SEARCH · PubMed Health

Results for “cortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 1,549 records · Page 86Linked to original sources

PubMed1995

Increased sensitivity to the sensorimotor gating-disruptive effects of apomorphine after lesions of medial prefrontal cortex or ventral hippocampus in adult rats.

Sensorimotor gating of the startle reflex is impaired in humans with schizophrenia and in rats after mesolimbic D2 dopamine receptor activation. The loss of startle gating after D2 activation in rats has been used as an animal model of impaired sensorimotor gating in schizophrenia, because the ability of antipsychotics to restore startle gating in D2-activated rats correlates significantly with antipsychotic clinical potency. Substantial evidence indicates that the pathophysiology of schizophrenia includes structural and functional deficits in prefrontal and temporal regions, particularly the dorsolateral prefrontal cortex and the hippocampus and parahippocampal gyrus. The present study assessed startle gating in adult rats after ibotenic acid lesions of the medial prefrontal cortex or ventral hippocampus. Medial prefrontal cortex lesioned rats exhibited normal startle amplitude and normal sensorimotor gating, as reflected by prepulse inhibition (PPI) of the startle reflex. Hippocampus lesioned rats exhibited elevated startle amplitude, and similar to rats with medial prefrontal cortex lesions, did not show significant changes in basal PPI. Low doses of the mixed dopamine agonist apomorphine did not significantly reduce PPI in sham lesioned rats, but significantly disrupted PPI in both medial prefrontal cortex- and ventral hippo-campus lesioned rats. These data are consistent with the hypothesis that cell damage in frontal and temporal cortex increases the sensitivity to the sensorimotor gating-disruptive effects of dopamine receptor activation.

Animals↗

PubMedDate not supplied

Information synthesis in key parts of the cerebral cortex as the basis of subjective experience.

This paper discusses a number of principles of the organization of cerebral processes underlying subjective experiences. The concept developed here suggests that these experiences arise as a result of the synthesis of different types of information, this synthesis occurring in various parts of the cortex which have key roles in this mental function. The synthesis is made using information arriving from the external environment, information extracted from memory, and information arriving from motivational centers. The concept is based on studies of the cerebral mechanisms of perception and thought. Experiences are demonstrated to arise as a result of the synthesis, by neurons in the projectional cortex, of data describing the physical and informational properties of a stimulus; the mechanism of the synthesis is a circular movement of excitation from the projectional to the associative regions of the cortex, then to the hippocampus and motivational centers, with return of excitation to the projectional cortex. It is also demonstrated that the process of thought involves convergence of cortical connections on defined centers, which are called interaction foci. Different thought operations are associated with their own specific interaction focus topographies: in imaginative thinking, foci are located in the temporo-parietal cortex, while abstract thinking foci in the frontal cortex. It is suggested that information arriving by means of neural connections is compared and synthesized in interaction foci, and that this provides the basis for decision-making. The final part of this paper addresses the functional importance of mental phenomena and their possible effects on cerebral processes.

Cerebral Cortex↗

PubMed1993

Mechanism of decreased arachidonic acid in the renal cortex of rats with diabetes mellitus.

The purpose of this study was to investigate the roles of decreased synthesis and increased consumption in the depression of arachidonic acid levels in renal cortex and glomeruli of rats with streptozotocin-induced diabetes mellitus. In diabetic rats, arachidonic acid was depressed 33.2% in renal cortex, 47.4% in liver and 66.1% in heart compared to values of control rats. delta 6 Desaturase activity was depressed in renal cortex, liver and heart of diabetic rats to 53.3, 55.5 and 63.7%, respectively, of control values. delta 5 Desaturase activity was also depressed 43.7, 55.5 and 47.6% in renal cortex, liver and heart of diabetic rats, respectively. In other rats the activities of five enzymes involved in the synthesis and esterification of arachidonic acid were measured in renal cortex and in isolated glomeruli. Both tissues from diabetic rats showed depressed activities of delta 5 and delta 6 desaturases, increased activities of long-chain acyl-CoA synthetase and 1-acyl-sn-glycero-3-phosphocholine acyltransferase and no change in the activity of elongase as compared to those in control tissues. Malondialdehyde, an end product of lipid peroxidation, was lower in the renal cortex of diabetic rats than in control rats, whereas beta-oxidation of linoleic acid and arachidonic acid were similar in diabetic and in control rats. Basal and stimulated prostaglandin E2 synthesis were significantly higher in isolated glomeruli from diabetic rats compared to those in control rats. In isolated tubules, prostaglandin E2 synthesis was similarly low in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyl-CoA Dehydrogenase, Long-Chain↗

