Simultaneous recordings from pericruciate pyramidal tract and non-pyramidal tract neurons; response to stimulation of inhibitory pathways.
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Animals↗
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Subcortical topography and proportions of the pyramidal tract.
The pyramidal tract (PT) was dissected in 30 normal human hemispheres according to the method of Klingler. The various dimensions as well as the cerebral landmarks were studied. The pyramidal tract is built up like a fan in the white matter by a thin layer of fibers of 2.8-3.5 mm in thickness. The fibers converge toward the internal capsule to a solid fiber tract with a lateral and apdiameter of 7.8 +/- 1.6 mm and 17.5 +/- 2.1 mm, respectively. This configuration of the PT presents different possibilities of damage during surgery. The evaluation of the three-dimensional course of the PT is possible by using three cerebral landmarks, the precentral gyrus, the entrance into the internal capsule and the posterior limb of the internal capsule. Their topography is described. Additionally the pyramidal tract can be defined medially by the sulcus cinguli and the roof of the lateral ventricle and laterally by the superior sulcus circularis Insulae. The possible displacement of the PT by space occupying lesions and the intra-operative orientation is discussed.
Adult↗
[Integrated function of the cerebral cortex (with special reference to the nature of the pyramidal cells and function of the pyramidal tract)--the motor area and 2 types of pyramidal tract cell].
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Animals↗
Synaptic inhibition in pyramidal tract neurons: membrane potential and conductance changes evoked by pyramidal tract and cortical surface stimulation.
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Animals↗
Responses of the pyramidal tract to stimulation of the baboon's motor cortex.
1. The arm area of the baboon's precentral motor cortex was stimulated by brief surface-anodal pulses, and the discharge of the corticospinal tract (the ;pyramidal tract waves') was recorded by an electrode resting on the dorsolateral surface of the cervical spinal cord.2. Some properties of the pyramidal tract waves were described, and they were also studied in relation to the firing of single cortico spinal fibres.3. The results led to the conclusion that the later pyramidal tract waves (the ;I waves') were almost exclusively due to a semi-synchronous repetitive discharge of the same fast cortico spinal fibres as those responsible for the initial wave (the ;D wave').4. Some problems concerning the origin and significance of the I waves were discussed.
Action Potentials↗
[Adrenoleukodystrophy with high signal intensity areas in bilateral pyramidal tracts from internal capsule through medullary pyramids on MRI].
We reported a case of adrenoleukodystrophy in which MRI showed high signal intensity areas in the pyramidal tracts from the internal capsule through the medullary pyramids. A 20-year-old man was admitted with complaints of slowly progressive spastic paraparesis of one and a half year duration. He had no mental deterioration, visual disturbance or sensory impairment. His maternal cousin died of adrenoleukodystrophy at the age of 13 years old, after showing progressive visual disturbance, dementia and quadriplegia. On admission, neurological examination revealed spastic tetraparesis and exaggerated deep tendon reflexes with pathological reflexes. Examination of the mental function and cranial nerves were normal. There were no sensory abnormalities in all modalities. Routine laboratory data including hematological studies, urinalysis, serum electrolytes and enzymes were all normal. Endocrinological examinations showed no adrenocortical insufficiency, and testicular function was normal. Cerebrospinal fluid, EEG, needle EMG and nerve conduction studies were also normal. CT scan showed a mild ventricular enlargement and no low density areas were seen in the cerebral white matter. Spin-echo MRI (SE 2,000/100, 2,000/40) revealed continuous high signal intensity areas in the pyramidal tracts from the internal capsule through medullary pyramids bilaterally. There were no abnormal findings in the spinal cord on MRI. Electrophysiologically, the brain-stem auditory evoked potentials (BAEPs) were abnormal and suggested the presence of bilateral dorsal brain stem lesions. Short latency somatosensory evoked potentials (SEPs) obtained by the bilateral tibial nerve stimulation revealed slowing of the central conduction time, showing delayed P37 latency and normal peripheral conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenoleukodystrophy↗
Retrograde cortical aand axonal changes following lesions of the pyramidal tract.
