Sentence examples for ventral column from inspiring English sources

A typical myelin structure around a node of Ranvier in an ex vivo spinal ventral column is shown in Figure 1A.

To quantify glutamate toxicity on impulse conduction, a double sucrose gap chamber (Supplementary Figure S2) [19] was used to record CAP from a 4-cm ventral column from guinea pig spinal cord.

Compound action potential (CAP) measurements in an ex vivo spinal cord ventral column were carried out by using a double sucrose gap chamber [19], as shown in Supplementary Figure S2.

To evaluate the role of Ca2+ influx in paranodal myelin damage, we incubated the spinal ventral column in oxygenated Krebs' solution supplemented with 250 µg/mL Ca2+ ionophore A23187.

Tentatively, in the control antibody-treated monkeys, the two animals exhibiting the least spontaneous recovery had lesions with large estimated volumes (Table 1 and Fig. 5) and were thus possibly subjected to a lesion that affected more of the ventral column, the dorsal column and the rubrospinal tract than in the other monkeys (Fig. 1B).

In Dogs 4 and 5, the ventral column was dorsally deviated in relation to the intervertebral space, compatible with a disc protrusion, between the 11th and 12th thoracic vertebrae and between the 13th thoracic vertebra and the 1st lumbar vertebra, respectively.

These paddle-like electrodes are applied to the dorsal and ventral columns of the spinal cord for stimulation of cough, and respiration function and chronic, and intractable pain.

In control spinal ventral columns perfused with normal oxygenated Krebs' solution, the CAPs showed little change during 4 h [27].

Application of 100 µM 4-AP to ventral columns without glutamate treatment did not significantly affect the CAP amplitude or width [30].

It was found that incubation of glutamate-treated spinal ventral columns with 4-AP for 1 h restored the CAP amplitude to 157±20% of the value after glutamate treatment/washing and before 4-AP application (Figure 3E and 3F).

Although there were no evidences for the motor neuron loss at this stage, a wide-spread axonal degeneration in the spinal tracts of the lateral and ventral columns was evident, particularly in Als2−/−;SOD1H46R mice (Figure 3A).