scholarly journals Cerebellar Golgi cells in the rat receive multimodal convergent peripheral inputs via the lateral funiculus of the spinal cord

2006 ◽  
Vol 577 (1) ◽  
pp. 69-80 ◽  
Author(s):  
Tahl Holtzman ◽  
Abteen Mostofi ◽  
Chia Ling Phuah ◽  
Steve A. Edgley
Keyword(s):  
Spinal Cord ◽  
Golgi Cells ◽  
Lateral Funiculus

scholarly journals Neuropathology of Experimental 3-nitro-4-hydroxyphenylarsonic Acid Toxicosis in Pigs

1986 ◽  
Vol 23 (4) ◽  
pp. 454-461 ◽  
Author(s):  
S. Kennedy ◽  
D. A. Rice ◽  
P. F. Cush
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Axonal Degeneration ◽  
Histopathologic Examination ◽  
Dorsal Region ◽  
Dorsal Funiculus ◽  
Lateral Funiculus ◽  
Discrete Area ◽  
Cervical Level ◽  
Peripheral Regions

Twenty pigs were fed a diet containing 187.5 mg kg−1 of 3-nitro-4-hydroxyphenylarsonic acid (3-nitro). Ten pigs were euthanized at intervals up to 29 days, 3-nitro was withdrawn from the diet of the remaining pigs on day 30, and these animals were subsequently euthanized at intervals up to 49 days after commencement of the experiment. A nervous syndrome characterized by clonic convulsive episodes inducible by exercise, developed at day 11. Paraparesis was apparent at day 22 progressing to paraplegia by day 33 (3 days after cessation of 3-nitro feeding). Histopathologic examination revealed myelin and axonal degeneration in the white matter of the spinal cord coincident with the onset of nervous signs. Marchi-positive degeneration was present in the dorsal funiculus at cervical level at day 22. Lesions intensified with increasing duration of toxicosis and while degenerate fibers were seen in all funiculi, there was preferential involvement of the fasciculi gracilis and cuneatus, the peripheral regions of the ventral and lateral funiculi, and a discrete area of the dorsal region of the lateral funiculus. Peripheral and optic neuropathies were evident from day 32 but were always mild and focal. The experiment establishes 3-nitro as a central-peripheral neurotoxicant of pigs.

Role of histamine in posttraumatic spinal cord hyperemia and the luxury perfusion syndrome

1976 ◽  
Vol 44 (1) ◽  
pp. 16-20 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Thomas F. Doyle
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Related Phenomenon ◽  
Spinal Cord Trauma ◽  
Normal Range ◽  
Content Type ◽  
Lateral Funiculus ◽  
Receptor Sites ◽  
Luxury Perfusion

✓ The authors studied the effect of pretreatment of monkeys with antihistamines on hyperemia observed in the lateral funiculus of the spinal cord after severe experimental spinal cord trauma. After administration of Chlorpheniramine and Metiamide, the spinal cords were traumatized with a 600 gm-cm injury. Blood flow in the lateral funiculus at the injury site was then determined hourly for 6 hours. The blood flow at this site remained in the normal range at all times in all animals. Neither a hyperemia nor an ischemia could be demonstrated. This finding reaffirms the authors' previous observation that ischemia does not exist in the lateral funiculus after severe experimental spinal cord trauma, and explains the previous observation of hyperemia as a histamine-related phenomenon, easily blocked by the administration of Chlorpheniramine and Metiamide, potent antihistamines which together block both the H1 and H2 receptor sites.

Position of Spinothalamic Tract Axons in Upper Cervical Spinal Cord of Monkeys

2000 ◽  
Vol 84 (3) ◽  
pp. 1180-1185 ◽  
Author(s):  
Xijing Zhang ◽  
Christopher N. Honda ◽  
Glenn J. Giesler
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Dynamic Range ◽  
Cervical Spinal Cord ◽  
High Threshold ◽  
Spinothalamic Tract ◽  
Antidromic Activation ◽  
Lateral Funiculus ◽  
Upper Cervical ◽  
Low Threshold

Percutaneous upper cervical cordotomy continues to be performed on patients suffering from several types of severe chronic pain. It is believed that the operation is effective because it cuts the spinothalamic tract (STT), a primary pathway carrying nociceptive information from the spinal cord to the brain in humans. In recent years, there has been controversy regarding the location of STT axons within the spinal cord. The aim of this study was to determine the locations of STT axons within the spinal cord white matter of C2 segment in monkeys using methods of antidromic activation. Twenty lumbar STT cells were isolated. Eleven were classified as wide dynamic range neurons, six as high-threshold cells, and three as low-threshold cells. Eleven STT neurons were recorded in the deep dorsal horn and nine in superficial dorsal horn. The axons of the examined neurons were located at antidromic low-threshold points (<30 μA) within the contralateral lateral funiculus of C2. All low-threshold points were located ventral to the denticulate ligament, within the lateral half of the ventral lateral funiculus (VLF). None were found in the dorsal half of the lateral funiculus. The present findings support our previous suggestion that STT axons migrate ventrally as they ascend the length of the spinal cord. Also, the present findings indicate that surgical cordotomies that interrupt the VLF in C2 likely disrupt the entire lumbar STT.

