title: Effects of assisted feeding on Wobbler mouse motoneuron disease and on serotonergic and peptidergic sprouting in the cervical spinal ventral horn.
abstract: The 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. Immunocytochemisty 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.
authors.affiliation: Department of Neuroscience, The University of Florida Brain Institute, College of Medicine, Gainesville 32610, USA. bose@ufbi.ufl.edu
authors.forename: P
authors.initials: P
authors.lastname: Bose
authors.forename: R
authors.initials: R
authors.lastname: Fielding
authors.forename: L L
authors.initials: LL
authors.lastname: Vacca-Galloway
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000235:genetics; D001522:Behavior, Animal / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D004435:Eating / Q000502:physiology*; D007150:Immunohistochemistry; D051379:Mice; D008818:Mice, Neurologic Mutants / Q000502:physiology*; D016472:Motor Neuron Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology* / Q000523:psychology; D009333:Neck; D009479:Neuropeptides / Q000502:physiology*; D009929:Organ Size / Q000502:physiology; D012701:Serotonin / Q000502:physiology*; D013116:Spinal Cord / Q000254:growth & development*
chemical_list: D009479:Neuropeptides; D012701:Serotonin