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PubMed1990

Antibody to a soluble protein purified from brain selectively labels layer V corticofugal projection neurons in rat neocortex.

An antibody to a soluble protein (protein 36) isolated and purified from rat brain labels the cell bodies and processes of pyramidal cells within layer V of the rat neocortex. We have used the fluorescent retrograde axonal tracer, Fast blue, in combination with FITC immunocytochemistry to determine the projection sites of the cortical neurons detected by this antibody. Retrogradely labeled pyramidal tract neurons and corticotectal neurons are labeled with the protein 36 antibody, but the callosally projecting neurons within layer V are not. Thus within the neocortex the antibody to protein 36 may selectively detect a particular class of neuron, the corticofugal projection neurons of layer V.

Animals↗

PubMed1990

Microinjection of TRH analogs into the raphe pallidus stimulates gastric acid secretion in the rat.

The effects of microinjection of the stable thyrotropin-releasing hormone (TRH) analog, RX 77368, [pGlu-His-(3,3'-dimethyl)-Pro-NH2] into the raphe pallidus on gastric acid secretion were studied in urethane-anesthetized rats with gastric fistula. RX 77368 microinjected into the raphe pallidus at doses of 0.07, 0.7 and 7.7 pmol induced a dose-dependent net stimulation of gastric acid secretion (7 +/- 4, 50 +/- 7 and 61 +/- 12 mumol/h respectively). The peak acid response was reached within 30 min and returned to basal level 90 min post-injection. The stimulatory effect was abolished by bilateral cervical vagotomy and pirenzepine pretreatment (1 mg/kg, i.v.). RX 77368 (7.7 pmol) microinjected into the inferior olive or pyramidal tract induced smaller or no gastric acid secretory response. These results demonstrate that chemical stimulation of the raphe pallidus increases gastric acid secretion through vagal pathways and peripheral muscarinic receptors. These data suggest that the nucleus raphe pallidus may be involved in vagal modulation of gastric acid secretion in the rat.

Animals↗

PubMed1990

Effects of protein kinase C inhibitor H-7 on membrane properties and synaptic responses of neocortical neurons of awake cats.

Electrophysiological effects of intracellularly pressure-injected H-7, an inhibitor of protein kinase C, were investigated in neocortical neurons of awake cats. H-7 reduced spontaneous and depolarizing current-induced firing activity and increased the latency and apparent threshold of action potentials elicited by depolarizing currents. Slow afterhyperpolarizations following action potentials and depolarizing pulses increased after injection of H-7, without detectable changes in the time course of the fast components of the action potentials. H-7 induced increases in IPSPs evoked by stimulation of the ventrolateral thalamus (VL) or the pyramidal tract (PT). Besides slight increases in the amplitude of IPSPs measured at peak, H-7 induced pronounced increases in the amplitude measured 50-100 ms after stimulation and in the total duration of IPSPs. EPSPs evoked by VL or PT stimulation did not show measurable alterations after injection of H-7. The effects occurred 2-15 min after injection of H-7 and lasted at least 90 min without essential changes in the baseline values of resting membrane potential or input resistance. The results suggest that in addition to playing a role in regulating membrane excitability, protein kinase C influences the inhibitory synaptic mechanisms of neocortical neurons.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1994

Neostriatal modulation of motor cortex excitability.

The influence of the basal ganglia motor loop on motor cortex function was examined by pharmacologically altering neostriatal activity while monitoring the electrical stimulation thresholds for eliciting movements of the ipsilateral and contralateral motor cortex in ketamine anesthetized rats. Repeated unilateral intraneostriatal infusions (1-3) of the glutamate agonist, kainic acid (0.1 microliter, 75 ng), or glutamate (0.3 microliter, 1.65 micrograms) reliably increased ipsilateral but not contralateral cortical thresholds. Single infusions of kainic acid (0.3 microliter, 150 or 225 ng) elevated ipsilateral cortical thresholds for 30-45 min; with glutamate (0.3 microliter, 1.65 micrograms), the change lasted less than 10 min. Antidromically identified striatonigral projection neurons (n = 8) located approximately 500 microM from the infusion cannula, showed either increased firing (n = 4) for less than 10 min following glutamate infusion or no change from their non-firing state (n = 4). Non-antidromically activated neurons (n = 3) were all excited by the infusion, although an interval of inhibition preceded or followed the excitation in two cases. Infusions (0.3 microliter) of inhibitory agents (GABA, 31 and 310 ng; muscimol 34.2 ng; and DNQX 34.2 ng) did not alter cortical threshold, nor did saline vehicle. Lesion of the ventrolateral but not ventromedial thalamic nucleus prevented the modulation of cortical thresholds following intraneostriatal infusion of 225 ng kainic acid. Thus the neostriatal alteration of cortical thresholds indicates a modulation of cortical excitability via thalamic projections and not the outcome of competing descending cortical and neonstriatal influences converging on motorneurons. These results suggest that tonic feedforward modulation of the motor cortex and the pyramidal tract by the basal ganglia can be inhibitory.

