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PubMed1986

Anatomical studies on the nucleus reticularis tegmenti pontis in the pigmented rat. I. Cytoarchitecture, topography, and cerebral cortical afferents.

The nucleus reticularis tegmenti pontis (NRTP) is a precerebellar reticular nucleus that has been found to be related to cerebropontocerebellar pathways and, more recently, to eye movements. The present study investigates the cytoarchitecture, the topography, and the cerebral cortical projections to the NRTP in the pigmented rat. The cytoarchitecture and topography of the NRTP was determined by examination of Nissl-stained material sectioned in the transverse and sagittal planes. Two cytoarchitectonically distinct portions of the NRTP are apparent; a central subdivision (NRTPc) composed of large multipolar, small spherical, and fusiform neurons, and a pericentral subdivision (NRTPp) composed of loosely packed small fusiform and spherical neurons. The NRTPc is located dorsal to the medial lemniscus and pyramidal tracts over the caudal two-thirds of the pons. It extends caudodorsally to the region just rostral and ventral to the abducens nucleus. The NRTPp is adjacent to the lateral margins of the NRTPc, rostrally, and lies ventral to the caudal portions of the NRTPc. Large injections of horseradish peroxidase (HRP) were made into the cerebellum in order to determine the degree to which each subdivision of the NRTP contributes to the cerebellar projection. A high percentage of NRTPc neurons and a lower percentage of NRTPp neurons were labeled. These differences in labeling density and neuronal morphology noted above confirm the appropriateness of subdividing the NRTP into central and pericentral subdivisions. The cerebral cortical afferents to the NRTP were examined by placing small iontophoretic injections of HRP into the NRTPc and NRTPp. A systematic examination of all cortical areas revealed that the HRP-labeled neurons are entirely localized within pyramidal layer V of three major cortical areas: the ipsilateral prefrontal cortex (Brodmann areas 8, 8a, 11, and 32); the ipsilateral motor and somatosensory cortices (Brodmann areas 2, 4, 6, and 10), and the bilateral cingular cortex (Brodmann areas 24a, 24b, 29c, and 29d). By far, the heaviest cortical labeling with HRP injections into the medial NRTPc is within the cingular cortex that may, in the rat, be homologous to the frontal eye field of the cat and monkey. In contrast, injections involving the lateral NRTPc or the NRTPp produced labeling within wide regions of the cortex with the greatest number in the somatomotor cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2002

Lewy bodies in Betz cells of the motor cortex in a patient with Parkinson's disease.

Lewy bodies (LBs) were observed in the giant pyramidal cells of Betz in the motor cortex of a patient with Parkinson's disease (PD) of 8-year duration. The patient had shown typical clinical features of PD. No dementia or pyramidal tract signs had been observed. The LBs, found in 8 of 747 Betz cells counted (1.1%), appeared as homogeneous or laminated, spherical inclusions with a clear surrounding halo and were strongly immunoreactive for alpha-synuclein. To our knowledge, this is the first demonstration of LBs in Betz cells. Considering the significant loss of neurons in the predilection sites for LBs, it is possible that in this patient, the motor cortex was also involved in the disease process of PD.

Humans↗

PubMed1993

Distribution of the inositol 1,4,5-trisphosphate receptor, P400, in adult rat brain.

The distribution of the inositol 1,4,5-trisphosphate receptor protein, P400, was investigated in adult rat brain by immunocytochemistry with the monoclonal antibody 4C11 raised against mouse cerebellar inositol 1,4,5-trisphosphate receptor protein. Immunoreactive neuronal cell bodies were detected in the cerebral cortex, the claustrum, the endopiriform nucleus, the corpus callosum, the anterior olfactory nuclei, the olfactory tubercle, the nucleus accumbens, the lateral septum, the bed nucleus of the stria terminalis, the hippocampal formation, the dentate gyrus, the caudate-putamen, the fundus striatum, the amygdaloid complex, the thalamus, the caudolateral part of the hypothalamus, the supramammillary nuclei, the substantia nigra, the pedunculopontine tegmental nucleus, the ventrotegmental area, the Purkinje cells in the cerebellum, the dorsal cochlear nucleus, the subnucleus oralis and caudalis of trigeminal nerve, and the dorsal horn of the spinal cord. Immunoreactive fibres were found in the medial forebrain bundle, the globus pallidus, the stria terminalis, the pyramidal tract, the spinal tract of trigeminal nerve, and the ventral horn of spinal cord. Nerve fibres forming a dense plexus ending in terminal-like boutons were detected in relation to nonimmunoreactive neurons of the dentate, interpositus, and fastigial nuclei of the cerebellum and around neurons of the vestibular nuclei. This receptor protein binds a specific second messenger, inositol 1,4,5-trisphosphate, which produces a mobilization of intracellular Ca2+ and a modulation of transmitter release.

