Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cerebral Decortication”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

Effect of substantia nigra stimulation on identified neurons in the VL-VA thalamic complex: comparison between intact and chronically decorticated cats.

The effects of substantia nigra (SN) stimulation on the activity of the nucleus ventralis lateralis of the thalamus (VL) have been studied. The VL cells were identified as relay or non-relay cells among the cerebellothalamocortical pathway on the basis of orthodromical activation from the cerebellum and antidromical activation from the cortex. Certain experiments were performed after wide pericruciate decortication in order to eliminate the response due to unavoidable activation of corticofugal fibers. These results show that nigrothalamic neurons exert an inhibitory effect on VL cells. This inhibition was observed on the relay as well as on non-relay cells and was strong enought to suppress the cerebellar monosynaptic excitatory input. Thus the SN can modulate the information running along the cerebellothalamocortical pathway. The topographic localization of inhibited cells suggests that the SN controls the activity of the thalamic neurons which interfere with axial and proximal musculature.

Animals↗

Decortication abolishes place but not cue learning in rats.

The experiments examined whether decorticate rats are able to acquire a place learning strategy, as compared with a cue learning strategy, to successfully navigate from one place to another and whether the hippocampus, in the absence of the neocortex, contributes to successful performance. Decorticate rats, with or without hippocampectomy, were unable to locate an "invisible" platform submerged at a fixed place in a tank of cool water (made opaque by milk), rather they scrabbled at the edges of the tank and failed even to initiate search strategies. They were able to learn to swim directly to the platform if it was visible. Their ability to find the hidden platform was not enhanced by presurgical experience or two-stage ablations with training before and after ablations. When pretrained on the cue task and tested on the place task, they learned to inhibit scrabbling at the tank edges and "search" in a haphazard fashion for the hidden platform, but they never learned to swim directly toward it. When decorticate rats, trained on the cue task, received superior colliculus or basal ganglia removal in a second operation, cue learning was abolished. Hippocampal removal after decortication left performance on the cue task unaffected. The results demonstrate: (1) the integrity of the neocortex is essential for place learning; (2) the brainstem, including superior colliculus and basal ganglia, is sufficient for cue learning; and (3) in the absence of the neocortex the hippocampus plays no role in guiding either type of navigation. It is concluded that sensorimotor subsystems of the forebrain play a special role as detector-response systems for guiding behaviour in response to constellations of distal stimuli, whereas subcortical structures are sufficient for navigation to a single stimulus.

Animals↗

Discharges of forelimb spindle primary afferents during locomotor activity in the decorticate cat.

In the acute decorticate cat, the discharge patterns of single spindle primary afferents from various forelimb muscles during locomotion have been examined in relation to the extrafusal activity. In a given muscle under isometric conditions, the activation of spindle primary endings was closely related to that of extrafusal muscle fibers. Since this increase in spindle discharge could occur in the absence of detectable electromyographic activity in the parent muscle, it resulted, at least to some extent from an enhanced activity in gamma efferents. The data are discussed in relation to previous studies of forelimb efferent activity and hindlimb fusimotor control in the same preparation.

Animals↗

Immunohistochemical localization of metabotropic glutamate receptors mGluR1a and mGluR2/3 in the rat basal ganglia.

Metabotropic glutamate receptors (mGluRs), which couple glutamate to second messengers, have important roles in the regulation of movement by the basal ganglia. We used two polyclonal antisera to mGluR1a and mGluR2/3 and confocal laser microscopy to investigate the localization of these receptors in the basal ganglia of the rat. The mGluRs were visualized in combination with an antibody to tyrosine hydroxylase (TH), an antibody to microtubule-associated protein 2 (MAP2, a dendritic marker), or SV2 (an antibody to a protein associated with presynaptic terminals). In the neostriatum, punctate mGluR1a immunoreactivity (ir) was present in the neuropil. This staining did not colocalize with MAP2-ir or SV2-ir and was not altered by decortication or unilateral 6-hydroxydopamine (6-OHDA) lesions. In the globus pallidus and substantia nigra pars reticulata, however, mGluR1a-ir was tightly clustered along large MAP2-ir dendrites. In contrast to the variations in mGluR1a-ir staining, similar punctate neuropil mGluR2/3-ir staining was observed within all basal ganglia structures. In the neostriatum, these puncta were abundant; unlike mGluR1a, many mGluR2/3-ir puncta colocalized with SV2-ir, and striatal mGluR2/3-ir puncta were markedly reduced in number after decortication. Neither mGluR1a-ir nor mGluR2/3-ir could be detected in TH-ir soma within substantia nigra pars compacta, or in TH-ir striatal terminals. Overall, our observations suggest that mGluR1a and mGluR2/3 receptors have distinct cellular localizations in different components of the basal ganglia circuitry and are likely to subserve distinct functions. Our data support the presence of mGluR2/3 on the terminals of corticostriatal afferents, where they may regulate glutamate release. In contrast, mGluR1a appears to be a postsynaptic receptor of neurons in the neostriatum, globus pallidus, and substantia nigra pars reticulata.