PubMed2004

Plasticity at hippocampal to prefrontal cortex synapses is impaired by loss of dopamine and stress: importance for psychiatric diseases.

The direct hippocampal to prefrontal cortex pathway and its changes in synaptic plasticity is a useful framework for investigating the functional operations of hippocampal-prefrontal cortex communication in cognitive functions. Synapses on this pathway are modifiable and synaptic strength can be turned up or down depending on specific patterns of activity in the pathway. The objective of this review will be to summarize the different studies carried out on this topic including very recent data and to underline the importance of animal models for the development of new and effective medications in psychiatric diseases. We have shown that long-term potentiation (LTP) of hippocampal-prefrontal synapses is driven by the level of mesocortical dopaminergic (DA) activity and more recently that stress is also an environmental determinant of LTP at these cortical synapses. Stimulation of the ventral tegmental area at a frequency known to evoke DA overflow in the prefrontal cortex produces a long-lasting enhancement of the magnitude of hippocampal-prefrontal cortex LTP whereas a depletion of cortical DA levels generates a dramatic decrease in this LTP. Moreover, hippocampal stimulation induces a transient but significant increase in DA release in the prefrontal cortex and an optimal level of D1 receptor activation is essential for LTP expression. We recently investigated the impact of stress on hippocampal-prefrontal LTP and demonstrated that exposure to an acute stress causes a remarkable and long-lasting inhibition of LTP. Furthermore, we demonstrated that tianeptine, an antidepressant which has a unique mode of action, and clozapine an atypical antipsychotic when administered at doses normally used in human testing are able to reverse the impairment in LTP. Stressful life events have a substantial causal association with psychiatric disorders like schizophrenia and depression and recent imaging studies have shown an important role of the limbic-cortical circuit in the pathophysiology of these illnesses. Therefore, we proposed that agents capable of reversing the impairment of plasticity at hippocampal to prefrontal cortex synapses have the potential of becoming new therapeutic classes of antidepressant or antipsychotic drugs.

Animals↗

PubMed1998

Investigation of the subtypes of alpha2-adrenoceptor mediating prejunctional inhibition in rat atrium and cerebral cortex.

We have investigated the subtype of alpha2-adrenoceptor mediating prejunctional inhibition of neurotransmission in rat atrium in comparison with the alpha2-adrenoceptor mediating prejunctional inhibition in rat cerebral cortex. In rat atrium and cerebral cortex, prejunctional alpha2-adrenoceptors were investigated in terms of the ability of alpha2-adrenoceptor antagonists to increase the stimulation-evoked overflow of tritium in tissues pre-incubated with [3H]-noradrenaline. The relatively non-selective alpha2-adrenoceptor antagonist yohimbine and the alpha2D-adrenoceptor selective antagonist BRL 44408 had potencies in rat atrium which were similar to their potencies in rat cerebral cortex. The antagonists ARC 239, HV 723, WB 4101, prazosin, chlorpromazine and abanoquil, which have low affinity for alpha2D-adrenoceptors, significantly increased stimulation-evoked overflow at lower concentrations in rat atrium than rat cerebral cortex. Antagonist potency at prejunctional alpha2-adrenoceptors was correlated with antagonist affinity at alpha2-adrenoceptor ligand binding sites in membranes of rat kidney (alpha2B) and submandibular gland (alpha2D), and human recombinant alpha2C-adrenoceptors labelled with [3H]yohimbine. The correlation between ligand binding sites and the functional receptor in the rat cerebral cortex was significant only for the alpha2D-adrenoceptor ligand binding site (r=0.87, n=8, P<0.01) as compared to the alpha2B-adrenoceptor (r=0.32, n.s.) or alpha2C-adrenoceptor (r=0.12, n.s.) ligand binding sites. The correlation between ligand binding sites and the functional receptor in the rat atrium was not significant for any ligand binding site, with r=0.64, 0.68 and 0.67 for the alpha2D-, the alpha2B- and the alpha2C-adrenoceptor ligand binding sites, respectively. It is concluded that the functional prejunctional alpha2-adrenoceptor of rat cerebral cortex closely resembles the alpha2D-adrenoceptor ligand binding site of rat submandibular gland, but the rat atrium may contain two subypes of prejunctional alpha2-adrenoceptor, alpha2D and another subtype, possibly alpha2B or alpha2C.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1998

