US
dc.contributor.authorVaccaGalloway, LLen_US
dc.date.accessioned2012-06-26T06:24:24Z-
dc.date.available2012-06-26T06:24:24Z-
dc.date.issued1999en_US
dc.identifier.citationBrain Research Bulletin, 1999, v. 48 n. 4, p. 429-439en_US
dc.identifier.issn0361-9230en_US
dc.identifier.urihttp://hdl.handle.net/10722/151541-
dc.description.abstractThe Wobbler mouse is used as a model of human motoneuron disease (MND). During the disease progress, the significant loss of motoneurons in cervical spinal cord and cranial motor nuclei leads to the progressive loss of motor function in the forelimb, head, and neck regions. The loss of cutting and chewing ability that results in the inability to feed properly might lead to a lower mean body weight (b. wt.) that is generally one-half that of the normal phenotype littermate controls. Nutritional deficit might also influence neuronal processes sprouting in the cervical spinal ventral horn. To determine whether nutritional deficits contribute to the wt. loss, and influence the progress of MND as well as its sprouting phenomenon, Wobbler and normal phenotype control littermates were dropper-fed three times daily on a regular laboratory diet of Rat Chow. Weight measurements and behavioral tests were taken to monitor the disease. Immunocytochemistry of serotonin, substance P, and leucine enkephalin were conducted in the cervical spinal cord to investigate if any alteration occurred on the previously reported values in ad lib-fed animals. Organ wts. were measured to determine where nutritional benefit was incurred. Although mean wt. loss in Wobblers was reduced, wt. differed significantly from the control values after dropper feeding. However, the progress of the disease or alteration of neurotransmitters containing neuronal processes were not affected by nutritional factors. Therefore, nutritional intake affects wt. gain, but is not a primary consideration in the progress of MND. Behavioral deficits and neurotransmitter alterations are probably directly caused by motoneuron losses.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/brainresbullen_US
dc.relation.ispartofBrain Research Bulletinen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newborn - Geneticsen_US
dc.subject.meshBehavior, Animal - Physiologyen_US
dc.subject.meshBody Weight - Physiologyen_US
dc.subject.meshEating - Physiologyen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Neurologic Mutants - Physiologyen_US
dc.subject.meshMotor Neuron Disease - Metabolism - Pathology - Physiopathology - Psychologyen_US
dc.subject.meshNecken_US
dc.subject.meshNeuropeptides - Physiologyen_US
dc.subject.meshOrgan Size - Physiologyen_US
dc.subject.meshSerotonin - Physiologyen_US
dc.subject.meshSpinal Cord - Growth & Developmenten_US
dc.titleEffects of assisted feeding on Wobbler mouse motoneuron disease and on serotonergic and peptidergic sprouting in the cervical spinal ventral hornen_US
dc.typeArticleen_US
dc.identifier.emailFielding, R:fielding@hku.hken_US
dc.identifier.authorityFielding, R=rp00339en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0361-9230(99)00024-6en_US
dc.identifier.pmid10357076-
dc.identifier.scopuseid_2-s2.0-0033103320en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033103320&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume48en_US
dc.identifier.issue4en_US
dc.identifier.spage429en_US
dc.identifier.epage439en_US
dc.identifier.isiWOS:000080317900011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBose, P=7103009659en_US
dc.identifier.scopusauthoridFielding, R=7102200484en_US
dc.identifier.scopusauthoridVaccaGalloway, LL=6602468305en_US

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