摘要:

THE functional significance of reorganization in somatosensory cortex following peripheral denervation has not been thoroughly addressed. In this paper, two distinct hypotheses dealing with this issue are discussed. The first is the hypothesis of functional respecification. This influential view suggests that sets of partially deafferented cortical neurons, which respond to new peripheral inputs and acquire new receptive fields, undergo corresponding changes in perceptual meaning. Excitation of these neurons by stimulation of their novel receptive fields is thought to result in a change in referral of sensation from the original (now denervated) skin fields to the newly acquired skin fields. The second hypothesis is that of functional conservation. This equally plausible alternative is that sets of partially deprived neurons, although they respond to novel peripheral inputs, retain their original perceptual meaning. Excitation of these neurons by stimulation of their new receptive fields is thought to evoke sensation formerly mediated by those neurons, and hence is still projected to the original, now denervated skin regions or phantom. Behavioral evidence strongly suggests that cortical reorganization after peripheral denervation does not result in major functional respecification, but that the original perceptual function mediated by those neurons is preserved.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

DAY-OLD chicks were trained on one-trial passive avoidance task, using methyl-anthranilate (MeA) as an aversive substance. Bilateral pharmacological manipulation of the intermediate hyperstriatum ventrale was performed by intracerebral application of an α2-noradrenergic agonist, clonidine (5 μM), or an antagonist, rauwolscine (300 μM). Only rauwolscine application (pre- or post-training) induced significant memory impairment. Quantitative receptor autoradiography was used to determine the kinetic properties of the binding sites for [3H]clonidine or [3H]rauwolscine in MeA-trained or water-trained (control) chicks, in forebrain areas known to be involved in avoidance learning. Scatchard analysis revealed that MeA-training resulted in a significant bilateral upregulation in the number of [3H]rauwolscine binding sites (Bmax) in the area of hyperstriatum ventrale. These findings suggest the importance of activation of α2-noradrenergic receptors in aversive learning in chicks.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

THE present study was designed to investigate the effects of infusions into reticular nucleus of thalamus (NRT) or intracerebroventricular (i.c.v.) infusions of muscarinic M1and M2receptor subtype selective drugs on thalamocortically generated neocortical high voltage spindles (HVSs) in awake immobile rats. NRT administration of 2.0 and 20.0 μg McN-A-343, a muscarinic M1agonist, and 20.0 μg methoctramine, a muscarinic M2antagonist, suppressed HVSs. The results suggest that the blockade of presynaptic M2receptors and activation of post-synaptic M1receptors in the NRT suppress thalamo-cortical oscillations and increase neocortical electrical arousal.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

GLIAL fibrillary acidic protein (GFAP) is an intermediate filament protein expressed primarily in astrocytes. We have tested whether GFAP protects against mechanical stress by inducing percussive head injury in GFAP-null mice with a weight drop device. When mice were positioned on a foam bed which allowed head movement at impact, all 14 wild-type mice tested survived, but 12 of 15 GFAP-null mice died within a few minutes. The cause of death appeared to be upper cervical spinal cord injury resulting in respiratory arrest. When the foam bed was replaced by a firm support, both GFAP-null and wild-type mice survived. These results indicate that mice lacking GFAP are hypersensitive to cervical spinal cord injury caused by sudden acceleration of the head.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

STUDIES of regional cerebral blood flow in patients with schizophrenia have led to the idea that dysfunctional neurocircuitry may play a role in patients' cognitive deficits. The present PET study was designed to explore this idea by comparing the functional neural networks associated with semantic processing for patients and normal controls through structural equation modeling (path analysis). The patients showed significantly different neural interactions among frontal regions, between the frontal and temporal cortices, and between the frontal lobe and anterior cingulate than controls. These discrepancies were especially striking given there were minimal group differences in task performance. Results suggest that schizophrenia involves a neural abnormality that is evident in functional networks during cognitive performance.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