Nociceptin inhibits noradrenaline release in the mouse brain cortex via presynaptic ORL1 receptors.

A fourth type of opioid receptor, termed ORL1, has been cloned and nociceptin (also known as orphanin FQ) has been identified as an endogenous ligand at this receptor. We examined whether nociceptin affects the release of noradrenaline in the brain. For this purpose, cerebral cortex slices from the mouse, rat or guinea-pig were preincubated with [3H]noradrenaline and then superfused with medium containing desipramine and rauwolscine. Tritium overflow was evoked electrically (0.3 Hz) or by introduction of Ca2+ 1.3 mM into Ca2+-free K+-rich (15 mM) medium. Nociceptin 1 microM reduced the electrically evoked tritium overflow from mouse, rat and guinea-pig brain cortex slices by 80, 71 and 36%, respectively. Naloxone 10 microM did not change the effect of nociceptin. All subsequent experiments were performed on mouse brain cortex slices and in the presence of naloxone 10 microM. The concentration-response curve of nociceptin (maximum inhibition by 80%, pEC50 7.5) was shifted to the right by the non-selective ORL1 receptor antagonist naloxone benzoylhydrazone and the selective ORL1 receptor antagonist [Phe1psi(CH2-NH)Gly2]-nociceptin(1-13)NH2 (pA2 6.6 and 7.2, respectively). Naloxone benzoylhydrazone did not affect the evoked overflow by itself whereas [Phe1psi(CH2-NH)Gly2]nociceptin(1-13)NH2 caused an inhibition by maximally 35% (pEC50 7.0; intrinsic activity alpha 0.45). The inhibitory effect of [Phe1psi(CH2-NH)Gly2]-nociceptin(1-13)NH2 was counteracted by naloxone benzoylhydrazone. Nociceptin also reduced the Ca2+-evoked tritium overflow in mouse brain cortex slices superfused in the presence of tetrodotoxin. This effect was also antagonized by naloxone benzoylhydrazone, which, by itself, did not affect the evoked tritium overflow. In conclusion, nociceptin inhibits noradrenaline release more markedly in the mouse than in the rat or guinea-pig brain cortex. The effect of nociceptin in the mouse brain cortex involves ORL1 receptors, which are located presynaptically on noradrenergic neurones.

Animals↗

PubMed1997

Blockade of serotonin-2C receptors by mesulergine reduces ocular dominance plasticity in kitten visual cortex.

We have investigated the role of serotonin-2C (5-HT2C) receptors in modulation of ocular dominance plasticity in kitten visual cortex. A small quantity of the 5-HT2C receptor blocker, mesulergine, was infused into the visual cortex of one hemisphere of 5- to 7-week-old kittens using osmotic minipumps, while the control hemisphere received vehicle solution. At the same time, one eyelid of the experimental animals was sutured shut. The ocular dominance distributions in the visual cortex (area 17) were assessed using extracellular recording methods after 1 week of combined mesulergine infusion and monocular deprivation. We found that the majority of the neurons remained binocularly responsive in the mesulergine-treated hemisphere, while most of the neurons recorded were either unresponsive or only weakly responsive to the deprived eye in the control hemisphere. Local infusion of mesulergine into the kitten visual cortex thus reduced the shift of ocular dominance that normally occurs in animals of these ages following monocular deprivation. The blocking effect seems to be distance-dependent and therefore dose-dependent: the farther away the recording sites were from the injection site, the fewer binocularly responsive cells were found. These results are relevant to previous findings indicating transient overexpression of 5-HT2C receptor in visual cortex of kittens at these ages. The data suggest that the 5-HT2C receptor system may be involved in the formation and modification of ocular dominance columns in the developing visual cortex.

