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PubMed1999

Effects of mild traumatic brain injury on immunoreactivity for the inducible transcription factors c-Fos, c-Jun, JunB, and Krox-24 in cerebral regions associated with conditioned fear responding.

We have previously demonstrated that mild traumatic brain injury (TBI) of the right parietal cortex results in a relatively selective deficit in conditioned fear responding. However, this behavioural deficit is very consistent and unrelated to the extent of the cortical necrotic lesion. We were therefore interested in determining if other brain regions might show a consistent response to mild TBI, and therefore, more reliably relate to the behavioural change. Increased expression of inducible transcription factors (ITFs) has been used to study which brain regions respond to a variety of events. In the present study, we examined the expression patterns of immunoreactivity (IR) for four ITFs (c-Fos, c-Jun, JunB, and Krox-24) at 3 h after mild fluid percussion TBI. Changes in ITF expression were only observed ipsilateral to the side of TBI. The clearest changes were observed in brain regions known to be involved in conditioned fear responding, such as the amygdala complex and hippocampal formation and several cortical regions. In contrast, no changes in IR for any of the ITFs were observed in the striatum, nucleus accumbens, nucleus basalis magnocellularis, septum or periacqueductal grey. Unlike the extent of visible damage to the cortex at the site of impact, the overexpression of ITFs showed a notable consistency between animals subjected to TBI. This consistency in regions known to be involved in conditioned fear responding (i.e., amygdala complex and hippocampal formation) lead us to suggest that it is these changes, rather than the more variable cortical necrotic lesion, that is responsible for the behavioural deficits we observe following mild TBI. Importantly, our results demonstrate that like the hippocampus, the amygdala is a sub-cortical structure particularly sensitive to the effects of mild brain trauma and underline the fact that cerebral regions distant from the location of the fluid impact can be affected.

Amygdala↗

PubMed2004

The anatomy of anosognosia for hemiplegia: a meta-analysis.

Anosognosia for hemiplegia is the denial of the contralesional motor deficits that may follow brain damage. Although this disturbance has been reported in the neurological literature since the beginning of the last century, only few longitudinal studies have addressed the issue of the anatomical substrate of the disorder. Here we present a comprehensive review of the literature on anosognosia for hemiplegia from 1938 to 2001, taking into account some of its clinical, epidemiological and anatomical aspects. In particular, an attempt has been made to identify the intra-hemispheric lesion locations most frequently associated to the denial behaviour. Our review shows that anosognosia for hemiplegia most frequently occurs in association to unilateral right-sided or bilateral lesions of different brain areas (cortical and/or subcortical). It seems to be equally frequent when the damage is confined to frontal, parietal or temporal cortical structures, and may also emerge as a consequence of subcortical lesions. Interestingly, the probability of occurrence of anosognosia is highest when the lesion involves parietal and frontal structures in combination, if compared to other combinations of lesioned areas. This pattern of lesions suggests the existence of a complex cortico-subcortical circuit underlying awareness of motor acts that, if damaged, can give raise to the anosognosic symptoms.

Adult↗

PubMed2001

Changes in the auditory-evoked potentials induced by fear-evoking stimulations.

It is long established that the inferior colliculus is involved in conveying all kinds of auditory information to higher cortical structures. Moreover, gradual increases in the electrical stimulation of this structure produces progressive aversive responses from vigilance, through freezing, until escape. Recently, we have shown that microinjections of the excitatory amino acids, N-methyl-D-aspartate (NMDA) and glutamate, into the inferior colliculus mimic these aversive effects. In the present study, we extend these observations showing that unilateral microinjections of 5 nmol of glutamate into the inferior colliculus--a dose that causes freezing behavior--in rats with bilateral recording electrodes into this structure produce an increase in the magnitude of the collicular-evoked potential in the ipsilateral side of the injection in relation to saline-injected animals. Besides, the application of two kinds of fear-evoking stimulations--light as a conditioned stimuli (CS) and ultrasound signals at the frequency of 22 kHz--also produced an increase in the amplitude of the evoked potentials recorded from the inferior colliculus in comparison to control situations without aversive stimuli presentations. These data support previous reports showing that fast-acting excitatory amino acid receptors in this midbrain region are involved in the processing of auditory information. Moreover, fear-eliciting stimulations, such as light-CS and ultrasound signals, increase acoustically evoked firing of neurons in the central nucleus of the inferior colliculus of rats.

Acoustic Stimulation↗

PubMed2006

[Part I: Face recognition].