INVESTIGATING the release mechanism of nerve growth factor (NGF) the possible cooperation of SNAREs (target (t)-and vesicular (v)-soluble NSF attachment protein receptors) which form a fusion core during docking of synaptic vesicles at the plasma membrane was examined. Cleavage of those proteins by clostridium toxins shows that SNAP-25 (synaptic vesicle associated protein) and syntaxin are involved but not synaptobrevin 2. α-Latrotoxin, which effects the release of neurotransmitters by acting on the fusion core, also induces Ca2+-independent NGF release. Taken together, the results indicate the formation of a fusion core during regulated NGF release and implicate the existence of NGF vesicles.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

PATIENTS with severe paralysis of limbs, face and vocal apparatus may be intelligent and aware and yet, tragically, unable to communicate. We describe a communication link for such a ‘locked-in’ patient with amyotrophic lateral sclerosis. We recorded action potentials in her brain over several months by means of an electrode that induces growth of myelinated fibers into its recording tip. She was able to control the neural signals in an on/off fashion. This result is an important step towards providing such patients with direct control of their environment by interfacing with a computer. Additionally, it indicates that restoration of paralyzed muscles may be possible by using the signals to control muscle stimulators.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

CEREBELLAR granule cells (CGC) are amongst the most abundant neuronal cells in the mammalian central nervous system.In vitro, they undergo apoptosis when deprived of depolarizating concentrations of KCl, providing an interesting system to study neuronal apoptosis. Despite its significance, the intracellular mechanisms that follow an apoptotic insult are poorly understood. Bisindolylmaleimide, a specific protein kinase C (PKC) inhibitor, blocks cell death and apoptosis with an optimal concentration of 10 μM. Bisindolylmaleimide also blocks apoptosis up to 7 h after KCl deprivation, suggesting that it blocks a secondary process. Ro-31-8220, another PKC inhibitor, also blocks apoptosis, but it is less effective, probably due to its lack of specificity. A possible PKC role in increasing the transcription or activating protein(s) involved in neuronal apoptosis is proposed.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BUFFERED propionic acid was injected s.c. into rats twice a day at 8 h intervals from the 6 to 21 days of age. Control rats received saline in the same volumes. The animals were weighed and killed by decapitation at 23 days. Whole brain and cerebral cortex were weighed and synaptic plasma membranes were prepared from cortex for the determination of Na+,K+-ATPase and Mg2+-ATPase activities. Body, whole brain and cortical weights were similar in the two groups, suggesting that propionic acid does not cause malnutrition in rats. Na+,K+-ATPase activity was significantly reduced by 30% in membranes from the propionate-treated group, whereas Mg2+-ATPase activity was not. In another set of experiments, synaptic plasma membranes were prepared from cerebral cortex of 23-day-old rats and incubated with propionic acid at final concentrations ranging from 0.1 to 2.0 mM. Na+,K+-ATPase activity, but not Mg2+-ATPase activity, was inhibited by 22–32%. Since propionic acid concentrations in plasma of chronically treated rats and of propionic acidaemic children are of the same order of magnitude as those testedin vitro, the results suggest that the inhibition of Na+,K+-ATPase activity may be related to the neurological dysfunction of patients affected by propionic acidaemia.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

IN the present study, we tested the hypothesis that interleukin (IL)-10 down-regulates human microglial cell IL-8 release by inhibiting activation of nuclear factor kappa B (NF-κB). Immunohistochemical staining demonstrated that IL-10 markedly suppressed lipopolysaccharide (LPS)-and IL-1β-stimulated IL-8 expression. NF-κB involvement was suggested by the finding that pyrrolidinedithiocarbamate, a known inhibitor of NF-κB activation, blocked LPS-and IL-1β-induced IL-8 production. Consistent with our hypothesis, IL-10 treatment of LPS-and IL-1β-stimulated microglia was associated with a marked decrease in NF-κB translocation from the cytoplasm to the nucleus.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID