Primary afferent depolarization of C fibres in the spinal cord of the cat

1978 ◽  
Vol 56 (1) ◽  
pp. 154-157 ◽  
Author(s):  
O. Calvillo

The excitability of primary afferent terminals of cutaneous C fibres was tested in the spinal cord of decerebrated cats. C fibre terminal excitability was decreased in the spinal state, and increased by conditioning volleys that activated only A fibres of another cutaneous nerve and by stimulating hair mechanically. It is suggested that C fibre input and therefore nociceptive information to the central nervous system is susceptible to presynaptic control by segmental and suprasegmental mechanisms.

1983 ◽  
Vol 61 (6) ◽  
pp. 626-631 ◽  
Author(s):  
Ante L. Padjen ◽  
Toshio Hashiguchi

The mechanism of primary afferent depolarization (PAD) was studied in the isolated frog spinal cord using intrafibre recording (microelectrodes filled with 0.6 M potassium sulfate) from large myelinated axons of dorsal roots. Standard current–clamp technique was used to obtain voltage–current (V–I) relationship. It was found that: (i) PAD is voltage dependent: its amplitude and rate of rise are increased with hyperpolarization; (ii) the slope of the linear part of the V–I curve obtained during PAD is decreased compared with the V–I curve at rest; (iii) the PAD equilibrium potential, estimated by extrapolation, ranged from −66 to −40 mV. These results suggest that PAD is associated with an increase in conductance of primary afferent terminals and thus seem to provide the first experimental evidence for the hypothesis that shunting of primary afferent membrane is the mechanism of presynaptic inhibition in the vertebrate nervous system.


1979 ◽  
Vol 57 (10) ◽  
pp. 1157-1167 ◽  
Author(s):  
B. R. Sastry

The effects of iontophoretically applied γ-aminobutyric acid (GABA), (−)-nipecotic acid (NCA), 2,4-diaminobutyric acid (DABA), and pentobarbital were examined on the thresholds for antidromic activation of single group I muscle afferents, in decerebrated spinal cats. GABA decreased the threshold for antidromic activation of the majority of the afferents. During this decrease in the threshold, the preterminal axons were depolarized. This depolarization was decreased by a prior depolarization, but increased by a hyperpolarization, of the afferent. During the depolarization of the afferent produced by GABA, the size of the orthodromic action potential was decreased. Iontophoretically applied bicuculline antagonized the effect of GABA on the threshold for antidromic activation of the afferents. NCA, DABA, and pentobarbital potentiated the action of GABA on the afferent terminal excitability. Pre-treatment of the animals with semicarbazide, which reportedly depletes spinal GABA, resulted in a reduction in the threshold produced by a conditioning stimulation of other group I afferents. GABA decreased the threshold for antidromic activation of the nonterminal regions of the afferents when applied near the stimulation sites. The amounts of GABA required to produce a decrease in the threshold of the nonterminal afferents were greater than those required to produce a comparable effect on the terminal regions of the fibres. Iontophoretically applied NCA and bicuculline, in amounts that were adequate to alter the effects of applied GABA, failed to affect the nerve stimulation-induced decrease in the threshold for antidromic activation of the fibres. Intravenously injected bicuculline, however, antagonized the actions of GABA as well as of the reduction in the threshold produced by nerve stimulation.These results indicate that (1) GABA-induced increase in the excitability of group I afferent terminals is associated with a depolarization of the afferent, (2) the uptake of iontophoretically applied amino acid into the spinal cord tissue appears to limit its action on the afferent terminal excitability, (3) GABA has a preterminal depolarizing action on group I muscle afferents, and (4) primary afferent depolarization produced by nerve stimulation may be of diffuse origin and, hence, cannot be significantly affected by iontophoretically applied NCA and bicuculline.


2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.


1963 ◽  
Vol 44 (3) ◽  
pp. 475-480 ◽  
Author(s):  
R. Grinberg

ABSTRACT Radiologically thyroidectomized female Swiss mice were injected intraperitoneally with 131I-labeled thyroxine (T4*), and were studied at time intervals of 30 minutes and 4, 28, 48 and 72 hours after injection, 10 mice for each time interval. The organs of the central nervous system and the pituitary glands were chromatographed, and likewise serum from the same animal. The chromatographic studies revealed a compound with the same mobility as 131I-labeled triiodothyronine in the organs of the CNS and in the pituitary gland, but this compound was not present in the serum. In most of the chromatographic studies, the peaks for I, T4 and T3 coincided with those for the standards. In several instances, however, such an exact coincidence was lacking. A tentative explanation for the presence of T3* in the pituitary gland following the injection of T4* is a deiodinating system in the pituitary gland or else the capacity of the pituitary gland to concentrate T3* formed in other organs. The presence of T3* is apparently a characteristic of most of the CNS (brain, midbrain, medulla and spinal cord); but in the case of the optic nerve, the compound is not present under the conditions of this study.