Faces represent a crucial vector of interhuman communication. The message transmitted by the face has multiple features. Recognition of each feature can be impaired independently or in combination with others. In order to understand the behavioral consequences of such impairments, which can be a major social handicap, we first must specify the neural networks involved in face recognition. We propose in this first part to present the systems involved in face recognition, in particular the question of identity and prosopagnosia. Different neural networks are indeed implicated in the recognition of invariant facial features such as identity, gender, ethnicity, and recognition of variant features like facial expression and eye gaze. This paper is illustrated by some of our scalp and intracranial electrophysiological studies performed in humans allowing us to describe some aspects of face recognition dynamics combining an excellent spatial and temporal resolution. Intracranial recordings were performed in drug refractory epileptical patients implanted with depth electrodes. These studies demonstrate that numerous deep brain and cortical structures participate early and sometimes in a sustained manner in face recognition.

Face↗

PubMed1988

Renin in mesoblastic nephroma: an immunohistochemical study.

Congenital mesoblastic nephroma (CMN) is the most common renal tumor of early infancy. It is usually evident at birth as an abdominal mass and is composed of spindle-shaped cells resembling smooth muscle cells and fibroblasts. There is macroscopic and microscopic infiltration of the surrounding kidney and entrapped tubules and glomeruli are common at the edge of the tumor. In this report, we describe a case of CMN associated with hyperreninaemia and hypertension. We examined the tumor from this case and 11 other cases for the presence of renin using a polyclonal antibody to human kidney renin. Hypertension was present in three of four additional cases for which records were available. Immunoreactive renin was present in ten of the 12 cases studied. In all of these cases, intense staining was present in vessels within the areas of the trapped cortex. In seven cases, renin was identified in the walls of vessels within the tumor itself without identifiable adjacent cortical structures. These findings indicate that CMN may often be associated with primary reninism in early infancy.

Humans↗

PubMed1999

Vertebrate slit, a secreted ligand for the transmembrane protein roundabout, is a repellent for olfactory bulb axons.

The olfactory bulb plays a central role in olfactory information processing through its connections with both peripheral and cortical structures. Axons projecting from the olfactory bulb to the telencephalon are guided by a repulsive activity in the septum. The molecular nature of the repellent is not known. We report here the isolation of vertebrate homologs of the Drosophila slit gene and show that Slit protein binds to the transmembrane protein Roundabout (Robo). Slit is expressed in the septum whereas Robo is expressed in the olfactory bulb. Functionally, Slit acts as a chemorepellent for olfactory bulb axons. These results establish a ligand-receptor relationship between two molecules important for neural development, suggest a role for Slit in olfactory bulb axon guidance, and reveal the existence of a new family of axon guidance molecules.

Animals↗

PubMed1998

The anatomy of the central control of posture: consistency and plasticity.

Posture is usually thought to be steered by brainstem and cortical structures that have access to the motoneurons and their premotor interneurons of the axial and neck muscles. The present paper describes these pathways and their relation with gaze control structures. All these systems belong to the medial component of the so-called voluntary motor system. On the other hand, in the cat there also exist several postures that are not steered by the somatic, but by the emotional motor system. Examples are arching of the back and mating postures. The pathways thought to be involved in these behaviours are described. They belong to the lateral component of the emotional motor system and, especially in case of mating postures, are extremely plastic. They have been demonstrated to be almost 10 times as strong in oestrus than in non-oestrus cats.

Animals↗

PubMed1998

Neonatal cryoanesthesia affects the morphology of the visual cortex in the adult rat.

Hypothermia is often employed as an anesthetic for manipulations of neonatal animals. We previously reported [J. Nuñez, J.M. Juraska, The effect of neonatal cryoanesthesia on the gross size of the splenium of the corpus callosum, Dev. Psychobiol. 30 (1997) 259; J. Nuñez, J.M. Juraska, The size of the splenium of the rat corpus callosum: influence of hormones, sex ratio and neonatal cryoanesthesia, Dev. Psychobiol., in press.] that the area of the splenium of the adult rat corpus callosum negatively correlated with the time neonatal pups spent in the cold. In the present study, we examined the effect of exposure to neonatal hypothermia (0, 15, 30 and 60 min at 4 degreesC, within 2 h of birth) on the thickness and volume of the binocular (Oc1B) and monocular (Oc1M) fields of the adult rat visual cortex. The number of neurons and glia in layer 2/3 in these areas was also assessed in the 0 and 60 min cold-exposed groups. Cryoanesthesia significantly decreased the length, thickness, volume and number of neurons and glia in both Oc1M and Oc1B. We also observed significant effects of cold exposure on the thickness of individual cortical layers, with some layers affected more than others after differential exposure times. Sex differences (males greater than females) were observed in a number of measures after varying amounts of time in cold and in the absence of cold exposure, in confirmation of previous work from our lab [S.N.M. Reid, J.M. Juraska, Sex differences in the gross size of the rat neocortex, J. Comp. Neurol. 321 (1992) 442-447; S.N.M. Reid, J.M. Juraska, Sex differences in neuron number in the binocular area of the rat visual cortex, J. Comp. Neurol. 321 (1992) 448-455.]. The present study points to the potential confound of using cryoanesthesia on neonatal animals to study cortical structure or function.