Animals↗

PubMed1992

Stimulation of three areas of the primary motor cortex interrupts micturition in dogs.

To clarify the area of the motor cortex (M1) in dogs, which corresponds to the cortical area participating in voluntary interruption of micturition in humans, the cortical portions related to the external urethral sphincter were first clarified by recording of somato-sensory evoked potentials, and then systematic cortical stimulation was performed in anesthetized and paralyzed dogs. The hypogastric, pelvic and pudendal nerves innervating the lower urinary tract and rectum were severed to eliminate the secondary reflexes. Five foci were recognized in the cortical potentials evoked after stimulation of the pudendal nerve. These foci existed in the sacral (Sacral-S) and hind leg (Leg-S) areas of the somato-sensory cortex (S1), and in the sacral (Sacral-M), hind leg (Leg-M) and trunk (Abd-M) areas of the M1. Stimulation of the three M1 foci, but not the two S1 foci, provoked centrifugal firings of the pudendal urethral branch. The firings disappeared after cutting of the ipsilateral bulbar pyramis. When the M1 foci were stimulated during the micturition reflex, the reflex discharge of a pelvic vesical branch was interrupted concomitantly with firings of the urethral branch. The interruption was still induced after the pyramidotomy. Pulse train stimulation of these M1 foci reset the cycles (about 2 Hz) in the alternative rhythmic firings of the urethral and vesical branches, which are known to be formed in the pontine micturition center [31,32]. These results suggest that the pyramidal cells in the three M1 foci inhibit the pontine micturition center and concomitantly contract the external urethral sphincter through the pyramidal tract. The possible roles of these M1 foci were discussed.

Animals↗

PubMed2002

Contributions of the motor cortex to the control of the hindlimbs during locomotion in the cat.

Although the corticospinal tract is not essential for the production of the basic locomotor rhythm in cats, it does contribute to the regulation of locomotion, particularly in situations in which there is a requirement for precise control over paw placement or limb trajectory. Lesions of the dorsolateral funiculi at the low thoracic level (T(13)) that completely interrupted both the cortico- and rubrospinal pathways produced long-term deficits in locomotion on a level surface. These deficits included a paw-drag that was probably caused both by a loss of cortico- and rubrospinal input to motoneurones controlling distal muscles as well as by a change in the relative timing of muscles acting around the hip and knee. Smaller lesions produced similar deficits from which the cats recovered relatively quickly. Cats with the largest lesions of the dorsolateral funiculi were unable to modify their gait sufficiently to step over obstacles attached to the treadmill belt even 3-5 months postlesion. These results imply that the medial pathways, the reticulo- and vestibulospinal pathways, are unable to fully compensate for damage to the lateral pathways. Single unit recordings from identified pyramidal tract neurones (PTNs) within the hindlimb representation of the primary motor cortex (area 4) showed that a substantial proportion of neurones (67%) significantly increased their discharge frequency when the cats modified their gait to step over obstacles attached to the treadmill belt. Of those PTNs that showed increased activity during the swing phase, populations of neurones were activated at different times. A large proportion of PTNS discharged early in swing, in phase with knee flexors such as the semitendinosus. Others discharged slightly later, in phase with the activity of ankle flexors, such as tibialis anterior, while still others discharged at the end of swing, in phase with digit dorsiflexors, such as the extensor digitorum brevis. We suggest that different populations of cortical neurones may specifically modify the activity of selected groups of close synergistic muscles during different parts of the swing phase. We further suggest that these modifications are mediated, in part, by groups of interneurones that are involved in determining the base locomotor rhythm. This provides a means by which the changes specified by the descending signal from the motor cortex may be smoothly, and appropriately, incorporated into the locomotor cycle.