1985 ◽  
Vol 55 ◽  
Author(s):  
F. Terry Hambrecht

ABSTRACTNeural prostheses which are commercially available include cochlear implants for treating certain forms of deafness and urinary bladder evacuation prostheses for individuals with spinal cord disorders. In the future we can anticipate improvements in bioelectrodes and biomaterials which should permit more sophisticated devices such as visual prostheses for the blind and auditory prostheses for the deaf based on microstimulation of the central nervous system.


1908 ◽  
Vol 54 (226) ◽  
pp. 560-561
Author(s):  
David Orr ◽  
R. G. Rows

At a quarterly meeting of this Association held last year at Nottingham, we showed the results of our experiments with toxins upon the spinal cord and brain of rabbits. Our main conclusion was, that the central nervous system could be infected by toxins passing up along the lymph channels of the perineural sheath. The method we employed in our experiments consisted in placing a celloidin capsule filled with a broth culture of an organism under the sciatic nerve or under the skin of the cheek; and we invariably found a resulting degeneration in the spinal cord or brain, according to the situation of the capsule. These lesions we found to be identical in morphological type and anatomical distribution with those found in the cord of early tabes dorsalis and in the brain and cord of general paralysis of the insane. The conclusion suggested by our work was that these two diseases, if toxic, were most probably infections of lymphogenous origin.


1947 ◽  
Vol s3-88 (1) ◽  
pp. 55-63
Author(s):  
R. A. R. GRESSON ◽  
I. ZLOTNIK

1. The Golgi material of the pyramidal cells of the cerebral cortex, the Purkinje cells of the cerebellum, and the multipolar cells of the medulla oblongata and ventral horns of the spinal cord of the sheep is present as filaments and as irregularly shaped bodies. In some of the cells, particularly in the lamb (Sheep V), the Golgi material has the appearance of a network. As it is frequently present as separate bodies it is suggested that it may always consist of discrete Golgi elements which are sometimes situated in close proximity or in contact with one another. Filamentous Golgi elements are present in the basal part of the cell processes. 2. An examination of neurones from the corresponding regions of the central nervous system of sheep infected experimentally with louping-ill showed that the Golgi material undergoes changes consequent upon the invasion of the cells by the virus. The Golgi material undergoes hypertrophy, and at the same time there is a reduction in the number of filamentous Golgi elements and a reduction in the amount of Golgi substance present in the cell processes. These changes are followed by fragmentation. All the neurones of a particular region are not affected equally at the same time. The Golgi material of the Purkinje cells tends to form groups in the cytoplasm prior to fragmentation. In the multipolar cells of the medulla oblongata the hypertrophy of the Golgi material is not as great as in the other regions of the central nervous system. The Golgi material of the motor nerve-cells of the ventral horns of the spinal cord undergoes considerable hypertrophy which is followed by a grouping of the Golgi elements and fragmentation.


2017 ◽  
Vol 37 (8) ◽  
pp. 820-828 ◽  
Author(s):  
Guilherme Konradt ◽  
Daniele M. Bassuino ◽  
Klaus S. Prates ◽  
Matheus V. Bianchi ◽  
Gustavo G.M. Snel ◽  
...  

ABSTRACT: This study describes suppurative infectious diseases of the central nervous system (CNS) in domestic ruminants of southern Brazil. Reports from 3.274 cattle, 596 sheep and 391 goats were reviewed, of which 219 cattle, 21 sheep and 7 goats were diagnosed with central nervous system inflammatory diseases. Suppurative infectious diseases of the CNS corresponded to 54 cases (28 cattle, 19 sheep and 7 goats). The conditions observed consisted of listerial meningoencephalitis (8 sheep, 5 goats and 4 cattle), suppurative leptomeningitis and meningoencephalitis (14 cattle, 2 goats and 1 sheep), cerebral (6 cattle and 2 sheep), and spinal cord (7 sheep) abscesses, and basilar empyema (4 cattle and 1 sheep). Bacterial culture identified Listeria monocytogenes (9/54 cases), Escherichia coli (7/54 cases), Trueperella pyogenes (6/54 cases) and Proteus mirabilis (1/54 cases). All cases diagnosed as listeriosis through histopathology yielded positive immunostaining on immunohistochemistry, while 12/17 of the cases of suppurative leptomeningitis and meningoencephalitis presented positive immunostaining for Escherichia coli. Meningoencephalitis by L. monocytogenes was the main neurological disease in sheep and goats, followed by spinal cord abscesses in sheep. In cattle, leptomeningitis and suppurative meningoencephalitis was the most frequent neurological disease for the species, and E. coli was the main cause of these lesions. Basilar empyema, mainly diagnosed in cattle, is related to traumatic injuries, mainly in the nasal cavity, and the main etiologic agent was T. pyogenes.


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