Aging↗

PubMed1992

Dissociation of spatial navigation and visual guidance performance in Purkinje cell degeneration (pcd) mutant mice.

Spatial learning in rodents requires normal functioning of hippocampal and cortical structures. Recent data suggest that the cerebellum may also be essential. Neurological mutant mice with dysgenesis of the cerebellum provide useful models to examine the effects of abnormal cerebellar function. Mice with one such mutation, Purkinje cell degeneration (pcd), in which Purkinje cells degenerate between the third and fourth postnatal weeks, were evaluated for performance of spatial navigation learning and visual guidance learning in the Morris maze swim-escape task. Unaffected littermates and C57BL/6J mice served as controls. Separate groups of pcd and control mice were tested at 30, 50 and 110 days of age. At all ages, pcd mice had severe deficits in distal-cue (spatial) navigation, failing to decrease path lengths over training and failing to express appropriate spatial biases on probe trials. On the proximal-cue (visual guidance) task, whenever performance differences between groups did occur, they were limited to the initial trials. The ability of the pcd mice to perform the proximal-cue but not the distal-cue task indicates that the massive spatial navigation deficit was not due simply to motor dysfunction. Histological evaluations confirmed that the pcd mutation resulted in Purkinje cell loss without significant depletion of cells in the hippocampal formation. These data provide further evidence that the cerebellum is vital for the expression of behavior directed by spatial cognitive processes.

Age Factors↗

PubMed2000

Prior electrical stimulation of the inferior colliculus sensitizes rats to the stress of the elevated plus-maze test.

Besides its primary function in the transmission of acoustic signals, the inferior colliculus (IC) is involved in conveying auditory information of aversive nature to higher cortical structures. In the field of anxiety research, one widely used animal model is the electrical stimulation of a given structure supposed to be involved in the neural circuitry underlying emotional behavior. Indeed, electrical stimulation of the inferior colliculus produces fear-like responses. Moreover, prior exposure to stressful events sensitizes rodents' responsivity to fearful stimuli when they are subsequently tested in the elevated plus-maze. Based on these evidence it seems to be important to know whether animals stimulated in the inferior colliculus would show a heightened behavioral responsivity to subsequent stressful events. To this end, we examined the temporal course of the effects of the electrical stimulation of this midbrain region (5, 10 and 15 min afterward) on the conventional and ethological measures of the behavior of rats exposed to the elevated plus-maze test. Prior electrical stimulation of the inferior colliculus produced an 'anxiogenic' profile in the elevated plus-maze, i.e. a significant reduction in the number of entries and time spent into the open arms. Still, previous electrical stimulation of the inferior colliculus caused a significant decrease in rearing, scanning, peeping out, head dipping and end-arm activity while increased immobility. All these changes occurred after 5 min of inferior colliculus electrical stimulation. Therefore, stimulation of the inferior colliculus causes a heightened responsivity to anxiogenic stimuli inherent to the elevated plus-maze test. These findings bring additional support to the proposed role of this midbrain structure in the elaboration of adaptive responses to stressful situations.

Animals↗

PubMed2001

Brain strategies for reading in the second language are determined by the first language.

Brain activation associated with reading was investigated in ten normal Japanese volunteers (five highly literate in both Japanese and English) and ten American native English speakers (five highly literate in both English and Japanese) in order to determine the neuroanatomic substrates employed in reading the first language (L1), and to determine the effect of L1 on the neurosubstrates involved in reading the second language (L2). The study was performed using blood oxygenation level dependent (BOLD) contrast functional magnetic resonance imaging (fMRI) on a high-field (3.0T) system specifically optimized for fMRI. The activation patterns in Japanese subjects reading Japanese (L1) were substantially different from the patterns obtained in American subjects reading English text (L1). The activation patterns reading L2 were virtually identical to the patterns seen when reading L1 in both Japanese and English natives highly literate in both language systems. The results demonstrated that the neuroanatomical substrates underlying the cognitive processing of reading are differentially determined based on the language system. The study further indicates that the cognitive processes for reading in the second language involve the same cortical structures employed for the first language, supporting the hypothesis that the second language represents the cognitive extension of the first language.

