title: Effects of H-reflex up-conditioning on GABAergic terminals on rat soleus motoneurons.
abstract: To explore the role of spinal cord plasticity in motor learning, we evaluated the effects of H-reflex operant conditioning on GABAergic input to rat spinal motoneurons. Previous work indicated that down-conditioning of soleus H-reflex increases GABAergic input to soleus motoneurons. This study explored the effect of H-reflex up-conditioning on GABAergic input. Of nine rats exposed to H-reflex up-conditioning, up-conditioning was successful (H-reflex increase >or= 20%) in seven and failed (change < 20%) in two. These rats and eight naive control (i.e. unconditioned) rats were injected with cholera toxin subunit B-conjugated Alexa fluor 488 into the soleus muscle to retrogradely label soleus motoneurons. Sections containing soleus motoneurons were processed for GAD(67) [one of the two principal forms of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD)] with an ABC-peroxidase system. Two blinded independent raters counted and measured GABAergic terminals on these motoneurons. Unlike successful down-conditioning, which greatly increased the number of identifiable GABAergic terminals on the motoneurons, up-conditioning did not significantly change GABAergic terminal number. Successful up-conditioning did produce slight but statistically significant increases in GABAergic terminal diameter and soma coverage. These results are consistent with other data indicating that up- and down-conditioning are not mirror images of each other, but rather have different mechanisms. Although the marked changes in GABAergic terminals with down-conditioning probably contribute to H-reflex decrease, the modest changes in GABAergic terminals associated with up-conditioning may be compensatory or reactive plasticity, rather than the plasticity responsible for H-reflex increase. As a variety of spinal and supraspinal GABAergic neurons innervate motoneurons, the changes found with up-conditioning may be in terminals other than those affected in successful down-conditioning.
authors.affiliation: Laboratory of Nervous System Disorders, Wadsworth Center, New York State Department of Health and State University of New York, Albany, NY 12201, USA.
authors.forename: Shreejith
authors.initials: S
authors.lastname: Pillai
authors.forename: Yu
authors.initials: Y
authors.lastname: Wang
authors.forename: Jonathan R
authors.initials: JR
authors.lastname: Wolpaw
authors.forename: Xiang Yang
authors.initials: XY
authors.lastname: Chen
mesh_terms: D000818:Animals; D003216:Conditioning, Operant / Q000502:physiology*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006181:H-Reflex / Q000502:physiology*; D006801:Humans; D008297:Male; D009046:Motor Neurons / Q000502:physiology*; D018482:Muscle, Skeletal / Q000294:innervation*; D009473:Neuronal Plasticity / Q000502:physiology; D017729:Presynaptic Terminals / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1