Animals↗

PubMed1984

The organization of projections from the cortex, amygdala, and hypothalamus to the nucleus of the solitary tract in rat.

Direct projections from the forebrain to the nucleus of the solitary tract (NTS) and dorsal motor nucleus of the vagus in the rat medulla were mapped in detail using both retrograde axonal transport of the fluorescent tracer True Blue and anterograde axonal transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). In the retrograde tracing studies, cell groups in the medial prefrontal cortex, lateral prefrontal cortex (primarily ventral and posterior agranular insular cortex), bed nucleus of the stria terminalis, central nucleus of the amygdala, paraventricular, arcuate, and posterolateral areas of the hypothalamus were shown to project to the NTS and in some cases also to the dorsal motor nucleus of the vagus. The prefrontal cortical areas projecting to the NTS apparently overlap to a large degree with those cortical areas receiving mediodorsal thalamic and dopaminergic input. The retrogradely labeled cortical cells were situated in deep layers of the rat prefrontal cortex. The anterograde tracing studies revealed a prominent topography in the mediolateral termination pattern of forebrain projections to the rostral part of the NTS and to the dorsal pons. The projections to the NTS were generally bilateral, except for projections from the central nucleus of the amygdala and bed nucleus of the stria terminalis which were predominantly ipsilateral. The prefrontal cortical projections to the NTS travel through the cerebral peduncle and pyramidal tract and terminate throughout the rostrocaudal extent of the NTS. Specifically, the prefrontal cortex innervates dorsal portions of the NTS (lateral part of the dorsal division of the medial solitary nucleus, dorsal part of the lateral solitary nucleus and the caudal midline region of the commissural nucleus), areas which receive relatively sparse subcortical projections. These dorsal portions of the NTS receive major primary afferent projections from the vagal and glossopharyngeal nerves. In contrast, the subcortical projections, which travel through the midbrain and pontine tegmentum, terminate most heavily in the ventral portions of the NTS, i.e., the area immediately dorsal and lateral to the dorsal motor nucleus of the vagus. Only the paraventricular hypothalamic nucleus has substantial terminals throughout the dorsal motor nucleus of the vagus. Hypothalamic cell groups innervate the area postrema and, along with the prefrontal cortex, innervate the zone subjacent to the area postrema.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

PubMed1986

Role of corticobulbar projection neurons in cortically induced rhythmical masticatory jaw-opening movement in the guinea pig.

The role of the pyramidal tract (PT) in the induction of the rhythmical masticatory activity (RMA) of the anterior digastric motoneurons by repetitive stimulation of the cortical masticatory area (CMA) was studied in the ketamine-anesthetized guinea pig. The coronal section of the medial brain stem at the pontine level did not show any effect on the cortically induced RMA in the digastric EMG, as long as the majority of the PT fibers was spared of the section. In contrast, unilateral section of the PT at the pontine level abolished the RMA in the digastric EMG induced by repetitive stimulation of the ipsilateral CMA, while that induced by the contralateral CMA stimulation was not affected by the PT section. The threshold of repetitive PT stimulation for induction of the RMA of the digastric EMG was much higher at the levels caudal to the facial nucleus than that at more rostral levels, and no RMA was induced by the PT stimulation at the caudal bulbar levels even at the supramaximal intensities for RMA induction of the PT stimulation at more rostral levels. Single shocks applied to the PT at the caudal bulbar levels did not evoke any antidromic field potential in the CMA. Single shocks applied to the CMA evoked a negative field potential in the medial bulbar reticular formation (MBRF) mainly on the contralateral side after a monosynaptic latency, which was largest in amplitude in the region including the most dorsal portion of the nucleus reticularis paragigantocellularis and the area dorsally adjacent to it (dPGC). Stimulation of the oral portion of the nucleus reticularis gigantocellularis (GC) evoked an antidromic negative field potential in the ipsilateral dPGC. Intracellular recording from neurons in the dPGC demonstrated that neurons were located in the dPGC that responded with EPSPs after a monosynaptic latency to single shocks applied to the contralateral CMA and with antidromic spike potentials to stimulation of the oral portion of the ipsilateral GC (GCo). Single shocks applied to the dPGC evoked antidromic field potential in the area in the contralateral cerebral cortex corresponding with the CMA. Injection of horseradish peroxidase (HRP) into the dPGC on one side retrogradely labeled the pyramidal cells with HRP bilaterally in the cerebral cortical area corresponding with the CMA. The number and density of the labeled cells on the contralateral side far exceeded those on the ipsilateral side.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1999

The role of synchrony and oscillations in the motor output.