Adult↗

PubMed2002

The role of TNF-alpha in amygdala kindled rats.

In the present study, the interaction between epileptogenesis and the immune system were studied in a kindling model. First, the effects of a single administration of TNF-alpha (5.0 microg/kg, i.p.) on seizure and EEG activity were investigated in amygdala-kindled rats. TNF-alpha treated rats showed more prolonged epileptiformic discharges than control rats. TNF-alpha also induced a decrease in the power of delta band and an increase in theta and alpha activity. In addition, a marked increase in the power of beta and gamma band was observed. The EEG changes were most numerous in the frontal cortex and amygdala. All effects were registered 24 h after TNF-alpha administration. Finally, electrical stimulation enhanced the level of TNF-alpha in blood serum from 1.9 +/- 1.5 to 12.7 +/- 3.8 pg/ml and in brain tissue 56.8 +/- 6.0 to 109.2 +/- 6.0 pg/mg, as was determined via the ELISA method. It can be concluded that there is a mutual facilitative interaction of both epileptogenic and cytokine-derived mechanisms on this type of seizure. The changes in the power spectrum of the EEG after TNF-alpha might contribute to intensify thalamic-derived facilitation of epileptic discharge in cortical structures.

Amygdala↗

PubMed2000

Glial glutamate transporter mRNAs in the genetically absence epilepsy rat from Strasbourg.

Recent studies support a critical role for the glutamatergic system and glutamate transporters in the pathogenesis of epilepsy. The glial glutamate transporters GLT-1 (L-glutamate transporter) and GLAST (L-glutamate/L-aspartate transporter) are known to be responsible for the majority of glutamate reuptake from the synaptic cleft and constitute one mechanism by which extracellular glutamate levels may be controlled. The present study therefore compared GLT-1 and GLAST mRNA levels in the genetically absence epilepsy rat from Strasbourg (GAERS) with those of age-matched non-epileptic controls. The GAERS rat has been proposed as an animal model of inherited human absence epilepsy, displaying recurrent, generalised, non-convulsive seizures that originate from thalamic and cortical structures. In situ hybridisation with 35S-labelled oligonucleotide probes demonstrated substantial and significant increases in GLT-1 mRNA levels in the ventromedial nucleus of the thalamus (VM) and the subthalamic nucleus (STN) of GAERS rats. Increases in GLAST mRNA were found in the primary somatosensory cortex (SS1) and temporal cortex (Te) of GAERS. These data, along with previous studies, suggest that regional imbalances in GABAergic and glutamatergic systems may be associated with the pathogenesis of absence seizures in GAERS.

ATP-Binding Cassette Transporters↗

PubMed1992

Myelitis and meningitis.

Animals with meningomyelitis have clinical neurologic signs that typically range from paraspinal discomfort to tetraplegia; however, most affected animals also show evidence of multifocal CNS involvement with brain stem and cerebral cortical structures being affected most commonly. The cause, duration, and host response to the disease process will determine the clinical signs in individual animals. Confirmation of a specific causative agent is difficult, but CSF analysis and immunotesting of serum and CSF yield the most rewarding diagnostic results. Successful treatment is based on formulation of an appropriate and aggressive therapeutic regimen. In some diseases, no effective treatment is available, and some animals may develop permanent neurologic disabilities.

Animals↗

PubMedDate not supplied

Ammonia and Alzheimer's disease.

