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PubMed1975

The role of cortical orientation in the control of the direction of ciliary beat in Paramecium.

The swimming behavior of many ciliate protozoans depends on graded changes in the direction of the ciliary effective stroke in response to depolarizing stimuli (i.e., the avoiding reaction of Paramecium). We investigated the problem of whether the directional response of cilia with a variable plane of beat is related to the polarity of the cell as a whole or to the orientation of the cortical structures themselves. To do this, we used a stock of Paramecium aurelia with part of the cortex reversed 180 degrees. We determined the relation of the orientation of the kineties (ciliary rows) to the direction of beat in these mosaic paramecia by cinemicrography of particle movements near living cells and by scanning electron microscopy of instantaneously fixed material. We found that the cilia of the inverted rows always beat in the direction opposite to that of normally oriented cilia during both forward and backward swimming. In addition, metachronal waves of ciliary coordination were present on the inverted patch, travelling in the direction opposite to those on the normal cortex. The reference point for the directional response of Paramecium cilia to stimuli thus resides within the cilia or their immediate cortical surroundings.

Animals↗

PubMed1995

Temporal dynamics and regional distribution of [14C]serine uptake into mouse brain.

In order to examine the uptake of L-serine into brain structures and brain metabolic compartments, L-[U-14C]serine was injected into tail vein of mice. The uptake was examined 30 min, 90 min, 3 h and 5 h after injection by both quantitative autoradiography of coronal brain sections and by biochemical analysis. Brain radioactivity was extracted and partitioned into protein associated pellets, metabolites soluble in aqueous phase and lipids soluble in the organic phase. Most of the radioactivity was found in the aqueous phase, about 10% was incorporated into lipids. Among phospholipids the highest label was found in phosphatidylserine, then in phosphatidylethanolamine and in phosphatidylcholine, it amounted to 52%, 30% and 18% of label by 90 min after injection, respectively. The brain distribution of L-serine uptake resembled that described for strychnine-insensitive [3H]glycine binding, with cortical structures being preferentially labelled.

Animals↗

PubMed2003

Differential brain activations during intentionally simulated and subjectively experienced paralysis.

INTRODUCTION: Distinguishing conversion disorder from malingering presents a significant challenge as the diagnosis ultimately depends on the patient's subjective report and the clinician's suspicion of an intention to deceive. Using hypnosis to manipulate the intentionality of movement inhibition in the same subjects, we used positron emission tomography (PET) to determine whether failure to move during intentionally simulated and subjectively experienced paralysis is mediated by different neural structures. METHODS: Using a within-subject design, 12 normal, hypnotised subjects were tested under two paralysis conditions during the same scanning session. Half of the scans were performed with the suggestion that the left leg was paralysed (subjectively experienced paralysis condition) and half with the leg normal but with the instruction that paralysis should be feigned (intentionally simulated paralysis condition). RESULTS: Relative increases in brain activation were seen in the right orbitofrontal cortex, right cerebellum, left thalamus, and left putamen during subjectively experienced paralysis compared to intentionally simulated paralysis, although a previously reported activation of the right anterior cingulate cortex was not seen. During intentionally simulated paralysis compared to subjectively experienced paralysis relative increases in brain activation were seen in the left ventrolateral prefrontal cortex, and a number of right posterior cortical structures. CONCLUSIONS: Our results suggest that subjectively experienced paralysis has a different neural basis to intentionally simulated paralysis. These findings have theoretical and clinical implications for malingering and related attempts to unravel the neuropsychological basis for conversion hysteria.

Journal Article↗

PubMed2004

Effects of very low birthweight on brain structure in adulthood.