Animals↗

PubMed1997

Lesions of the entorhinal cortex disrupt behavioral and neuronal responses to context change during extinction of discriminative avoidance behavior.

Rabbits given either electrolytic lesions of the entorhinal cortex or sham-lesions were trained to prevent a foot-shock by stepping in an activity wheel after one tone, a positive conditioned stimulus (CS+), and to ignore a different tone, a negative conditioned stimulus (CS-). Neuronal activity was recorded simultaneously in the basolateral nucleus of the amygdala, the CA1 cell field of hippocampus, anterior cingulate cortical area 24b and posterior cingulate cortical area 29c/d. The activity of neurons in the entorhinal cortex was recorded in the controls. Acquisition of conditioned avoidance responses (CRs) was not affected by lesions of the entorhinal cortex. Discriminative neuronal activity (greater neuronal responses to the CS+ than to the CS-) during CR acquisition was significantly enhanced in hippocampal area CA1 and attenuated in the basolateral amygdala in rabbits with lesions. Following acquisition to a criterion, two counterbalanced extinction tests were administered, one in the original context and the other in the presence of novel contextual stimuli. CR frequency was significantly reduced in controls but not in rabbits with lesions, during extinction with novel contextual stimuli, relative to performance in the original context. The rabbits with lesions also showed fewer inter-trial responses than controls during extinction in the original context but intertrial response frequency in rabbits with lesions did not differ from the frequency in controls during extinction in the novel context. Neurons in the basolateral amygdala in controls showed discriminative activity during extinction in the original context but not in the novel context. Amygdalar neurons in the rabbits with lesions did not show discriminative activity during extinction in either context. Posterior cingulate cortical neurons in control rabbits did not show discriminative activity during extinction in the original context but these neurons exhibited robust discriminative activity in the novel context. Posterior cingulate cortical neurons in rabbits with lesions showed discriminative activity in both extinction sessions. The results indicated that the entorhinal cortex does not play a significant role in the acquisition of discriminative avoidance behavior, under the employed conditions of training. However, the interactions of neurons in the entorhinal cortex, amygdala and cingulate cortex are essential for contextual modulation of CRs during extinction.

Amygdala↗

PubMed2001

Ischemia increases prostaglandin H synthase-2 levels in retina and visual cortex in piglets.

BACKGROUND: Ischemia increases levels of prostaglandin H synthase-2 (PGHS-2) in neonatal brain and cerebral vasculature, but effects on the developing visual system are unknown. We examined the effects of ischemia on PGHS-2 mRNA and protein levels in the retina and visual cortex in anesthetized piglets. METHODS: Ten minutes of complete retinal and brain ischemia was induced by increasing intracranial pressure. After 2-12 h of reperfusion, samples of retina and visual cortex were collected for determinations of levels of PGHS-2 mRNA (RNase protection assay) or protein (immunohistochemistry and western blotting). Tissues also were obtained from control animals. RESULTS: Levels of PGHS-2 mRNA were undetectable in control animals but showed a dramatic increase at 2-4 h in the cortex and retina in animals exposed to ischemia. Detectable but limited PGHS-2 immunoreactivity (IR) was present in the retina and visual cortex from control animals. In piglets not subjected to ischemia, PGHS-2 IR was localized mainly to the outer limiting membrane and to the Muller cells. Ischemia induced a marked increase in PGHS-2 IR in the neural retina, with the greatest increase in the photoreceptor layer. PGHS-2 levels in whole retina also increased at 8 h after ischemia. In the intact visual cortex PGHS-2 IR was evident in layers II and V. Ischemia increased the intensity of IR in layers II/III as well as layer V. CONCLUSIONS: Detectable amounts of PGHS-2 protein are present in the piglet retina and visual cortex under normal conditions, but levels are markedly increased 8-12 h after ischemic stress. Enhanced PGHS-2 levels after ischemic stress may contribute to delayed pathological changes of the visual system in the neonate.