Following lesions of the pyramidal tract in hamsters, retrograde changes were studied in the sensorimotor cortex and in the pyramidal tract axons proximal to the lesion, at survival times ranging from 2 weeks to 14 months. Severe cell shrinkage occurred in layer 5 pyramidal neurons as early as 2 weeks, but there was no cell loss among these neurons even with long survival times. Use of the Fink-Heimer method for degenerating axons revealed that the pyramidal tract proximal to the lesion had undergone a retrograde axon degeneration which, in some respects, resembled anterograde degeneration. The retrograde axon degeneration began at the lesion site and advanced slowly rostralwards with time involving increasingly greater numbers of fibers. However, even at the longest survival times the degeneration fell off markedly at pontine levels. The results indicate that this process represents a true retrograde fiber degeneration (as opposed to an indirect Wallerian degeneration) which appears to reach a point of equilibrium such that a partially shrunken pyramidal cell is maintaining a partially degenerated axon.
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[Aberrant pyramidal tract: a study with Sudan III stain].
The aberrant pyramidal tracts in the pontine medial lemnisci were studied, using standard Sudan III stain, in six cases of chronic pyramidal tract degeneration. Three of the six cases had bilateral or unilateral cerebral destructive lesions, one cervical hematomyelia with rare retrograde pyramidal tract degeneration, one classical amyotrophic lateral sclerosis, and one atypical motor neuron disease with striatonigral degeneration. Except for the latter two cases the aberrant pyramidal tract degeneration was confirmed bilaterally or on the side ipsilateral to the pyramidal tract degeneration in the pontine base. This degeneration could also be found, on careful examination, with other stains, i.e., H & E, Luxol fast blue-periodic acid Schiff and modified Bielschowsky. Significant change was not observed in the medullary medial lemniscus in any case. The different results observed in the aberrant pyramidal tract between the destructive and degenerative disorders might be pathogenetically important. Reservation, however, may be required since the number of the cases of degenerative disorders in this study was limited. A possible factor for this difference is the survival length which might have erased degradation products altogether. Another factor is the sensitivity of Sudan III in comparison with the Marchi's method which might demonstrate more subtle evidence of degeneration but with its intrinsic capricious staining characteristics. The physiological role of the aberrant pyramidal tract, which has been neglected in the recent textbooks of neuroanatomy, may become of clinical interest with high-quality MRI in cases such as isolated cranial motor nerve palsy without concomitant paralysis of the extremities.
Adult↗
[Synaptic processes in neurons of the cat pericruciate cortex evoked by pyramidal tract stimulation].
The influences of pyramidal tract stimulation on the activity of neurons in the pericruciate cortex were investigated on 423 neurons (81 neurons were studied intracellularly and 342--extracellularly), 78 of them having background activity. Pyramidal stimulation is shown to evoke not only antidromic spikes (0.5-16.0 ms latency) in the pyramidal cells, but also lateral and recurrent PSPs in the pyramidal and unidentified units of all cortical layers. IPSPs were observed in 46.7% of the investigated neurons, EPSPs--in 21.0%, mixed responces--in 26.0%. The latency of IPSPs was 1.5-14.0 ms, their amplitude ranged from 1.3 to 17.0 mV, the duration of the rising phase varied from 4 to 18 ms and the whole duration was 18-120 ms reaching sometimes 250-500 ms. In 30% of cases it was possible to divide the IPSPs into two phases: a fast one with a duration of 10-20 ms and a slow one. The latency of IPSPs was 2.6-19.0 ms, their amplitude--1.0--7.8 mV and duration--from 10.0 to 50.0 ms. The antidromic discharge in the pyramidal tract inhibited the background activity for 200-400 ms in 51.2% of spontaneously active units; acceleration was observed in 19.5% and mixed effect in 7.4% of units. The participation of pyramidal axonal collaterals and cortical interneurons in generation of the described processes is discussed.
Action Potentials↗
Redirected growth of pyramidal tract axons following neonatal pyramidotomy in cats.