Very-low-birthweight (VLBW) individuals are at high risk of brain injury in the perinatal period. We wished to determine how such early brain lesions affect brain structure in adulthood. Thirty-two VLBW adults (20 female, 12 male) and 18 term, normal birthweight sibling control individuals (nine female, nine male) underwent structural MRI at a mean age of 23 years 4 months (range 17 to 33 years; SD 3.4). Images were analyzed using an automated tissue segmentation algorithm in order to estimate whole brain tissue class volumes in native space. Images were then warped to a template image in standard space. There was no significant between-group difference in whole brain, grey matter, white matter, or total cerebral spinal fluid (CSF) volumes. However, lateral ventricular volume was significantly increased by 41% in those with VLBW. The ratio of grey to white matter was also significantly increased (by 10%) in those with VLBW. Group comparison maps showed widespread changes in the distribution of grey and white matter, and relative excess of ventricular CSF, in the brains of VLBW individuals. Increased ventricular volume predicted decreased grey matter in subcortical nuclei and limbic cortical structures, and decreased periventricular white matter. We conclude that these diffuse abnormalities of grey and white matter are a consequence of the interaction of perinatal brain injury and ongoing neurodevelopmental processes.

Adolescent↗

PubMedDate not supplied

Clinical hypnosis modulates functional magnetic resonance imaging signal intensities and pain perception in a thermal stimulation paradigm.

OBJECTIVE: This study was designed to describe regional changes in blood oxygenation level dependent signals in functional magnetic resonance images (fMRI) elicited by thermal pain in hypnotized subjects. These signals approximately identify the neural correlates of the applied stimulation to identify neuroanatomic structures involved in the putative effects of clinical hypnosis on pain perception. METHODS: After determination of the heat pain threshold of 12 healthy volunteers, fMRI scans were performed at 1.5 Tesla by using echoplanar imaging technique during repeated painful heat stimuli. Activation of brain regions in response to thermal pain during hypnosis (using a fixation and command technique of hypnosis) was compared with responses without hypnosis. RESULTS: With hypnosis, less activation in the primary sensory cortex, the middle cingulate gyrus, precuneus, and the visual cortex was found. An increased activation was seen in the anterior basal ganglia and the left anterior cingulate cortex. There was no difference in activation within the right anterior cingulate gyrus in our fMRI studies. No activation was seen within the brainstem and thalamus under either condition. CONCLUSION: Our observations indicate that clinical hypnosis may prevent nociceptive inputs from reaching the higher cortical structures responsible for pain perception. Whether the effects of hypnosis can be explained by increased activation of the left anterior cingulate cortex and the basal ganglia as part of a possible inhibitory pathway on pain perception remains speculative given the limitations of our study design.

Brain↗

PubMed1992

Regional distribution and in vivo binding of the atypical antipsychotic drug remoxipride. A biochemical and autoradiographic analysis in the rat brain.

The regional brain distribution and binding of the antipsychotic benzamide drug remoxipride was studied in the male rat. After i.v. injections of 3H-remoxipride (1 mumol.kg-1) more than 85% of the radioactivity was identified as authentic remoxipride in brain by using reversed-phase liquid chromatography. Autoradiographic and spectroscopic analysis showed that 3H-remoxipride was distributed relatively even in different brain areas, with exception of the following structures, which showed highest drug concentrations: the choroid plexus, septum, medial part of the caudate nucleus, different areas of the thalamus and hypothalamus situated close to the cerebral ventricles. A closer analysis of the autoradiograms showed a gradient of radioactivity extending from the cerebral ventricles to the deeper parts of the brain at 30 minutes after injections. After 60 minutes radioactivity was detected throughout all forebrain dopamine receptive areas. These findings suggest that remoxipride enters the cerebrospinal fluid (CSF) via the vascular bed of the choroid plexus and that it enters the brain interstitial fluid from the CSF. In the caudate nucleus, nucleus accumbens, olfactory tubercle and olfactory bulb 30-40% of the radioactivity was reduced by pretreatment with the dopamine D-2 selective drug raclopride. In addition, small, but significant, reductions (10-15%) of 3H-remoxipride derived radioactivity was found in the neocortex, hippocampus and the cerebellum, suggesting that remoxipride interacts with a D-2 receptor also in these cortical structures. Taken together, these studies show that after i.v. injections, 3H-remoxipride enters the brain primarily in unmetabolized form when given in doses that affect DA receptor mediated behaviours, that it distributes to most areas throughout the neuraxis and that it binds to D-2 receptors in different parts of the basal ganglia, neocortex, hippocampus and cerebellum.