Animals↗

Synaptic localization of striatal NMDA, quisqualate and kainate receptors.

Striatal binding of labeled glutamate to N-methyl-D-aspartate (NMDA) receptors, D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) to quisqualate receptors and kainate to kainate receptors was examined in rats which had received unilateral decortications or unilateral striatal quinolinic acid lesions. One week after decortication, there were no significant changes in NMDA, quisqualate or kainate receptors in the striatum ipsilateral to the lesion, when compared to the striatum contralateral to the lesion. In contrast, binding to NMDA receptors was reduced by 92%, to quisqualate receptors by 80% and to kainate receptors by 81% in striatum 3 months after quinolinic acid lesions. The reduction in NMDA receptor binding was significantly greater than the loss of quisqualate or kainate receptors. These results suggest that NMDA, quisqualate and kainate receptor recognition sites are located postsynaptically in the striatum. These results also have implications for the quinolinic acid model of Huntington's disease.

Animals↗

Habituation of heart rate in functionally decorticate rats.

Habituation of acoustically evoked heart rate responses and retention of this habituation was studied in functionally decorticate rats. An improved technique to induce cortical spreading depression (CSD) resulted in a pronounced and continuous depression of electroencephalographic activity. In Experiment 1, short-term habituation (STH) was demonstrated in decorticate rats and surgical controls; long-term habituation (LTH, 24 hr) occurred only in intact animals. In Experiment 2, only CSD groups were used. As in the first experiment, STH but not LTH was obtained under CSD. However, there was clear evidence that habituation could be retained subcortically for 30 min. It is concluded that the rat's cortex is not necessary for habituation of acoustically evoked heart rate responses and retention of this habituation over a moderately long interval. However, the results suggest that the cortex is involved in LTH and that the neuronal substrates of STH and LTH are, in significant part, different.

Acoustic Stimulation↗

Frontal decortication eliminates drug-induced ascorbic acid release in the striatum but not the nucleus accumbens of freely moving rats.

The mechanism of morphine-, methamphetamine-, and nicotine-induced ascorbic acid (AA) release in the striatum and nucleus accumbens (NAc) is not well understood. In the present study, the roles of the corticostriatal and corticoaccumbens pathways in drug-induced AA release were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD). The results showed that morphine (20 mg/kg), methamphetamine (3.0 mg/kg), or nicotine (1.5 mg/kg) intraperitoneally (i.p.) significantly stimulated AA release in the striatum to more than 180%, 190%, and 140% compared with saline groups, respectively. These effects could be completely eliminated by frontal decortication, or antagonized by MK-801 (1.0 mg/kg). Moreover, methamphetamine or nicotine also significantly induced AA release in the NAc to more than 180% and 150% compared with saline groups, respectively. However, these effects could not be eliminated by frontal decortication. Although the effects of methamphetamine or nicotine in the NAc could be antagonized by MK-801, two-way ANOVA analysis did not show a significantly interaction between MK-801 and methamphetamine, or nicotine. The results indicates that the corticostriatal glutamatergic pathway may be a common and necessary pathway in drug-induced AA release in the striatum, but the corticoaccumbens glutamatergic pathway may not be crucial in drug-induced AA release in the NAc. The present study implies that different mechanisms might be involved in drug-induced AA release in the striatum and the NAc in rats.