After the pyramidal tract at the pontomedullary junction in neonatal cats had been cut and the ipsilateral frontoparietal cortex injected with intra-axonal markers at 40 to 74 days of age, cortical axons were labeled in aberrant pathways that descended into the caudal medulla and spinal cord. Some labeled axons from the damaged pyramidal tract crossed the midline, descended with fibers in the intact pyramidal tract through the pyramidal decussation, and entered the lateral corticospinal tract. Another group of aberrant projections descended bilaterally along the ventrolateral edge of the medulla and either ended in the lateral reticular nuclei or continued into the spinal cord. Finally, some axons descended individually through the central medullary tegmentum and ended bilaterally in the spinal trigeminal, dorsal column, and lateral reticular nuclei. Although these findings suggest that pyramidal tract axons regenerate after injury, the findings from a second series of experiments refute this conclusion. In 2- to 5-day-old cats, the fluorescent dye Fast Blue was injected into the spinal cord, and 7 to 8 days later the contralateral pyramidal tract was cut. In these animals, there were never any cortical neurons retrogradely labeled with Fast Blue in the frontoparietal cortex ipsilateral to the pyramidotomy, although numerous neurons were labeled contralaterally. Control experiments confirmed that the interval between the Fast Blue injections and the pyramidotomies was long enough for retrogradely labeling cortical neurons, that the spinal cord injections did not adversely affect the retrogradely labeled cortical neurons, and following axotomy dying cortical neurons could be demonstrated directly using silver impregnation techniques. We conclude that neonatal pyramidotomy causes the death of all axotomized cortical neurons in kittens, and, therefore, the aberrant cortical projections seen caudal to the lesion must be redirected, late-developing, and undamaged cortical axons, and not regenerated axons.
Animals↗
The mode of activation of pyramidal tract cells by intracortical stimuli.
1. Direct and indirect effects of intracortical stimulattion on pyramidal tract cells were compared in the monkey and in the cat under barbiturate or chloralose anaesthesia. The hind-limb motor areas were explored, that in the monkey only within the convex part of the precentral gyrus. The intracortical stimuli were applied in the nearest vicinity of pyramidal tract cells, where antidromic spike potentials of single cells were recorded. 2. Average records of descending volleys in corticospinal tract fibres were taken from the surface of the lateral funiculus or from its dissected fascicles. The sensitivity of the recording was sufficient to detect responses in single fibres. 3. The latencies of the earliest descending volleys evoked by weak intracortical stimuli were compared with the latencies of the antidromic spike potentials of pyramidal tract cells evoked by stimulation of the lateral funiculus at a low lumbar level (same conduction distance). Only in about one third of cases these latencies were similar and compatible with a direct activation of pyramidal tract cells. In the remaining cases they indicated mono- or polysynaptic activation of pyramidal tract cells. 4. Latencies of the later components of the descending volleys indicated that they were due to indirect activation of pyramidal tract cells in practically all cases. 5. The components of the descending volleys attributable to the indirect activation of pyramidal tract cells were greatly increased when repetitive intracortical stimuli were applied instead of single ones. 6. The investigation leads to the conclusion that a weak intracortical stimulation is relatively ineffective in a direct excitation of pyramidal tract cells and that the effects of such a stimulation are mainly indirect, especially when repetitive stimuli are used.
Animals↗
Course and termination of the pyramidal tract in the pig.
To study the pyramidal tract in the pig, the motor cerebral cortex of one side was defined electrophysiologically and subsequently excised. The animals operated were killed after 7, 11 and 14 days, and the cerebral hemisphere of the operated side, brain stem and spinal cord were removed for histological examination. The pyramidal tract proved to run ipsilaterally as far as the oral extremity of the 12th cranial nerve nucleus. The decussation, which exhausted itself almost completely at the level of the rostral extremity of the 1st cervical metamere, started here. After the limit just mentioned only rare isolated fibres were visible. Along its course, the pyramidal tract sent a small number of axons to the ipsilateral and contralateral nucleus of the 7th cranial nerve, while the fibres running from the opposite side to the reticular formation and to the hypoglossal nerve nucleus, cuneatus, gracilis and trigeminal spinal tract nuclei were more numerous.
