Potentiation of sensory responses in the anterior cingulate cortex following digit amputation in the anaesthetised rat.
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The anterior cingulate cortex (ACC) is important for processing different types of information, including sensory inputs. In the present study on anaesthetised rats, we recorded in vivo sensory responses of the ACC to peripheral electrical shocks. Peripheral electrical stimulation at high intensities sufficient to activate nociceptive sensory fibres elicited EPSPs within the ACC. Digit amputation caused long-lasting potentiation of ACC responses to peripheral electrical stimulation. Evoked field EPSPs remained enhanced for at least 120 min after the amputation. Because electrical shocks were delivered to the normal hindpaw, it is likely that plastic changes occur centrally in the spinal cord or the supraspinal structures following amputation. We also recorded field EPSPs of the ACC in response to focal cortical stimulation within the ACC. Like the sensory responses, field EPSPs produced by focal cortical stimulation within the ACC were potentiated after digit amputation, suggesting that long-lasting changes occurred locally within the ACC. Local blockade of peripheral activity by QX-314 at the amputated hindpaw 120 min after amputation did not significantly affect sensory responses induced within the ACC. Thus, peripheral ongoing inputs do not play an important role in maintaining potentiation within the ACC. Two pulses of hindpaw stimulation caused paired-pulse depression in the ACC. Local stimulation within the ACC also caused depression of sensory responses to hindpaw stimulation, suggesting that the population of synapses activated by local stimulation may overlap with that activated by peripheral hindpaw stimulation. Our results suggest that rapid enhancement of sensory responses can be observed in the ACC after amputation and that enhanced neuronal responses to subsequent somatosensory stimuli may contribute to phantom-limb pain. (+info)
Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia.
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The neonatal (PND 7) lesion of the ventral hippocampus (VH) with ibotenic acid represents a well-established experimental paradigm that recapitulates many schizophrenia-like phenomena. In order to investigate molecular changes that could contribute to long lasting consequences on brain function, we have investigated the effects of the VH lesion on the expression for the trophic factors FGF-2 and BDNF. We used RNase protection assay to measure their mRNA levels in cortical regions of prepubertal (PND 35) and young adult (PND 56) animals, both under basal condition as well as in response to an acute restraint stress. The expression of BDNF was not altered by the VH lesion in prefrontal (PFC) and frontal cortex (FC) of PND 35 or PND 56 rats. An acute restraint stress at PND 35 produced a significant increase of the neurotrophin expression in PFC of sham as well as lesioned animals. However in young adult animals a significant elevation of BDNF expression was observed only in sham rats. We also found that the VH lesion produced a significant reduction of basal BDNF mRNA levels in the cingulate cortex of young adult, but not prepubertal rats. This effect was not accompanied by changes in the acute modulation of the neurotrophin, which was up-regulated by stress in both experimental groups. Conversely the expression of FGF-2 at PND 35 and PND 56 was not altered by early postnatal VH lesion, and there were no major differences between sham and lesioned animals in response to the acute stress. The changes in trophic factor expression may be relevant for the long-term effects of VH lesion on synaptic plasticity and may determine an increased vulnerability of the brain under challenging situations. (+info)
Cortical activation by tactile and painful stimuli in hemispherectomized patients.
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Hemispherectomized patients are able to perceive tactile and painful stimuli on their nonparetic as well as paretic body halves. We have used functional MRI to study the cortical mechanisms underlying this preserved somatosensory capacity. Nonpainful brushing and painful heat were applied to the skin of the legs in four hemispherectomized patients and, for comparison, in four normal subjects. Cortical activation was studied with a 1.5 T scanner using a BOLD (blood oxygen level dependent) protocol. All patients rated both the brushing and the heat pain as almost equally intense on each leg and the ratings were similar to those in normals. Brushing on the nonparetic leg activated primary and secondary somatosensory cortices (S1 and S2) in all patients, similar to findings in normals. Brushing on the paretic leg activated S1 in two patients and S2 in one of these patients. Heat pain activated S2, insular cortex and anterior cingulate cortex to a similar degree for both legs, but the activation was weaker in the patients than in the normals. For the individual patient, there was generally no obvious correlation between cortical activation as studied with the BOLD technique and psychophysical performance. The findings from tactile stimulation of the nonparetic leg, that the activation was similar to the contralateral activation in normals, suggest that tactile information processing in the hemisphere contralateral to the stimulation is independent of the corpus callosum. In contrast, the pain activation for the nonparetic leg was weaker than in normals, suggesting that pain activation in the hemisphere contralateral to the stimulation is dependent on transcallosal information processing. The latter finding was corroborated by a subnormal capacity for pain localization on the nonparetic foot in two of the patients. The findings from stimulation of the paretic leg show that areas typically involved in the processing of tactile and painful stimuli can be activated by ipsilateral pathways directly from the periphery. The tactile-evoked ipsilateral S1 activation may be due to subcortical reorganization, since it was not observed in the normal subjects. (+info)
Brain activity during biofeedback relaxation: a functional neuroimaging investigation.