Animals↗

PubMed2000

"Rodent-like" and "primate-like" types of astroglial architecture in the adult cerebral cortex of mammals: a comparative study.

Previous observations disclosed that astroglia with interlaminar processes were present in the cerebral cortex of adult New and Old World monkeys, but not in the rat, and scarcely in the prosimian Microcebus murinus. The present report is a more systematic and comprehensive comparative analysis of the occurrence of such processes in the cerebral cortex of several mammalian species. Brain samples were obtained from adult individuals from the following orders: Carnivora (canine), Rodentia (rat and mouse), Marsupialia (Macropus eugenii), Artiodactyl (bovine and ovine), Scandentia (Tupaia glis), Chiroptera (Cynopteris horsfieldii and C. brachyotis), and Primate: Prosimian (Eulemur fulvus), non-human primate species (Cebus apella, Saimiri boliviensis, Callithrix, Macaca mulatta, Papio hamadryas, Macaca fascicularis, Cercopithecus campbelli and C. ascanius) and from a human autopsy. Tissues were processed for immunocytochemistry using several antibodies directed against glial fibrillary acidic protein (GFAP), with or without additional procedures aimed at the retrieval of antigens and enhancement of their immunocytochemical expression. The cerebral cortex of non-primate species had an almost exclusive layout of stellate astrocytes, with only the occasional presence of long GFAP-IR processes in the dog that barely crossed the extent of lamina I, which in this species had comparatively increased thickness. Species of Insectivora and Chiroptera showed presence of astrocytes with long processes limited to the ventral basal cortex. Interlaminar GFAP-IR processes were absent in Eulemur fulvus, at variance with their limited presence and large within- and inter-individual variability as reported previously in Microcebus murinus. In New World monkeys such processes were absent in Callithrix samples, at variance with Cebus apella and Saimirí boliviensis. Overall, the expression of GFAP-IR interlaminar processes followed a progressive pattern: bulk of non-primate species (lack of interlaminar processes)--Chiroptera and Insectivora (processes restricted to allocortex) < strepsirhini < haplorhini (platirrhini < catarrhini). This trend is suggestive of the emergence of new evolutionary traits in the organization of the cerebral cortex, namely, the emergence of GFAP-IR long, interlaminar processes in the primate brain. Interlaminar processes may participate in a spatially restricted astroglial role, as compared to the one provided by the astroglial syncytium. It is proposed that the widely accepted concept of an exclusively astroglial syncytium is probably linked with a specific laboratory animal species ("rodent-type" or, rather, "general mammalian-type" model) that misrepresents the astroglial architecture present in the cerebral cortex of most anthropoid adult primates ("primate-type" model), including man.

Aged↗

PubMed2002

Fluoxetine, but not other selective serotonin uptake inhibitors, increases norepinephrine and dopamine extracellular levels in prefrontal cortex.

RATIONALE: The selective serotonin uptake inhibitor (SSRI) fluoxetine has been shown to not only increase the extracellular concentrations of serotonin, but also dopamine and norepinephrine extracellular concentrations in rat prefrontal cortex. The effect of other SSRIs on monoamine concentrations in prefrontal cortex has not been thoroughly studied. OBJECTIVE: The aim of this study was to compare the ability of five systemically administered selective serotonin uptake inhibitors to increase acutely the extracellular concentrations of serotonin, norepinephrine and dopamine in rat prefrontal cortex. METHODS: The extracellular concentrations of monoamines were determined in the prefrontal cortex of conscious rats using the microdialysis technique. RESULTS: Fluoxetine, citalopram, fluvoxamine, paroxetine and sertraline similarly increased the extracellular concentrations of serotonin from 2- to 4-fold above baseline. However, only fluoxetine produced robust and sustained increases in extracellular concentrations of norepinephrine and dopamine after acute systemic administration. Fluoxetine at the same dose blocked ex vivo binding to the serotonin transporter, but not the norepinephrine transporter, suggesting that the increase of catecholamines was not due to non-selective blockade of norepinephrine uptake. Prefrontal cortex extracellular concentrations of fluoxetine at the dose that increased extracellular monoamines were 242 nM, a concentration sufficient to block 5-HT(2C) receptors which is a potential mechanism for the fluoxetine-induced increase in catecholamines. CONCLUSION: Amongst the SSRIs examined, only fluoxetine acutely increases extracellular concentrations of norepinephrine and dopamine as well as serotonin in prefrontal cortex, suggesting that fluoxetine is an atypical SSRI.