Animals↗

PubMed1979

Inhibition in penicillin-induced epileptic foci.

A previous study indicated that the early surface negative component (associated with recurrent inhibition) of the evoked potential recorded from cat pericruciate cortex, subsequent to pyramidal tract stimulation, was altered after application of penicillin to the cortical surface (Van Duijn et al. 1973). This suggested that decreased effectiveness of recurrent inhibition might be the basis for epileptogenicity of penicillin. To verify that recurrent inhibition is functionally decreased in the penicillin epileptic focus and to assess alternative sites for penicillin action, this phenomenon was investigated at the cellular level. Neurons were recorded extracellularly and response to stimuli monitored throughout the transition from normal cortex to epileptogenic cortex. Stimuli employed were peduncular stimulation (to test recurrent inhibitory pathways), epicortical stimulation (to test inhibitory pathways, bypassing the recurrent collateral system), and forepaw footpad shock (to test the responsiveness ofneurons to afferent input). In normal cortex, PT cells were inhibited by peduncular or epicortical stimulation and excited by forepaw stimulation, with the excitation followed by a period of inhibition. In the penicillin focus, inhibition was not observed in response to any of the 3 stimuli, and the excitatory response to forepaw stimulation was maintained. The bursting non-PT cells, most likely candidates for interneurons, exhibited excitation in response to peduncular and epicortical stimulation, consistent with involvement in inhibitory pathways. Nonetheless, in the penicillin focus, excitatory response to peduncular and epicortical stimulation was maintained. Excitatory response to forepaw stimulation was also maintained in the penicillin focus. The results demonstrate a loss of effectiveness of recurrent inhibition measured at the PT cell body in the penicillin focus. Further, the reduction in inhibitory feedback occurs in conjunction with maintained or enhanced excitability of the neurons which are most likely candidates for inhibitory interneurons. Thus, penicillin is most likely exerting its effect at the inhibitory synapses onto PT cells in the cortex, thereby allowing excitatory input to have greater influence on neuronal firing.

Animals↗

PubMed1979

Convulsive effects of 3-aminopyridine on cortical neurones.

The authors examined the effects of 3-aminopyridine (3-AP) on pyramidal tract neurones in the motor cortex of anesthetised cats. 3-AP proved to be a strong convulsive agent. Local application of 3-AP in concentrations of 15-20 mM resulted in typical paroxysmal alterations of neuronal activity: (a) enhancement of background firing, (b) augmentation of EPSPs, (c) depression of IPSPs and (d) single and serial paroxysmal depolarization shifts (PDSs). Serial PDSs were reflected by large synchronous waves in the surface ECoG.

Administration, Topical↗

PubMed1983

Studies on the human spontaneous electromyelogram (EMyeloG). II. Patients with peripheral nerve, root and spinal cord disorders.

Using an intrathecal recording technique the spontaneous electromyelogram (EMyeloG) was recorded in 44 patients having peripheral nerve, spinal root and lower motor neurone disorders (17 cases), suprasegmental spinal cord disorders (18 cases) and diffuse involvement of the posterolateral funiculus or spinal ganglia (9 cases). In the first 17 cases, labelled as 'afferent group,' the spontaneous EMyeloG was significantly reduced, parallelling the paucity of afferent signals entering the spinal cord. However, the spontaneous EMyeloG was found to be normal in cases with the diffuse anterior horn cell involvement and motor polyneuropathy. In the second 18 cases labelled as 'efferent group,' the spontaneous EMyeloG was more prominent and the amplitude and frequency of the spontaneous cord potentials were significantly increased. Especially in patients with spastic paraparesis various peripheral afferent stimuli could produce more significant facilitation of the EMyeloG in the 'efferent group' than in normal subjects. In the third group labelled as 'mixed group' a different type of abnormal spontaneous action potentials was observed in addition to increase of the spontaneous EMyeloG. These potentials were positive or mainly positive and their duration was long, being 10-25 msec. It was concluded that the human spontaneous EMyeloG recorded from an intrathecal electrode probably originates from the interneurones of the posterior horns, facilitated by peripheral afferent inputs and inhibited by suprasegmental descending pathways, especially the pyramidal tract.