Animals↗
Immunocytochemical localization of cell adhesion molecule L1 in developing rat pyramidal tract.
L1 is a representative of a family of carbohydrate neural cell adhesion molecules. The expression of L1 was studied during postnatal development of the rat pyramidal tract by immunohistology using polyclonal antibodies to L1 in spinal cord cervical intumescences. On postnatal day 1 (P1), L1 immunoreactivity was present in the entire dorsal funiculus, consisting of the ascending fasciculus gracilis and fasciculus cuneatus and the descending pyramidal tract. At that time the cervical pyramidal tract contains the first outgrowing corticospinal axons. At P4 both the fasciculus gracilis and the pyramidal tract are immunoreactive whereas the fasciculus cuneatus is negative. At P10 the pyramidal tract is intensely labelled whereas both ascending bundles are negatively stained. In the period between P4 and P10 the pyramidal tract is characterized by a massive outgrowth of corticospinal axons. During pyramidal tract myelination, between P10 and the end of the third postnatal week (P21), L1 immunoreactivity is progressively reduced. These observations suggest that L1 may play a prominent role in outgrowth, fasciculation and the onset of myelination of rat pyramidal tract axons. The differential L1 immunoreactivity of the pyramidal tract and the earlier developing ascending systems in rat dorsal funiculus indicate that this polyclonal antiserum is a useful differentiating marker for outgrowing fibre tracts.
Aging↗
Fetal occipital cortical neurones transplanted to the rostral cortex can extend and maintain a pyramidal tract axon.
In adult rats, cortical neurones that send axons through the pyramidal tract are confined to layer V, over the rostral two-thirds of the cerebral hemisphere. However, during the first postnatal week, many neurones in layer V in the occipital cortex (including the visual cortex) also extend axon collaterals through the pyramidal tract and into the spinal cord. These occipital corticospinal collaterals are completely eliminated over the subsequent 2 weeks, although their cells of origin do not die. We now report that when portions of the occipital cortex from fetal rats are transplanted to more rostral cortical regions of newborn rats, some of the transplanted neurones not only extend axons through the pyramidal tract, but also maintain these axons beyond the stage at which they are normally eliminated. These results suggest that normally-eliminated cortical axons can be 'rescued' and, in the case of pyramidal tract neurones, the position of the neurones within the tangential plane of the cortex is a critical factor in determining which neurones retain and which lose their pyramidal tract collaterals.
Animals↗
Cortical pyramidal tract interneurones and their sensitivity to L-glutamic acid.
1. Pyramidal tract interneurones, defined as neurones which are activated synaptically as a result of pyramidal tract stimulation, have been identified in the rat cerebral cortex. The number of evoked spikes depended upon stimulus strength, and stimulation in a specific thalamic nucleus produced a burst of activity lasting for up to 1 sec.2. These cells are readily excited by a brief (50 msec) pulse of glutamate applied by micro-iontophoresis. Other, unidentified cells are not so responsive.3. Synaptically evoked spikes resulting from pyramidal tract stimulation can be blocked by the iontophoretic and I.P. administration of substances shown to antagonize glutamate excitation of cells.4. The results support suggestions that glutamic acid is a neurotransmitter in the cerebral cortex. The evidence presented further indicates that glutamic acid could be the transmitter released by the pyramidal tract.
Acetylcholine↗
Effects of infant versus adult pyramidal tract lesions on locomotor behavior in hamsters.