Animals↗

PubMed1999

Picrotoxin in the medial prefrontal cortex impairs sensorimotor gating in rats: reversal by haloperidol.

RATIONALE: Neuropathological data indicate a GABAergic dysfunction in the prefrontal cortex and hippocampus of schizophrenics. On this basis, the construct validity of an animal model of schizophrenia was tested. OBJECTIVE: This study assessed prepulse inhibition (PPI) of startle in rats after injections of the GABA antagonist picrotoxin into the prefrontal cortex and the ventral hippocampus. It was also tested if reductions in PPI are reversed by the dopamine antagonist haloperidol. PPI is a measure of sensorimotor gating and is impaired in schizophrenia patients. The hypothesis underlying this study was that blockade of prefrontocortical and hippocampal GABA receptors disrupts PPI in a dopamine-dependent way. This hypothesis was based on neuropathological data from schizophrenics indicating a loss of GABAergic neurons in the prefrontal cortex and hippocampus and on the observation that PPI is reduced in schizophrenics. METHODS: Picrotoxin (0, 5, 10 ng/0.5 microl) was infused through chronically indwelling cannulae into the medial prefrontal cortex (mPFC), into the lateral prefrontal cortex and into the ventral hippocampus. The effect on PPI was measured directly after picrotoxin infusion. The neuroleptic compound haloperidol (0.1 mg/kg) was administered intraperitoneally 30 min before testing. RESULTS: Picrotoxin in the mPFC dose-dependently reduced PPI and this effect was antagonized by systemic pretreatment with the dopamine antagonist haloperidol. No significant effects on PPI were observed after picrotoxin infusions into the lateral prefrontal cortex or into the ventral hippocampus. CONCLUSIONS: These findings indicate that acute blockade of GABA receptors in the mPFC impairs sensorimotor gating in a dopamine-dependent manner. Since PPI in rats has been shown to possess face, predictive, and construct validity as an animal model for some psychotic symptoms, we discuss the potential relevance of our findings for the pathophysiology of schizophrenia.

Animals↗

PubMed2002

Perceptual segregation of overlapping shapes activates posterior extrastriate visual cortex in man.

Objects in natural scenes are rarely seen in isolation, but are usually overlapping or partially occluding other objects. To recognize individual objects, the visual system must be able to segregate overlapping objects from one another. Evidence from lesions in humans and monkeys suggest that perceptual segregation of occluded or overlapping objects involves extrastriate visual cortex. In monkeys, area V4 has been shown to play an important role in recognizing occluded or poorly salient shapes. In humans, a retinotopic homologue of ventral V4 (V4v) has been described, but it is not known whether this area is also functionally homologous to area V4 in monkeys. In this study, we tried to localize the visual cortical regions involved in perceptual segregation of overlapping shapes using positron emission tomography (PET). Regional cerebral blood flow (rCBF) was measured in seven subjects while they discriminated the relative areas of simultaneously presented rectangular shapes. In the control condition, the shapes were displayed without overlaps; in a second condition, the shapes overlapped each other partially. In a third condition, the shapes did not overlap but had been reduced in salience by adding random noise to the stimuli. Contrasting the overlapping shape condition with the control condition identified a single region in the left posterior lateral occipital cortex. The rCBF in this region also increased, though more weakly, during discrimination of shapes embedded in noise, relative to the control condition. The region activated by segregation of overlapping shapes was located in the posterior occipital cortex close to the anterior border of area V2, near the average location of human V4v as determined by retinotopic mapping studies. The activation of this region of extrastriate visual cortex by a task that involved segregation of overlapping shapes is consistent with monkey V4 and human V4v being functionally homologous. We conclude that discrimination of overlapping shapes involves in particular a region of extrastriate visual cortex located in the left lateral occipital cortex and that this region may correspond to human V4v.