Animals↗

Recovery from early cortical damage in rats. II. Effects of experience on anatomy and behavior following frontal lesions at 1 or 5 days of age.

Perinatal cortical damage is often associated with significant overall shrinkage of the remaining cortex and severe behavioral impairments. Environmental experience was manipulated in order to determine if the anatomical and behavioral effects of neonatal frontal decortication might be attenuated by rearing in a complex environment. Rats received frontal decortication on the day of birth or 5 days later and were subsequently raised, along with littermate controls, in a complex environment or in standard laboratory cages. In adulthood, the animals were tested on a battery of behavioral tests which showed that enrichment markedly attenuated the effects of the early lesions, especially for the 5-day operates, even on tests such as tongue extension that would not be expected to benefit from specific practice in the complex environment. Analysis of the remaining cortex revealed that all groups raised in the complex environment developed thicker cortex, the increase being most dramatic in the rats given lesions at 5 days of age.

Animals↗

[Changes in evoked cortico-motor responses in the rat during aging and after partial decortication].

Some changes of the organization of cortical motor representations, which were revealed by means of the intracortical microstimulation (ICMS) in aged rats after unilateral partial decortication, were true consequences of the decortication, but had no significant relationship to the aging. Distributions of latent periods of contralateral hind-leg EMG-responses to the ICMS had no significant shifts both during aging and after the surgery. Values of short-latency responses of ipsilateral proximal and axial muscles to the ICMS were in late time periods, from 8 to 16 months after surgery, significantly lower than ones of contralateral homonymous muscles. It is supposed, that ipsi- and bilateral short-latency responses to the ICMS in proximal and axial muscles of operated rats during late time periods are relayed through some pathways from the brain stem to the spinal cord.

Age Factors↗

[Polarization of terminals of the primary afferents of the lumbar region of the spinal cord during fictitious locomotion].

Changes in electric polarization of lumbosacral primary afferent terminals were studied during fictious locomotion of immobilized decorticated and spinal cats. Fictitious locomotion was accompanied by a stable hyperpolarization of afferent terminals. In the presence of hyperpolarization a periodic depolarization took place with the rhythm of efferent activity. These tonic and phasic changes were observed in the terminals of all the studied groups of afferent fibres (cutaneous and muscle Ia and Ib). Periodic depolarization was in-phase indifferent ipsilateral lumbosacral segments. During fictitious gallop the changes in depolarization of primary afferent terminals were in-phase on different sides; during fictitious walking these periodic changes were of out-of-phase character. Physiological significance of changes in electric polarization of primary afferent terminals by the spinal locomotor generator is discussed on the basis of the data obtained.

Animals↗

Cellular and network models for intrathalamic augmenting responses during 10-Hz stimulation.

Repetitive stimulation of the thalamus at 7-14 Hz evokes responses of increasing amplitude in the thalamus and the areas of the neocortex to which the stimulated foci project. Possible mechanisms underlying the thalamic augmenting responses during repetitive stimulation were investigated with computer models of interacting thalamocortical (TC) and thalamic reticular (RE) cells. The ionic currents in these cells were modeled with Hodgkin-Huxley type of kinetics, and the results of the model were compared with in vivo thalamic recordings from decorticated cats. The simplest network model demonstrating an augmenting response was a single pair of coupled RE and TC cells, in which RE-induced inhibitory postsynaptic potentials (IPSPs) in the TC cell led to progressive deinactivation of a low-threshold Ca2+ current. The augmenting responses in two reciprocally interacting chains of RE and TC cells depended also on gamma-aminobutyric acid-B (GABAB) IPSPs. Lateral GABAA inhibition between identical RE cells, which weakened bursts in these cells, diminished GABAB IPSPs and delayed the augmenting response in TC cells. The results of these simulations show that the interplay between existing mechanisms in the thalamus explains the basic properties of the intrathalamic augmenting responses.

Animals↗

[Presynaptic mechanisms of the change in segmental responses accompanying the formation of the spinal locomotor generator in the cat].