Inhibition of primate spinothalamic tract neurons by stimulation in periaqueductal gray or adjacent midbrain reticular formation

1984 ◽  
Vol 51 (3) ◽  
pp. 450-466 ◽  
Author(s):  
K. D. Gerhart ◽  
R. P. Yezierski ◽  
T. K. Wilcox ◽  
W. D. Willis
Keyword(s):  
Spinal Cord ◽  
Reticular Formation ◽  
Dynamic Range ◽  
Periaqueductal Gray ◽  
Noxious Stimulation ◽  
Spinothalamic Tract ◽  
Antidromic Activation ◽  
Lateral Funiculus ◽  
C Fibers ◽  
Midbrain Reticular Formation

Recordings were made from spinothalamic tract (STT) cells in the lumbosacral enlargement of anesthetized monkeys. The cells were identified by antidromic activation from the contralateral ventral posterior lateral nucleus of the thalamus. Electrical stimulation at sites within the periaqueductal gray, the adjacent midbrain reticular formation, or the deep layers of the tectum were found to inhibit the activity of STT cells. In general, midbrain stimulation inhibited the background discharges and the responses of wide dynamic range cells evoked by innocuous and noxious cutaneous stimulation (29 of 37 cases). However, for six cells, midbrain stimulation preferentially inhibited the responses to noxious stimulation. The evoked responses of all 10 high-threshold cells were inhibited. In only two cases was midbrain stimulation ineffective, and no excitatory effects were observed. The mean latency to onset of inhibition resulting from midbrain stimulation was 24.9 +/- 7.2 ms (n = 35). The amount of inhibition produced by midbrain stimulation was graded with stimulus intensity. For example, trains of stimuli (333 Hz) at 50 microA produced a mean inhibition to 81.7 +/- 16.6% of control, while 200 microA resulted in a mean inhibition to 36.3 +/- 21.7%. Not only was the inhibition increased by the use of stronger current intensities, but the duration of inhibition was prolonged. Midbrain stimulation inhibited the responses of STT cells to volleys in both the A-fibers and the C-fibers of the sural nerve. However, there was a selective action in that the responses to C-fiber volleys were more strongly inhibited than were the responses to A-fiber volleys. Lesions placed in the white matter of the upper cervical spinal cord reduced the inhibition produced by stimulation in either the midbrain or the nucleus raphe magnus. The extent to which the inhibition was reduced was proportional to the extent of the cord lesions. However, even when there was an interruption of the entire lateral funiculus on the side of an STT cell and of the dorsal quadrant of the contralateral side, there was still substantial inhibition following stimulation in either brain stem site. It is concluded that while part of the inhibition is mediated by pathways descending in the dorsal lateral funiculus (DLF), at least some depends on pathways coursing through the ventral spinal cord. Inhibition of STT cells may contribute to the neuronal mechanism of the analgesia that results from stimulation in the periaqueductal gray matter in awake, behaving animals.

Spinal cord pathways involved in initiation of swimming in the stingray, Dasyatis sabina: spinal cord stimulation and lesions

1984 ◽  
Vol 51 (3) ◽  
pp. 578-591 ◽  
Author(s):  
B. J. Williams ◽  
C. A. Livingston ◽  
R. B. Leonard
Keyword(s):  
Spinal Cord ◽  
Rhythmic Activity ◽  
Descending Pathways ◽  
Pectoral Fin ◽  
Lateral Funiculus ◽  
Root Entry Zone ◽  
Before And After ◽  
Motor Nerves ◽  
Stimulation Experiments ◽  
A Site

In spinally transected stingrays, electrical stimulation of a site just ventral to the dorsal root entry zone or a site in the intermediate portions of the lateral funiculus produced rhythmic swimming like movements of the contralateral pectoral fin. Electromyographic (EMG) records collected during cord-stimulated rhythms had the same pattern of activity and sometimes the same intersegmental coordination as those collected during spontaneous swimming of the same animal. In paralyzed, high-spinal stingrays, the only stimulation sites that produced rhythmic activity (fictive swimming) in the pectoral fin motor nerves were in the intermediate portion of the lateral funiculus. The evoked rhythm occurred in the motor nerves that were contralateral to the stimulated side of the spinal cord. The effects of subtotal lesions of the rostral spinal cord on spontaneous swimming behavior were assessed by analysis of EMG records taken before and after the lesions were made. Severe deficits in swimming occurred after bilateral ablation of intermediate portions of the lateral funiculi. In agreement with previous results, the stimulation experiments indicate that the stingray spinal cord contains an inherent capacity to generate properly coordinated rhythmic swimming. The current experiments also suggest that the descending pathways(s) that normally functions to initiate swimming projects through the intermediate aspects of the lateral funiculi.

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