There is currently much interest in the synchronisation of neural discharge and the potential role it may play in information coding within the nervous system. We describe some recent results from investigations of synchronisation within the motor system. Local field potentials (LFPs) and identified pyramidal tract neurones (PTNs) were recorded from the primary motor cortex of monkeys trained to perform a precision grip task. The LFPs showed bursts of oscillatory activity at 20-30 Hz, which were coherent with the rectified electromyographs (EMG) of contralateral hand and forearm muscles. This oscillatory synchronisation showed a highly specific task dependence, being present only during the part of the task when the animal maintained a steady grip and not during the movement phases before or after it. PTNs were phase-locked to LFP oscillations, implying that at least part of the coherence between cortical activity and EMG was mediated by corticospinal fibres. The phase locking of the PTNs to LFP oscillations produced task-dependent oscillatory synchronisation between PTN pairs, as assessed by the single-unit cross-correlation histogram. Recordings were also made from normal human subjects performing a precision grip similar to that used in the monkey recordings. Pairs of EMGs recorded from intrinsic hand and forearm muscles showed 20-30 Hz coherence, which modulated during task performance, being present only during periods of steady contraction. We suggest that these changes in EMG-EMG synchronisation reflect changing levels of synchronous drive from the corticospinal system. The generation of oscillations in the cortex is discussed in the light of results from a model of local cortical circuits. Other modelling work has shown that synchrony in the corticospinal inputs could act to recruit motoneurones more efficiently, producing more output force from a muscle than asynchronous inputs firing at the same mean rate. A speculative hypothesis is presented on the role of synchronous oscillations in the motor system, which is consistent with experimental observations to date.

Animals↗

PubMed1975

Delayed hypoxic encephalopathy without cognitive dysfunction.

Three days after an episode of hypoxia, a 20-year-old man developed profound motor deficit in the absence of behavioral or cognitive disturbance. Previous reviews of delayed hypoxic encephalopathy have stressed behavioral and cognitive disturbances as the initial symptoms. This patient's pyramidal tract dysfunction in the absence of higher cortical dysfunction serves to illustrate that delayed hypoxic encephalopathy is predominantly a white matter rather than a gray matter disorder.

Adult↗

PubMed1977

Macular cherry-red spots and beta-galactosidase deficiency in an adult. An autopsy case with progressive cerebellar ataxia, myoclonus, thrombocytopathy, and accumulation of polysaccharide in liver.

An adult patient with macular cherry-red spots, a gargoyle-like physical appearance, cerebellar ataxia, myoclonus, convulsive seizures, and pyramidal tract signs showed a profound deficiency of beta-galactosidase in liver and brain. Thrombocytopathy of undetermined etiology was evident since childhood, and the patient died of intracranial bleeding at age 22. Cerebral ganglioside pattern was normal. Hepatic mucopolysaccharides were not increased. GM1-gangliosidosis and mucopolysaccharidosis were ruled out by those analytical data. However, a large amount of amylopectin-like polysaccharide was found to be accumulated in liver. Hepatocyte contained numerous inclusion bodies with granulofibrillary structure similar to Lafora bodies, corpora amylacea, and inclusion bodies in glycogenosis type IV. This case seems to represent a new inborn metabolic disease closely related to GM1-gangliosidosis and mucopolysaccharidosis. The primary metabolic defect is not known at present.

Adult↗

PubMed1977

Prognosis in hereditary amyotrophic lateral sclerosis.

Two different forms of hereditary amyotrophic lateral sclerosis (ALS) has been separated according to duration of illness. A rapid course with short survival as seen in sporadic ALS is usual, but a comparatively benign type with a mean survival of 12 years has been reported in some families. Four patients from an ALS-afflicted family with five affected members in three generations were examined and then followed up. A conspicuous variability in progression among the patients was observed, with death occurring from 26 months to 12 years after onset; one patient is alive 13 years after onset. Wide differences were also found with respect to initial site of involvement and pyramidal tract signs. Three other families with this mixed pattern of prognosis have been reported previously. Affected individuals within involved families had either short or long duration of the disease, rather than displaying a continuum. However, in view of the existence of a type of hereditary ALS with marked intrafamilial variability, prognosis, even in the presence of previous benign cases, should be cautiously given.