Animals↗

PubMedDate not supplied

Cortical and subcortical structures involved in recognition memory: neurophysiological and anatomical studies.

Recordings of neuronal activity were made in cortical and subcortical structures of monkeys performing visual recognition memory tasks in which the novelty/familiarity of the stimuli was varied. A population of neurons with memory-like activity was recorded in a periventricular region at the border of the anterior thalamus and dorsal hypothalamus. These neurons responded with decreases in firing rate to novel stimuli and increases in firing rate to the same stimuli when they were familiar. The calculated memory spans of these neurons ranged from 7 to hundreds of intervening trials. The afferent connections of this region were traced by an injection of HRP into the periventricular region. Retrogradely labeled cells were observed in the ventromedial prefrontal cortex, the ventromedial temporal cortex, amygdala, medial thalamus and supramammillary region. Recordings were then made in the hippocampus and ventromedial temporal cortex. A population of neurons in the ventromedial temporal cortex responded maximally to the first presentation of a stimulus, reflecting the novelty or recency of the stimulus presentation. In contrast, such neurons were not observed in the CA fields or subiculum of the hippocampal formation. These studies suggest that a system of brain structures involving the temporal cortex and periventricular region provide one mechanism whereby monkeys are able to recognise and respond to visual stimuli differing in their novelty and familiarity.

Animals↗

PubMed1996

Magnetic resonance imaging of human brain function.

BACKGROUND: Previously the exclusive domain of the technology of positron emission tomography, functional MRI is now proving capable of mapping functional regions of the human cortex in near real time during specific task activations or in response to any hemodynamic stress. Of particular interest is the opportunity to observe secondary cortical responses, activation due to imagined tasks, memory function, time-resolved pathways through cortical regions, and activation in sub-cortical structures. METHODS AND RESULTS: One method of functional MRI uses blood oxygenation changes, which can be imaged continuously while functional centers are being stimulated. Image intensity can become darker if there is more deoxygenated blood and brighter if more oxygenated blood enters the brain. This concepts works in all perfused tissues in the body, and allows use of the blood oxygenation mechanism to image neuronal activation. A second method takes advantage of the fact that the protons within the MRI slice are always partially saturated by the rapid rate of imaging. As blood flow delivers unsaturated blood water protons into an imaged slice, these arterially-delivered protons will appear very bright in the image. Visualization of this effect is accomplished by simple image subtraction or by comparison of intensity changes as a function of the paradigm application frequency. Using either approach leads directly to a functional map. CONCLUSIONS: At present, clinical applications are rapidly moving toward routine non-invasive mapping of distortions of the functional motor and somatosensory cortex and other cortical regions as a result of brain tumors. Other clinical applications include the observation of the effect of degenerative diseases such as multiple sclerosis. Alzheimer's disease, stroke, migraine, epilepsy, and other diseases causing neuronal loss and Parkinsonism. Functional MRI and its applications will continue to grow exponentially throughout the decade.

Brain↗

PubMed1997

Chronic focal neocortical epileptogenesis: does disinhibition play a role?