Cerebellar Ataxia↗

PubMed1986

Electrical stimulation over the human vertebral column: which neural elements are excited?

Supramaximal percutaneous electrical stimuli applied over the human cervical vertebral column produce maximal compound muscle action potentials (CMAPs) in abductor digiti minimi. It is important to know which neural elements are excited by these stimuli and experiments were performed to answer this question. With stimulating electrodes placed progressively lateral to the midline, submaximal CMAPs with the same latency are produced. With shocks over the cervical vertebrae in the midline, the threshold for excitation of arm muscles is much lower than for excitation of leg muscles. Comparison of conduction time from the cervical column to more distal sites on the ulnar nerve by direct measurement and by F wave latency determination shows that the latter exceeds the former by 1.6 msec. Collision experiments in which paired shocks were given at the wrist and Erb's point or the wrist and cervical column showed that recovery from blocking as interstimulus interval lengthened was similar for the two sites, and that it was possible to detect F waves from the proximal stimulus. The latency of CMAPs evoked from midline surface stimuli was identical to that from a needle stimulus near the C8 root. It is concluded that electrical stimuli applied over the cervical vertebrae in the midline excite the motor roots at their exit from the spinal canal. This finding has implications for clinical studies of pyramidal tract and proximal peripheral nerve conduction.

Action Potentials↗

PubMed1992

Thyrotropin-releasing hormone analog injected into the raphe pallidus and obscurus increases gastric contractility in rats.

The present study was performed to investigate the influence of the chemical stimulation of medullary raphe nuclei by the stable TRH (thyrotropin-releasing hormone) analog, RX 77368, on gastric contractility. Urethane-anesthetized rats were acutely implanted with miniature strain gauge force transducers on the corpus of the stomach for continuous recording of gastric contractility. Traces were analyzed by computer. Microinjections of vehicle or RX 77368 into the raphe pallidus or raphe obscurus were performed using pressure injection of 50 nl through glass micropipettes 30 min following basal recording of gastric contractility. RX 77368 (0.7-77 pmol) dose dependently stimulated gastric contractility when microinjected into the raphe pallidus and raphe obscurus. The stimulation of gastric contractions induced by microinjection of RX 77368 (77 pmol) into these raphe nuclei was completely blocked by vagotomy and prevented (raphe obscurus) or reduced (raphe pallidus) by atropine. RX 77368 (7.7-77 pmol) microinjected into the inferior olive, pyramidal tract, medial lemiscus was ineffective. These results demonstrate that chemical stimulation of the raphe pallidus and obscurus by RX 77368 stimulates gastric contractility through vagal and muscarinic pathways. These data suggest a role for medullary raphe nuclei in the central vagal regulation of gastric contractility.

Animals↗

PubMed1983

Changes in extracellular potassium and calcium concentration and neural activity during prolonged electrical stimulation of the cat cerebral cortex at defined charge densities.

In cats anesthetized with nitrous oxide and halothane, ion-selecting microelectrodes were used to monitor changes in the concentration of potassium [K+]0 and calcium [Ca2+]0 in the extracellular compartment of the cerebral cortex during as long as 4 h of continuous stimulation of the cortical surface. At stimulus charge densities shown to induce only minimal localized histologic changes [20 microC/cm2 . ph at 50 pulses per second (pps)], [K+]0 at a depth of about 750 micrometers underwent only a transient increase at the beginning of stimulation, followed by a rapid return to the prestimulus concentration. [Ca2+]0 was unaffected. At a higher charge density (100 microC/cm2 . ph at 20 pps) there was a rapid transient increase in [K+]0, followed by a more gradual return to a plateau about 1 mM above the prestimulus value. [Ca+]0 usually underwent an initial increase followed by a slow decrease to a plateau value above 0.5 mM. At a charge density of 100 microC/cm2 . ph and 50 pps (shown in histological studies to induce significant neural damage), [Ca2+]0 slowly decreased to near or below 0.5 mM in the middle layers of the cortex. After 30 to 40 min of stimulation, [K+]0 underwent episodic fluctuations about a plateau value 0.5 to 1 mM above the prestimulus concentration. Simultaneous recordings of the compound action potential in the ipsilateral pyramidal tract indicated that these fluctuations were due to local changes in the excitability of intracortical circuitry conditioned by the intense stimulation. The results have implications for the possible interrelation of the changes in extracellular ionic concentrations and the early stages of stimulation-induced neural damage.