Adult↗

PubMed2001

Corticomuscular coherence in the 6-15 Hz band: is the cortex involved in the generation of physiologic tremor?

Physiologic tremor (PT) consists of a peripheral mechanical oscillation at the limbs' resonance frequency and an independent central component in the 6-15 Hz band. This central component has mainly been attributed to spinal interneuronal systems or subcortical oscillators but more recently also to cortical rhythms. We recorded PT electromyographically and accelerometrically from different parts of the arm in parallel to epicortical recordings from grid electrodes covering the primary sensorimotor areas of the contralateral cortex in six epileptic patients. Previous bipolar electrical stimulation of the cortical electrodes resulted in a somatotopic map of the primary cortex underlying the grid. Spectral and cross-spectral analysis including coherence spectra between epicortical electrodes and EMG and the corresponding phase spectra were performed off-line. We found significant corticomuscular coherence in the 6-15 Hz range in four out of the six patients. This coherence was focal on the cortex and it was distributed somatotopically mainly within the primary motor area. The frequency band of the coherence mostly corresponding to the EMG frequency remained stable with added inertia, while the main accelerometric frequency was clearly reduced following the resonance frequency. The phase spectra between electrocorticogram (ECoG) and EMG showed a clear delay between cortex and muscle in two of the patients, which was compatible with conduction in fast pyramidal pathways. These findings indicate that the 6-15 Hz coherence between cortex and EMG reflects a corticomuscular transmission of the oscillation rather than peripheral feedback to the cortex. We conclude that cortical networks are involved in the generation of physiologic tremor.

Adolescent↗

PubMed2002

Induction of persistent changes in the organisation of the human motor cortex.

Motor learning must involve changes in the organisation of the brain, and it seems axiomatic that afferent signals generated during repeated motor practice contribute to this. In this study, motor-point stimulation of the first dorsal interosseous (FDI) muscle was paired with transcranial magnetic stimulation of the human motor cortex on three successive days to determine whether repeated stimulation sessions result in enduring reorganisation of the motor cortex. This repeated "dual" stimulation induced significant changes in the excitability of the motor cortex together with expansion of the area of scalp from which these responses were elicited. The expansion in muscle representation was accompanied by large movements in the centre of gravity (CoG), suggesting a true reorganisation of the underlying cortical representational zone. The changes persisted for at least 2 days following the last stimulation session. It is concluded that repeated dual stimulation is capable of inducing long-lasting reorganisation within the motor cortex. These changes may be similar in nature to those seen in the motor cortex during motor learning. Moreover, these observations suggest that it may be possible to induce the motor cortex of patients who have suffered strokes to reorganise in a way that improves the voluntary control of the weakened muscles.

Adult↗

PubMed2003

Delayed reorganization of the shoulder representation in forepaw barrel subfield (FBS) in first somatosensory cortex (SI) following forelimb deafferentation in adult rats.