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The mechanisms by which cognitive processes influence states of bodily arousal are important for understanding the pathogenesis and maintenance of stress-related morbidity. We used PET to investigate cerebral activity relating to the cognitively driven modulation of sympathetic activity. Subjects were trained to perform a biofeedback relaxation exercise that reflected electrodermal activity and were subsequently scanned performing repetitions of four tasks: biofeedback relaxation, relaxation without biofeedback and two corresponding control conditions in which the subjects were instructed not to relax. Relaxation was associated with significant increases in left anterior cingulate and globus pallidus activity, whereas no significant increases in activity were associated with biofeedback compared with random feedback. The interaction between biofeedback and relaxation, highlighting activity unique to biofeedback relaxation, was associated with enhanced anterior cingulate and cerebellar vermal activity. These data implicate the anterior cingulate cortex in the intentional modulation of bodily arousal and suggest a functional neuroanatomy of how cognitive states are integrated with bodily responses. The findings have potential implications for a mechanistic account of how therapeutic interventions, such as relaxation training in stress-related disorders, mediate their effects. (+info)
The role of the striatum and hippocampus in planning: a PET activation study in Parkinson's disease.
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Previous work has identified the prefrontal cortex (PFC) and striatum as participating in the planning and selection of movements. We compared the brain activation patterns during planning in Parkinson's disease patients and age-matched controls using H(2)(15)O-PET and the Tower of London (TOL) task. In this study, our mildly affected Parkinson's disease group performed as well as the control group but showed a different pattern of neuronal activation. In the two groups, overlapping areas of the PFC were activated but, whereas the right caudate nucleus was activated in the control group, this was not evident in the Parkinson's disease patients. This suggests that normal normal frontal lobe activation can occur in Parkinson's disease despite abnormal processing within the basal ganglia. Moreover, right hippocampus activity was suppressed in the controls and enhanced in the Parkinson's disease patients. This could represent a shift to the declarative memory system in Parkinson's disease during performance of the TOL task, possibly resulting from insufficient working memory capacity within the frontostriatal system. (+info)
Bilateral focal cerebral angiomatosis associated with nervous signs in a cat.
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A case of cerebral angiomatosis in a cat was associated with neurologic signs characterized by clusters of severe generalized seizures. Bilaterally in the gray matter, most prominent in the cingulate gyrus, there was focal accumulation of garlandlike arrangements of blood vessels. Vessels exhibited activated, hypertrophic endothelial cells and thickening and progressive dystrophic mineralization of the basement membrane, with complete luminal obstruction of some affected vessels. Thickening of the basement membrane was due to accumulation of endothelium-derived proteins such as laminin and von Willebrand factor. Furthermore, moderate diffuse astrogliosis was observed. Findings indicate an idiopathic angiomatosis, with clinical signs possibly due to ischemia resulting from narrowing or complete obliteration of vessel lumina. Changes represent a unique endothelial cell-derived lesion within the brain not previously described in humans or domestic animals. (+info)
Temporary inactivation of the retrosplenial cortex causes a transient reorganization of spatial coding in the hippocampus.
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The ability to navigate accurately is dependent on the integration of visual and movement-related cues. Navigation based on metrics derived from movement is referred to as path integration. Recent theories of navigation have suggested that posterior cortical areas, the retrosplenial and posterior parietal cortex, are involved in path integration during navigation. In support of this hypothesis, we have found previously that temporary inactivation of retrosplenial cortex results in dark-selective impairments on the radial maze (Cooper and Mizumori, 1999). To understand further the role of the retrosplenial cortex in navigation, we combined temporary inactivation of retrosplenial cortex with recording of complex spike cells in the hippocampus. Thus, behavioral performance during spatial memory testing could be compared with place-field responses before, and during, inactivation of retrosplenial cortex. In the first experiment, behavioral results confirmed that inactivation of retrosplenial cortex only impairs radial maze performance in darkness when animals are at asymptote levels of performance. A second experiment revealed that retrosplenial cortex inactivation impaired spatial learning during initial light training. In both experiments, the normal location of hippocampal "place fields" was changed by temporary inactivation of retrosplenial cortex, whereas other electrophysiological properties of the cells were not affected. The changes in place coding occurred in the presence, and absence, of behavioral impairments. We suggest that the retrosplenial cortex provides mnemonic spatial information for updating location codes in the hippocampus, thereby facilitating accurate path integration. In this way, the retrosplenial cortex and hippocampus may be part of an interactive neural system that mediates navigation. (+info)
Impulsive choice induced in rats by lesions of the nucleus accumbens core.
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Impulsive choice is exemplified by choosing a small or poor reward that is available immediately, in preference to a larger but delayed reward. Impulsive choice contributes to drug addiction, attention-deficit/hyperactivity disorder, mania, and personality disorders, but its neuroanatomical basis is unclear. Here, we show that selective lesions of the nucleus accumbens core induce persistent impulsive choice in rats. In contrast, damage to two of its afferents, the anterior cingulate cortex and medial prefrontal cortex, had no effect on this capacity. Thus, dysfunction of the nucleus accumbens core may be a key element in the neuropathology of impulsivity. (+info)