Adult↗

PubMed1980

Progressive bulbar paralysis associated with neural deafness. A nosological entity.

A complete autopsy verification of progressive bulbar palsy associated with neural deafness was performed. Hearing loss and speech difficulties developed in a five-year-old girl. When she was 24 years old, clinical examination demonstrated deafness and bulbopontine paralysis together with retinitis pigmentosa, peripheral amyotrophies, pyramidal signs, and ataxia. The patients died at 27 years and the autopsy disclosed degenerative changes characterized by simple atrophy and loss of neurons accompanied by gliosis and loss of myelinated fibers. The structures principally affected were the anterior horns and the motor nuclei of the brain stem together with the eighth cranial nerve nuclei. Loss of myelinated fibers was found in the spinocerebellar and pyramidal tracts and in the fasciculus gracilis. Our study suggests that progressive bulbar paralysis with neural deafness should be considered as a nosological entity.

Adolescent↗

PubMed1982

Hereditary proximal spinal and bulbar motor neuron disease of late onset. A report of six cases.

Six cases of a comparatively rare motor neuron disease are described. Essential features of this syndrome include (1) X-linked inheritance; (2) adult onset in the fourth to fifth decades; (3) slow progression; (4) predominant proximal and bulbar muscle involvement; and (5) absence of sensory or pyramidal tract signs. The previously reported finding of gynecomastia was absent, whereas longitudinal midline furrowing of the tongue was present in only one case. Electromyography in five patients revealed neurogenic changes. Muscle biopsies in two patients showed fiber type grouping with type I fiber predominance. The coexistence of this form of motor neuron disease and diabetes mellitus is prominent in family 2. It is important to recognize that these patients have a chronic, slowly progressive illness. The prognosis for longevity is good, although severe disability is inevitable. Management includes reassurance, supportive therapy, genetic counseling, and periodic testing for diabetes.

Chromosomes↗

PubMed1986

The role of glutamate in neurotransmission and in neurologic disease.

Glutamate is the putative neurotransmitter of several clinically important pathways, including cortical association fibers, corticofugal pathways such as the pyramidal tract, and hippocampal, cerebellar, and spinal cord pathways. The excitatory actions of glutamate are mediated by multiple, distinct receptor types and potent receptor antagonists have recently been developed. Glutamate also has neurotoxic properties and can produce "excitotoxic" lesions reminiscent of human neurodegenerative disorders. Abnormally enhanced glutamatergic neurotransmission may cause excitotoxic cell damage and lead to the neuronal death associated with olivopontocerebellar atrophy, Huntington's disease, status epilepticus, hypoxia/ischemia, and hypoglycemia. Pharmacologic manipulation of the glutamatergic system may have great potential for the rational treatment of a variety of neurologic diseases.

Animals↗

PubMed1993

The clinical spectrum of unruptured intracranial aneurysms.

OBJECTIVE: A retrospective study was performed to delineate the clinical characteristics of symptomatic unruptured aneurysms. DESIGN: Patient histories, operative reports, and angiograms in 111 patients with 132 unruptured aneurysms were reviewed. SETTING: Tertiary care university hospital. PATIENTS: One hundred eleven patients with 132 unruptured intracranial aneurysms were studied. There were 85 women and 26 men, with a mean age of 51.2 years (age range, 11 to 77 years). Many patients were referred by community neurologists and neurosurgeons for further evaluation and neurosurgical management. RESULTS: Fifty-four symptomatic patients were identified. Group 1 (n = 19; mean aneurysm diameter, 2.1 cm) had acute symptoms: ischemia (n = 7), headache (n = 7), seizure (n = 3), and cranial neuropathy (n = 2). Group 2 (n = 35; mean aneurysm diameter, 2.2 cm) had chronic symptoms attributed to mass effect: headache (n = 18), visual loss (n = 10), pyramidal tract dysfunction (n = 4), and facial pain (n = 3). Group 3 (n = 57; mean aneurysm diameter, 1.1 cm) had asymptomatic aneurysms. CONCLUSIONS: Acute severe headache, comparable to subarachnoid hemorrhage headache, but without nuchal rigidity, was associated with the following mechanisms: aneurysm thrombosis, localized meningeal inflammation, and unexplained. Unruptured aneurysms may be misdiagnosed as optic neuritis or migraine, or serve as a nidus for cerebral thromboembolic events. Internal carotid artery and posterior circulation aneurysms were more likely to cause focal symptoms from mass effect than were anterior cerebral artery and middle cerebral artery aneurysms. Weeks to years may elapse before their diagnosis. The absence of subarachnoid blood does not exclude an aneurysm as a cause for acute or chronic neurologic symptoms.