Animals↗

PubMed1984

Effects of claustrum stimulation on spontaneous bioelectrical activity of motor cortex neurons in the cat.

Electrophysiologic interactions between claustrum and motor cortex neurons were investigated in the cat. A total of 136 neurons was recorded from the motor cortex in area 4 (90 cells) and in area 6 (46 cells). Ninety-eight of the total neurons were identified as pyramidal tract neurons (PTNs). Stimulation of the claustrum by single shocks or by trains of stimuli imposed on the tested PTNs a pure long-lasting inhibition, or a long-lasting inhibition preceded by a short early activation, or no effect. No functional localization of the effects of claustrum activation were found within the motor areas. The observed results are consistent with the hypothesis that the claustrum may play a role in movement organization.

Action Potentials↗

PubMed1986

Neuronal activity evoked by chronically implanted intracortical microelectrodes.

The averaged evoked compound action potentials (AECAPs) were recorded from the ipsilateral pyramidal tract of awake, unrestrained cats before, during, and after continuous electrical stimulation of the cerebral cortex via chronically implanted activated iridium or platinum-30% iridium (Pt30%Ir) microelectrodes. After stimulating 24 h at 20 pulses per second (pps), using charge-balanced, 200-microseconds pulse pairs of 40 to 80 microA (400 to 800 microC/cm2, 8 to 16 nC/phase (ph), 2 to 4 A/cm2), there was a transient elevation of the threshold of the early (direct) and of the alte (transynaptic) components of the AECAP. After cessation of continuous stimulation at 80 microA, the threshold of the early component of the AECAP remained elevated for as long as 24 h and the late component as long as 4 days, indicating significant but reversible depression of the electrical excitability of cortical neurons close to the microelectrodes. In three cats stimulated 23 h/day for 1 week, the AECAP also recovered to their prestimulus threshold. In contrast, pulsing for 24 h at 320 microA (3200 microC/cm2, 64 nC/ph, 16 A/cm2) produced marked elevation of the threshold of the AECAPs which was not reversed by 7 to 12 days after termination of intracortical stimulation. The electrical excitability of neurons adjacent to (unpulsed) microelectrodes 2 mm from the pulsed electrode was not affected. The observations reported here, in conjunction with the histologic results reported in the companion paper, indicate that both the Pt30%Ir and the iridium microelectrodes can be operated safely at currents to at least 80 microA, charge/ph of 16 A/cm2, and a charge density of 800 microC/cm2 X ph. However, on the basis of the electrophysiologic criteria, both types appear to be unsafe when pulsed at 320 microA (64 nC/ph, 3200 microC/cm2 X ph, 16 A/cm2).

Action Potentials↗

PubMed1986

Histopathologic evaluation of prolonged intracortical electrical stimulation.

Chronic stimulating microelectrodes fabricated from platinum-30% iridium (Pt-30%Ir) or activated iridium were implanted in assemblies of three in the left sensorimotor cortex of the cat and pulsed continuously at currents of 10 to 320 microA (100 to 3200 microC/cm2 X ph, 2 to 64 nC/ph) for periods of 24 h or for 23 h/day for 7 days. The microelectrodes had beveled tips with uninsulated geometric surface areas of 20 X 10(-6) cm2. Neuronal activity evoked by the focal stimulation was monitored by recording compound action potentials from the ipsilateral pyramidal tract. By this criterion neuronal activation thresholds were 5 to 15 microA (50 to 150 microC/cm2 X ph, 1 to 3 nC/ph) for both types of electrodes. Histologic evaluations of tissue surrounding the electrode tips were carried out by either light or electron microscopy. No neural damage was induced by 24 or 161 h of pulsing using either type of electrode at currents of 10 to 80 microA. Neural damage attributable to electrical stimulation per se was observed in a few sites pulsed with 320 microA (3200 microC/cm2 X ph, 64 nC/ph, 16 A/cm2) with Pt-30%Ir but not activated iridium electrodes of the same size. Electrode dissolution appears to be best correlated with charge density and current density. Dissolution of the Pt-30%Ir microelectrode tip was observed by scanning electron microscopy at charge densities as low as 200 microC/cm2 X ph (1 A/cm2), whereas erosion of activated iridium microelectrodes occurred only at the highest charge and current densities (3200 microC/cm2 X ph, 16 A/cm2). Thus, the activated iridium electrode is superior to Pt-30%Ir for chronic stimulations, from the standpoint of electrode tip stability, because with the former, in contrast to the alloy, detectable erosion occurred only at an intensity well above that required for activation of nearby neurons.