It is shown on unanesthetized immobilized decorticated cats that spinalization of the animal leads to depolarization of the central afferent terminals, decrease of early polysynaptic responses in motoneurons and dorsal root potentials (DRP) evoked by stimulation of the low-threshold cutaneous and muscle afferents, increase of early polysynaptic responses and DRP evoked by stimulation of high-threshold muscle afferents, reduction in the activity of intermediate nucleus interneurons mono- and polysynaptically connected with primary afferents, rise of the activity of interneurons di- and oligosynaptically connected with primary afferents. Injection of DOPA into spinal animals leads to opposite changes. Dependence between changes in the state of segmental neuronal apparatus and the level of spinal locomotor generator activity are discussed on the basis of the data obtained.

Animals↗

The distribution and function of DL-[3H]2-amino-4-phosphonobutyrate binding sites in the rat striatum.

The binding of the glutamate-like radioligand, DL-[3H]2-amino-4-phosphonobutyrate (DL-[3H]APB), to L-glutamate-sensitive sites in the rat striatum was investigated. A single, saturable population of binding sites, indistinguishable from that characterized previously on rat whole brain synaptic membranes, was identified. The effects of specific lesions of the striatum: decortication; striatal injection of kainic acid; and 6-hydroxydopamine injections into the substantia nigra, were also examined. Specific DL-[3H]APB binding in the striatum was elevated significantly following decortication. An increase in the number of binding sites was found to be responsible for this enhancement in binding. Lesions of the postsynaptic targets of corticostriatal fibres reduced the number of DL-[3H]APB binding sites in the striatum without affecting binding site affinity. This finding suggests that L-APB sensitive excitatory amino acid receptors are located predominantly on membranes derived from structures postsynaptic with regard to the glutamatergic innervation. The possible physiological role of these receptors was examined using an in vitro release technique. Both L-glutamate and L-APB were found to facilitate potassium evoked [3H]dopamine release from striatal slices. This finding supports the proposed existence of functional acidic amino acid receptors on dopaminergic terminals in the striatum. These receptors may play an important role in the control of motor function.

Aminobutyrates↗

Striatal glutamatergic function: modifications following specific lesions.

The effects of specific lesions of the striatum: (a) hemidecortication; (b) striatal injection of (+/-) ibotenate; and (c) 6-hydroxydopamine injections into the substantia nigra, were investigated on specific [3H]glutamate binding to striatal membranes. One month after decortication, there was a substantial reduction of calcium-dependent, stimulated glutamate release from striatal slices, indicating effective loss of glutamatergic fibres. Striatal glutamate binding increased by approximately 30% and this supersensitivity could be attributed solely to an increased receptor density. Ibotenate lesions which destroy target neurones for the glutamatergic fibres (sparing terminals), reduced glutamate binding in the striatum, as did nigral 6-OHDA lesions which delete striatal dopaminergic terminals. This finding supports the concept of there being glutamate receptors on pre-synaptic dopamine terminals in the striatum, involved in regulation of dopamine release. 6-OHDA lesions also result in a supersensitivity of the dopamine receptors localized on the cortico-striatal afferent terminals, as evidenced by the enhanced ability of dopamine to inhibit the K+-evoked, calcium-dependent release of endogenous striatal glutamate.

Animals↗

Temporal resolution of gaps in noise by the rat is lost with functional decortication.

In Experiment 1 (n = 8), the rat's ability to detect brief gaps in white noise was measured by gap-produced inhibition of an acoustic startle reflex, elicited 100 ms after the gap. After bilateral application of KCl to the cortex, gaps as long as 15 ms provided no reflex inhibition; in contrast, the inhibitory threshold was between 2 and 4 ms in the saline control condition. In Experiment 2 (n = 13), noise pulses of 40, 50, or 70 dB were presented 20-500 ms before the startle stimulus, and in Experiment 3 (n = 5) noise offsets occurred so that the startle stimulus was presented at the end of a 2-30-ms gap. Noise pulses and offsets both inhibited reflex expression equally in saline- and KCl-treated animals. Differences between the normal (saline) functions of noise offsets and gaps suggest additional sensory processing with the longer lead time. The loss of gap sensitivity after KCl application indicates that gap processing, unlike pulses and offsets, depends on cortical mechanisms.

Animals↗

Subcortical nature of Pavlovian differentiation in the rabbit.