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. Behavioural, cognitive and memory dysfunctions are characteristic symptoms of AD. The formation of amyloid plaques is currently considered as the key event of AD. Other histological hallmarks of the disease are the formation of fibrillary tangles, astrocytosis, and loss of certain neuronal systems in cortical areas of the brain. A great number of possible aetiologic and pathogenetic factors of AD have been published in the course of the last two decades. Among the toxic factors, which have been considered to contribute to the symptoms and progression of AD, ammonia deserves special interest for the following reasons: (a) Ammonia is formed in nearly all tissues and organs of the vertebrate organism; it is the most common endogenous neurotoxic compounds. Its effects on glutamatergic and GABAergic neuronal systems, the two prevailing neuronal systems of the cortical structures, are known for many years. (b) The impairment of ammonia detoxification invariably leads to severe pathology. Several symptoms and histologic aberrations of hepatic encephalopathy (HE), of which ammonia has been recognised as a pathogenetic factor, resemble those of AD. (c) The excessive formation of ammonia in the brains of AD patients has been demonstrated, and it has been shown that some AD patients exhibit elevated blood ammonia concentrations. (d) There is evidence for the involvement of aberrant lysosomal processing of beta-amyloid precursor protein (beta-APP) in the formation of amyloid deposits. Ammonia is the most important natural modulator of lysosomal protein processing. (e) Inflammatory processes and activation of microglia are widely believed to be implicated in the pathology of AD. Ammonia is able to affect the characteristic functions of microglia, such as endocytosis, and cytokine production. Based on these facts, an ammonia hypothesis of AD has first been suggested in 1993. In the present review old and new observations are discussed, which are in support of the notion that ammonia is a factor able to produce symptoms of AD and to affect the progression of the disease.

Alzheimer Disease↗

PubMed2002

Neurobiology of ammonia.

Hyperammonemia resulting from inherited urea cycle enzyme deficiencies or liver failure results in severe central nervous system dysfunction including brain edema, convulsions and coma. Neuropathologic evaluation in these disorders reveals characteristic alterations of astrocyte morphology ranging from cell swelling (acute hyperammonemia) to Alzheimer Type II astrocytosis (chronic hyperammonemia). Having no effective urea cycle, brain relies on glutamine synthesis for the removal of excess ammonia and the enzyme responsible, glutamine synthetase, has a predominantly astrocytic localization. Accumulation of ammonia in brain results in a redistribution of cerebral blood flow and metabolism from cortical to sub-cortical structures. In addition to changes in astrocyte morphology, increased brain ammonia concentrations result in alterations in expression of key astrocyte proteins including glial fibrillary acidic protein, glutamate and glycine transporters and "peripheral-type" (mitochondrial) benzodiazepine receptors. Such changes result in alterations of astrocytic volume and increased extracellular concentrations of excitatory and inhibitory substances. In addition, the ammonium ion has direct effects on excitatory-inhibitory transmission via distinct mechanisms involving cellular chloride extrusion and postsynaptic receptor function. Acute ammonia exposure leads to activation of NMDA receptors and their signal transduction pathways. Chronic hyperammonemia also results in increased concentrations of neuroactive L-tryptophan metabolites including serotonin and quinolinic acid. Therapy in hyperammonemic syndromes continues to rely on ammonia-lowering strategies via peripheral mechanisms (reduction of ammonia production in the gastrointestinal tract, increased ammonia removal by muscle).

Ammonia↗

PubMed2002

Fundamental mechanisms of visual motion detection: models, cells and functions.

Taking a comparative approach, data from a range of visual species are discussed in the context of ideas about mechanisms of motion detection. The cellular basis of motion detection in the vertebrate retina, sub-cortical structures and visual cortex is reviewed alongside that of the insect optic lobes. Special care is taken to relate concepts from theoretical models to the neural circuitry in biological systems. Motion detection involves spatiotemporal pre-filters, temporal delay filters and non-linear interactions. A number of different types of non-linear mechanism such as facilitation, inhibition and division have been proposed to underlie direction selectivity. The resulting direction-selective mechanisms can be combined to produce speed-tuned motion detectors. Motion detection is a dynamic process with adaptation as a fundamental property. The behavior of adaptive mechanisms in motion detection is discussed, focusing on the informational basis of motion adaptation, its phenomenology in human vision, and its cellular basis. The question of whether motion adaptation serves a function or is simply the result of neural fatigue is critically addressed.

Adaptation, Physiological↗

PubMed2000

Impairment of motor imagery in putamen lesions in humans.

Patients with putamen or cortical lesions participated in a first- and third-person movement imagery task, each primarily engaging kinesthetic and visual imagery. The subjects were instructed to imagine themselves (first-person task) and a third party (third-person task) performing a sequence of three movements and to choose from a set of four photos the end posture resulting from the movements. The results demonstrated that, limb-specific imagery was impaired in both putamen and cortical lesions, in the first-, but not third-person task. Moreover, more than half of the errors made by cortical patients were with respect to the first movement, a finding consistent with motor cortex involvement in memory processes. Taken overall, the results provide evidence that the basal ganglia as well as cortical structures play an important role in the neural network mediating motor imagery.

Cerebral Infarction↗