Animals↗

PubMed1975

An unusual form of spinal muscular atrophy with mental retardation occurring in an inbred population.

Three sibs are described suffering from hereditary non-progressive spinal muscular atrophy with non-progressive mental retardation. One of them had in addition signs of pyramidal tract involvement. Muscular weakness was more pronounced proximally than distally and the neck muscles were severely involved. Th.ey all had small skulls and several associated congenital malformations were observed including syndactyly of the left hand in 1 patient. The patients belong to a small inbred community in the Netherlands. Erythropoietic protoporphyria was also present in the family but segregated independently. This combination of "congenital" mental retardation with "congenital" non-progressive spinal muscular atrophy is believed to represent a new syndrome, caused by a rare recessive gene.

Adult↗

PubMed1975

Reversible central nervous system dysfunction in folate deficiency.

An epileptic patient on chronic anticonvulsant drug therapy is described, in whom anaemia and neurological abnormalities including progressive dementia, bilateral pyramidal tract signs, incontinence and ataxia developed. Vitamin B12 serum levels and absorption were normal, but serum folic acid levels were low. Both the neurological disturbances and anaemia resolved following oral folic acid administration. This sequence of events in our patient suggests a cause and effect relationship between the folate deficiency and the coexistent, transient neurological syndrome.

Aged↗

PubMed1976

Plasma lactate in anterior horn cell disease.

This communication reports biochemical findings in 7 patients with anterior horn cell disease. The diagnosis was confirmed by evidence of denervation in the EMG and mukle biopsy with normal motor conduction velocities. In 4 of these patients, upper extremities were involved in a symmetrical fashion. In 1, the upper and lower extremities were involved in a symmetrical fashion. In the other 2, one upper or lower extremity were respectively involved in isolation. Pyramidal tract signs were evident in 2 patients of this group. Seventh cranial nerve and 12th cranial nerve involvement were seen in 2 patients. None of the patients manifested 8th cranial nerve dysfunction. All of these 7 patients showed elevation of raised fasting plasma lactate, with normal plasma citrate and plasma pyruvate values. This is in contrast to the altered citrate and pyruvate levels described by other workers in other cases of anterior horn cell disease. The significant biochemical relationship are discussed.

Adolescent↗

PubMed1977

Motor neurone disease with neurofibrillary tangles in a Brazilian woman.

The occurrence of neurofibrillary tangles in both the cerebral cortex and brain stem is typically seen in the Guam type of amyotrophic lateral sclerosis, but is exceedingly rare in the classical form of the disease. Only 3 cases of sporadic amyotrophic lateral sclerosis with such histopathologic features have so far been reported, all in the United States. A 49-year-old Brazilian woman had an 18-month history of amyotrophic lateral sclerosis involving predominantly the left-sided extremities with prominent bulbar signs. Autopysi disclosed moderate to severe loss of motor neurones in the hypoglossal nuclei and anterior spinal horns, absence of pyramidal tract demyelination, depigmentation of the substantia nigra and numerous neurofibrillary tangles in the hypothalamic region, parahippocampal gyrus, reticular substance of the mesencephalon and pons and in some brain stem nuclei. The topographical distribution of these changes was closely similar to that of Guamanian amyotrophic lateral sclerosis.

Alzheimer Disease↗

PubMed1978

Familial communicating syringomyelia.

Calssical cervical syringomyelia was found in 3 members of one family. All 3 underwent air myelogram, and a Chiari malformation type I and postural collapse of the spinal cord was found in each case. An affected 7-year-old boy was discovered after a clinical and radiological survey of 8 first-degree relatives on the basis of mild scoliosis, pyramidal tract signs in the lower limbs and enlarged sagittal diameter of the cervical canal. One other member had basilar impression of the skull but no neurological abnormalities. No positive correlation was found between either the size of the cystic cord enlargement or descent of the ectopic tonsils with the duration or severity of the neurological findings. Suboccipital decompressive craniotomy and upper cervical laminectomy in one case was followed by improvement in strength and sensation 1 year later. Progression in familial syringomyelia appears to occur through a mechanism identical to that in the sporadic form and surgery is therefore also indicated. In affected families, routine survey of close relatives for abnormal neurological signs, and radiological evidence of scoliotic deformity of the spine, enlarged cervical canal and bone abnormalities at the craniovertebral junction may prove valuable for early detection. A dominantly inherited, genetically determined malformation seems to be the probable mechanism of inheritance in this family.

Adolescent↗