Normal, hemidecorticated and decorticated rabbits were trained to criterion in a Pavlovian light-tone differentiation situation using the nictitating membrane preparation. Neither hemidecortication nor total neodecortication had any significant effect on the acquisition of Pavlovian conditional responses and both types of lesion were accompanied by differentiation performance which was as good as, or better than, that shown by normal controls. There was an indication however, that total neodecortication produced a slight retardation in the initial acquisition of conditional responses to the positive conditional stimulus. Both hemidecortication and bilateral neodecortication increased conditional response onset latencies but did not affect unconditional response latencies. These data are consistent with the notion that the essential substrate for Pavlovian conditioning is subcortical and that the breadth of stimulus feature extraction is reduced by neodecortication. In the course of this study it was noted that neodecortication reduced the asymptotic body weight of animals in both the lesioned groups.

Acoustic Stimulation↗

Visual and auditory cortical lesions following acquisition of an intensity discrimination in rats fail to disrupt cross-modal transfer.

The effect of visual or auditory decortication on cross-modal transfer of an intensity discrimination was examined in rats. Twenty animals were first trained under either visual-auditory (V-A) or auditory-visual (A-V) cross-modal transfer (CMT) in a shuttlebox using a shock avoidance pardigm. Prior to the second training session, five of the A-V animals received auditory ablations and five V-A animals received visual ablations. The other 10 animals served as controls and received sham operations. The results reveal that CMT occurred in both experimental groups following cortical ablations. It is possible that information regarding stimulus intensity was transferred from a cortical region used during the original training session to the cortex used in the second or retraining session, prior to surgery. Alternatively, it may be that some subcortical structure (e.g. the amygdala, superior colliculus, or reticular formation) may be involved in CMT of intensity.

Acoustic Stimulation↗

Modulation of cortical and pyramidal tract induced motor responses by electrical stimulation of the basal ganglia.

Two general mechanisms based on anatomical studies are possible for modulation of motor activity by the caudate nucleus and globus pallidus. These mechanisms are: (1) modulation of the output of cortical neurons that exert motor influences; and (2) modulation of subcortical neurons that exert motor influences. Differentiation between these two mechanisms was accomplished in the present study by two experimental approaches, both of which employed the conditioning-test paradigm. The first approach was an investigation of caudate nucleus or globus pallidus modulation (conditioning stimulus) of flexor responses of the anterior tibialis muscle elicited by electrical stimulation of the sensorimotor cortex (test stimulus) or pyramidal tract (test stimulus). These investigations were carried out in the intact and in decorticate cats. The second approach was an analysis of modulation or cortically induced pyramidal tract responses (direct and indirect, D-I potentials) by conditioning shock trains delivered to various loci within the caudate nucleus or globus pallidus. Both approaches were designed to determine whixh inhibitory and facilitatory motor influences of the basal ganglia occurred at a cortical or subcortical level. Simultaneous stimulation of a locus within the caudate nucleus and the sensorimotor cortex evoked either an enhancement, reduction or no alteration of the cortically induced increase in flexor responses (measured by Ia afferent activity, EMG, myogram). In contrast, no inhibitory influences occurred from caudate nucleus stimulation upon pyramidal tract induced flexor responses in either the intact or decorticate preparation. Inhibitory loci were distributed toward the rostral portion of the caudate nucleus, whereas facilitatory loci were distributed throughout; this distribution was statistically significant (chi2; P less than 0.01). Only enhancement or no influence upon cortical induced or pyramidal tract induced responses were obtained by conditioning stimuli to the globus pallidus. In the unanesthetized but immobilized cat, trains of shocks delivered to the caudate nucleus enhanced, reduced or had no influence upon the cortically evoked direct (D) and indirect (I) potentials recorded in the bulbar pyramidal tract. The distribution of facilitatory and inhibitory loci was organized in a similar fashion as in theanesthetized preparation. From these observations, a model was proposed in which the output of the caudate nucleus exerts both facilitatory or inhibitory modulation of the tonically active globus pallidus cells. The latter in turn predominantly or exclusively facilitate output of pyramidal tract neurons as well as the output of subcortical structures; both effects facilitate motor responses at the spinal level.

Animals↗