scholarly journals Electrical Stimulation of Low-Threshold Proprioceptive Fibers in the Adult Rat Increases Density of Glutamatergic and Cholinergic Terminals on Ankle Extensor α-Motoneurons

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0161614 ◽  
Author(s):  
Olga Gajewska-Woźniak ◽  
Kamil Grycz ◽  
Julita Czarkowska-Bauch ◽  
Małgorzata Skup
2004 ◽  
Vol 287 (4) ◽  
pp. H1721-H1729 ◽  
Author(s):  
Koji Miyazaki ◽  
Satoshi Komatsu ◽  
Mitsuo Ikebe ◽  
Richard A. Fenton ◽  
James G. Dobson

Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A1 receptors (A1R). The role of PKCε in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKCε was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKCε construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKCε was found localized primarily in transverse tubules. The A1R agonist chlorocyclopentyladenosine (CCPA) at 1 μM rendered an enhanced localization of PKCε in the t-tubular system. The β-adrenergic agonist isoproterenol (Iso; 0.4 μM) elicited a 29–36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Iso-produced increase in shortening in all three groups, the reduction caused by CCPA was greatest with PKCε overexpression. The CCPA reduction of the Iso-elicited shortening was eliminated in the presence of a PKCε inhibitory peptide. These results suggest that the translocation of PKCε to the t-tubular system plays an important role in A1R-mediated antiadrenergic actions in the heart.


2013 ◽  
Vol 231 (2) ◽  
pp. 165-177 ◽  
Author(s):  
Ali Jahanshahi ◽  
Lisa Schonfeld ◽  
Marcus L. F. Janssen ◽  
Sarah Hescham ◽  
Ersoy Kocabicak ◽  
...  

1976 ◽  
Vol 39 (3) ◽  
pp. 534-546 ◽  
Author(s):  
R. D. Foreman ◽  
J. E. Beall ◽  
J. D. Coulter ◽  
W. D. Willis

The effect of dorsal column stimulation on spinothalamic tract cells was investigated in anesthetized monkeys. The dorsal column stimuli were applied at midthoracic or at cervical levels of the cord, while the responses of spinothalamic tract cells of the lumbosacral enlargement were examined. A dorsal column volley depressed the activity of spinothalamic tract cells for about 150 ms. A similar depression was observed whether the spinothalamic tract cell was classified as hair activated, low, or high threshold, based on its response properties to cutaneous stimulation. The hair-activated and low-threshold spinothalamic tract cells were initially excited by the dorsal column volley, but often it was possible to demonstrate that a depression could be produced by stimuli which were too weak to cause excitation of these cells. Depression was produced both of the responses of spinothalamic tract cells to electrical stimulation of peripheral nerves and to mechanical stimulation of cutaneous nociceptors. A similar depression was produced by electrical stimulation of large afferents in peripheral nerves.The pathway mediating the depression of spinothalamic tract cells was shown to involve antidromic invasion of collaterals of dorsal column fibers. The best points for stimulation of the cord to produce a depression were over the ipsilateral dorsal column. A lesion interrupting the dorsal column eliminated the depression of cells below the lesion, whereas a lesion of much of the lateral column had no effect.The mechanism of the depression is likely to be complex. Apart from interactions at an interneuronal level, dorsal column volleys can be presumed to collide with sensory input from afferents which project up the dorsal column; collision would interfere chiefly with the responses of hair-activated and low-threshold spinothalamic tract cells. In addition, dorsal column volleys were shown to evoke inhibitory postsynaptic potentials in some spinothalamic tract neurons, and they also produced primary afferent depolarization, at least of large cutaneous afferemts.The excitation of hair-activated and low-threshold spinothalamic tract cells argues against their participation in signaling pain, since dorsal column stimulation in humans does not produce pain at stimulus intensities and frequencies which should activate such neurons. Alternatively, an ascending volley in the dorsal column or in other pathways may interfere with pain transmission in the brain.


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