We previously reported that 6-16 weeks after forelimb amputation in adult rats, neurons in layer IV of rat first somatosensory cortex (SI) in the forepaw barrel subfield (FBS) associated with the representation of the forepaw became responsive to new input from the shoulder (Pearson et al. 1999). These new shoulder-responsive sites in deafferented FBS had longer evoked response latencies than did sites in the shoulder representation located in the posterior part of the trunk subfield, hereafter referred to as the original shoulder representation. Furthermore, projection neurons in the original shoulder representation in both intact and deafferented adults did not extend their axons into the FBS, and ablation of the original shoulder representation cortex and/or the second somatosensory cortex (SII) failed to eliminate new shoulder input in the deafferented FBS (Pearson et al. 2001). These results led us to conclude that large-scale reorganization in FBS quite likely involved a subcortical substrate. In addition, the time course for large-scale cortical reorganization following forelimb amputation was unknown, and this information could shed light on potential mechanisms for large-scale cortical reorganization. In the present study, we extended our previous findings of large-scale cortical reorganization in the FBS by investigating the time course for reorganization following forelimb amputation. The major findings are: a) deafferented forelimb cortex remained unresponsive to shoulder stimulation during the 1st week following forelimb amputation; b) new responses to shoulder stimulation were first observed in deafferented forelimb cortex 2-3 weeks after forelimb amputation; however, the new shoulder input was restricted to locations in the former forearm cortex; c) islet(s) of new shoulder representation were first observed in deafferented FBS 4 weeks after amputation; these islets occupied a larger percentage of FBS in subsequent weeks; d) portions of FBS remained unresponsive as many as 4 months after deafferentation (maximum time examined between amputation and recording); and e) the increase in total size of the shoulder representation appeared to result from the establishment of new shoulder representations that were often discontinuous from the original shoulder representation. These findings provide evidence that forelimb amputation results in delayed reorganization of the FBS and we describe possible mechanisms and substrates underlying the reorganization.

Age Factors↗

PubMed2004

Perceptual learning of line orientation modifies the effects of transcranial magnetic stimulation of visual cortex.

Perceptual learning may be accompanied by physiological changes in early visual cortex. We used transcranial magnetic stimulation (TMS) to test the postulate that perceptual learning of a visual task initially performed at 60-65% accuracy strengthens visual processing in early visual cortex. Single pulse TMS was delivered to human occipital cortex at time delays of 70-154 ms after the onset of an odd-element, line orientation discrimination task. When TMS was delivered at a delay of 84 ms or later the accuracy of visual discrimination was transiently degraded in ten subjects. As visual performance in control trials without TMS improved with training, the absolute magnitude of TMS suppression of performance decreased in parallel. This result occurred both when TMS was delivered to broad areas of occipital cortex and when TMS was optimally delivered to early occipital cortex. No change in TMS suppression was observed when three new subjects were given feedback during an odd-element task that did not require substantial perceptual learning. Thus, perceptual learning improved visual performance and reduced TMS suppression of early visual cortex in parallel.

Adolescent↗

PubMed2000

"Third tier" ventral extrastriate cortex in the New World monkey, Cebus apella.

The ventral extrastriate cortex adjacent to the second visual area was studied in the New World monkey Cebus apella, using anaesthetised preparations. The visuotopic organisation and myeloarchitecture of this region demonstrate the existence of a distinct strip of cortex, 3-4 mm wide, with an ordered representation of the contralateral upper visual quadrant, up to 60 degrees eccentricity. This upper-quadrant representation is probably homologous to the ventral subdivision of the third visual complex (V3v) of Old World monkeys, also known as the ventral posterior area. The representation of the horizontal meridian in V3v forms its posterior and medial border with V2, while the upper vertical meridian is represented anterior and laterally, forming a congruent border with the fourth visual area (V4). Central visual fields are represented in posterior and lateral portions of V3v, in the inferior occipital sulcus, while the periphery of the visual field is represented anteriorly, on the tentorial surface. Cortex anterior to V3v, at the ventral occipitotemporal transition, had neurones that had poor visual responses. No representation of the lower quadrant was found adjacent to V3v in ventral cortex. However, we observed cells with perifoveal receptive fields centred in the lower quadrant immediately dorsal to V3v, around the junction of the inferior occipital and lunate sulci. These observations argue against the idea that V3v is an area restricted to the ventral cortex in New World monkeys and support the conclusions of previous anatomical studies in Cebus that showed a continuity of myeloarchitecture and connectional patterns between ventral and lateral extrastriate cortices. Together, these data suggest that V3v may be part of a larger area that extends into dorsolateral extrastriate cortex, overlapping to some extent with the caudal subdivision of the dorsolateral area described in other New World monkeys.

Animals↗