The role of the pyramidal tract in locomotion was studied in hamsters by analyzing their locomotor behavior after lesions of the medullary pyramidal tract. Animals with lesions either as adults or as infants were compared to determine whether early pyramidotomy results in greater functional recovery. Normal and pyramidotomized animals were filmed during locomotion on a runway consisting of either smooth or rough terrain to assess whether the uneven surface would accentuate locomotor deficits. Frame-by-frame analysis of the filmed behavior during all phases of the step cycle was carried out to determine positions of the joints of the forelimb and hindlimb during locomotion. Accuracy of limb placement on the rough terrain was determined by observations of consecutive step cycles. The results show that lesions of the pyramidal tract in both infant and adult hamsters affect locomotion first by causing a reduction in the yielding phase of the step cycle and second by producing inaccuracies of forelimb placement. Rough terrain accentuates deficits in forelimb placement during locomotion. Animals with lesions as infants and those with lesions as adults show surprisingly similar deficits in locomotion, with the exception that animals with lesions as infants show some behavioral compensation in hindlimb movement by developing a normal degree of yielding at the knee. In contrast, hamsters with lesions as either adults or infants never recover normal forelimb behavior in either yielding at the elbow or accuracy of forelimb placement. These results emphasize the sensorimotor role of the pyramidal tract, even in a relatively stereotyped behavior such as locomotion.(ABSTRACT TRUNCATED AT 250 WORDS)
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Neuronal chromatin changes in layer V pyramidal cells of somatomotor cortex after pyramidal tract lesions as demonstrated by [3H]actinomycin D binding.
Changes in chromatin structure of pyramidal tract neurons after medullary pyramidal tract lesions were examined autoradiographically utilizing [3H]actinomycin D (Act D) binding to nuclei in frozen sections of brain. After a right pyramidal tract lesion, the binding of Act D to nuclei of axotomized pyramidal neurons of somatomotor cortex layer V increased sharply at 1 and 5 days postoperation, compared with pyramidal cells of the left side or hippocampal control cells of the left hemisphere. At 3, 7, 9, and 11 days the axotomized cells showed significantly decreased binding compared with controls. The unoperated pyramidal cells showed a significantly decreased Act D binding at 2 h and 9 days postoperation compared with the ipsilateral hippocampal control cells. The data suggested that intrinsic neurons of the central nervous system had a response pattern of chromatin changes to axotomy that was basically similar to that of peripheral neurons (sensory ganglion cells). However, the response was compressed into the 1st week postoperation with only a brief reaction which might be correlated to axonal regeneration. This reaction was followed by a prolonged depression of Act D nuclear binding which may be associated with cellular atrophy.
Analysis of Variance↗
Immunoelectron microscopic localization of cell adhesion molecule L1 in developing rat pyramidal tract.
The glycoprotein L1 is a cell adhesion molecule that has been proposed to function in the peripheral nervous system in axon fasciculation and onset of myelination. In this report we localize L1 during the development of a major central pathway: the pyramidal tract. The (sub)cellular localization of L1 was determined both by pre-embedding staining on Vibratome sections and by immunogold labelling on ultracryosections in developing rat pyramidal tract at the fifth cervical segment. On arrival at the fifth cervical segment, i.e. at postnatal day 1, growth cones of pioneer fibres did not exhibit L1-immunoreactivity. In the contact zone between pyramidal tract growth cones and glial processes no L1-immunoreactivity was observed. A clear L1-immunoreactivity was noted on small unmyelinated other axons situated in the entrance area of the pyramidal tract growth cones. Also on later arriving, i.e. between postnatal days 2 and 10, small unmyelinated fasciculating pyramidal tract axons L1 were present. It is our impression that L1 is localized in an irregular patchy way on the outer side of the axonal membrane. During the onset of myelination, i.e. between postnatal days 10 and 14, L1 could not be detected on axons ensheathed by oligodendrocytic processes. When myelination is largely completed, i.e. at postnatal day 21, the L1 antigen could be localized within the axoplasma of both unmyelinated and myelinated pyramidal tract axons. Furthermore, L1 could be observed occasionally on small unmyelinated pyramidal tract axons. Whereas compact myelin was always L1-negative, L1 was noted periaxonally between the axolemma and compact myelin and at (para)nodal regions at the contact zone between axolemma and oligodendrocytic processes. From these results it may be deduced that: (1) L1 is involved in fasciculation of outgrowing later arriving pyramidal tract fibres: (2) L1 is not involved in the onset of myelination in this central tract; (3) L1 might play an additional adhesive role in myelinated rat pyramidal tract.
Aging↗