Acute Disease↗

PubMed1996

Clinical and neuroradiological findings in classic infantile and late-onset globoid-cell leukodystrophy (Krabbe disease).

In the present study the clinical course and imaging of early and late-onset forms of Krabbe disease are analyzed. We report on 11 patients with a biochemical diagnosis of galactosyl ceramide beta-galactoside deficiency. Two presented as the classic infantile form and died within the second year of life. In 9 children the first clinical signs, such as gait difficulties and visual failure, started after age 2 years. All these patients developed slow regression of motor and mental capacities, and most of them died within their first decade. In patients of both groups computed tomography (CT) and magnetic resonance imaging (MRI) were performed. In the late-onset form, hypodensities of the central white matter and pyramidal tracts were the leading radiological signs, whereas in the early-onset form, hyperdensities and cerebellar white matter lesions were also detected. From our results it becomes clear that variability of Krabbe disease refers not only to clinical manifestation but also to CT and MRI findings. Better knowledge of phenotypic and radiological diversity will help to understand the pathogenesis of the disease.

Age of Onset↗

PubMed1996

Aprosencephaly and cerebellar dysgenesis in sibs.

Aprosencephaly is a rare, lethal malformation sequence of the central nervous system that has been attributed to a postneuralation encephaloclastic process. We describe autopsy findings consistent with aprosencephaly in 2 fetuses conceived from a consanguineous mating (first cousins). Both showed anencephalic manifestations; however, the crania were intact, with fused sutures. The neuropathologic findings were essentially identical. Each fetus had complete absence of the telecephalon and pyramidal tracts, rudimentary diencephalic and mesencephalic structures, primitive cerebellar hemispheres, posterolateral clusters of primitive neural cells in the medullas suggesting an abnormality of neural migration, a normally-formed spinal cord, and retinal dysplasia within normally-formed globes. In addition, both fetuses manifested a peculiar perivascular mesenchymal proliferation seen only within the central nervous system. The similarity of these cases, coupled with parental consanguinity, suggests a primary malformation in brain development due to the homozygous representation of a mutant allele. We hypothesize that these patients may represent a defect in a gene important in brain development, the nature of which has yet to be elucidated.

Abnormalities, Multiple↗

PubMed1996

Development of spinal cord projections from neocortical transplants heterotopically placed in the neocortex of newborn hosts is highly dependent on the embryonic locus of origin of the graft.

Previous experiments based on heterotopic transplantation paradigms have indicated that the distribution of efferents developed by layer V pyramidal cells seems to be related to where in the neocortex the cells develop and not to where they were generated. The present study was undertaken in an attempt to obtain a quantitative estimation of the weight of extrinsic factors in the development of neocortical efferents. Fragments of embryonic (E15-E19) frontal or occipital cortex were grafted homotopically or heterotopically into the frontal or occipital cortex of newborn rats. As adults, the hosts received an injection of a retrograde tracer into the pyramidal tract decussation, and the distribution of the subsequent cell labeling was examined in each category of transplant. The mean numbers of labeled cells were 725 in frontal-to-frontal transplants and 250 in frontal-to-occipital transplants. In occipital-to-frontal transplants, the numbers of labeled cells were extremely low, ranging from 0 to 14. Finally, as expected, practically no cell labeling was found in occipital-to-occipital transplants. Thus, transplants of presumptive frontal origin systematically develop and maintain in adulthood a spinal cord projection even though they are placed in the host occipital cortex. Conversely, transplants of presumptive occipital origin are practically incapable of maintaining a spinal cord projection in adulthood even though they are placed in the host frontal cortex. It seems, therefore, that the generation of regional differences in efferent connectivity found in the mature cortex depends on early regional specification within the neocortical neuroepithelium.

Animals↗