Several lines of evidence have suggested that decreases in postsynaptic inhibition may have a role in epileptogenesis in cortical structures. However, other studies have suggested that GABAergic inhibition is spared, or even augmented in some forms of post-lesional epilepsy. In the studies described here, inhibitory events were recorded in two models of post-lesional chronic epileptogenesis. (i) As previously reported (D.A. Prince and G.-F. Tseng. J. Neurophysiol. 69: 1276-1291. 1993), epileptiform activity develops in slices from partially isolated rat neocortical islands 2-3 weeks after the initial in vivo lesion. In this model of post-traumatic epilepsy, large amplitude polyphasic inhibitory postsynaptic currents (IPSCs) in layer V pyramidal neurons are associated with each interictal epileptiform field potential. The frequency of spontaneous IPSCs as well as miniature IPSCs was significantly increased in neocortical slices from the epileptogenic chronically injured cortex versus controls. Immunocytochemical reactions for parvalbumin and calbindin, calcium binding proteins present in subgroups of GABAergic neurons, showed an increased staining of both neuropil and somata within the epileptogenic tissue. Immunoreactivity for glutamic acid decarboxylase (GAD) and GABA also appeared to be increased in the neuropil. (ii) Cortical microgyri resembling human malformations were produced by freeze lesions made transcranially in P0 rat cortex (K.M. Jacobs, M.J. Gutnick, and D.A. Prince. Cereb. Cortex, 6: 514-523. 1996). The boundary between the four-layered microgyrus and surrounding cortex become epileptogenic within about 2 weeks, as judged by evoked extracellular field potentials and cellular activities. Epileptogenesis in the surrounding cortex is not altered when the microgyrus itself is isolated by transcortical cuts. Patch-clamp recordings from layer V neurons in the epileptogenic zone showed that spontaneous IPSCs are larger and more dependent on glutamatergic synapses than in control neurons. The amplitudes of polysynaptic IPSCs evoked by threshold stimulation were also larger than in control cells. Although evaluation of inhibitory events in these models is still incomplete, results to date suggest that GABAergic inhibition may be enhanced in epileptogenic areas associated with chronic cortical injury. Sprouting of axonal arborizations of pyramidal cells onto interneurons, upregulation of GABAergic neurons, and perhaps sprouting of inhibitory axons that make increased numbers of contacts onto pyramidal cells may all contribute to the increased inhibitory drive. Results in these models do not support the disinhibitory hypothesis of chronic epileptogenesis.

Animals↗

PubMed2005

Different function of pedunculopontine GABA and glutamate receptors in nucleus accumbens dopamine, pedunculopontine glutamate and operant discriminative behavior.

The nucleus accumbens, as the main input structure of the ventral basal ganglia loop, is described as a limbic-motor interface. Dopamine input to nucleus accumbens modulates processing of concurrent glutamate input from limbic structures carrying motor and motivational information. There is evidence that these dopamine/glutamate interactions are fundamentally involved in response selection processes. However, the pedunculopontine tegmental nucleus (PPTg) in the brainstem is connected with limbic structures as well as dopaminergic midbrain areas, which also project to the nucleus accumbens. Furthermore, behavioral studies implicate the PPTg in complex, motivated behavior. Thus, the PPTg might be involved in motivated behavior by influencing response selection processes in the nucleus accumbens. In this study we used in vivo microdialysis in freely moving rats in order to inhibit (100, 200, 300 and 400 microm baclofen) or stimulate [5, 12.5, 25 or 50 micromalpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA)] the PPTg in animals that are performing an operant discrimination task for food reward. The behavioral consequences were correlated with dopamine and glutamate levels in nucleus accumbens and PPTg, respectively. PPTg inhibition by local GABAB receptors impaired the response rate and accuracy of performance in the operant discrimination task. PPTg stimulation by local AMPA receptors exclusively impaired the response rate. Both treatments blocked the performance-driven dopamine signal in nucleus accumbens, whereas glutamate in PPTg was enhanced after AMPA administration only. The data indicate that the PPTg functionally participates in a network of subcortical and cortical structures, which is responsible for the execution of motivated behavior and response selection processes.

Analysis of Variance↗

PubMed1987

[The effect of lidocaine on brain edema and neural function].

Recently lidocaine (Ld) has been reported to have beneficial effects on neural suppression caused by experimental cerebral ischemia or spinal cord injury. In this paper, the effects of Ld on brain edema, local cerebral blood flow (lCBF), and neural function in the thalamocortical and cortical structures were experimentally studied. Vasogenic brain edema was induced by exposure of the cat's cerebral surface to the air in the manner of Prados et al. The dura mater over the left cerebral hemisphere was resected, and the brain was exposed to room air for 12 hours. The animals were divided into two groups. In the control group of 31 cats, Ld was not administered. In the treated group of 8 cats, Ld (4.5 mg/kg) was given intravenously immediately after the beginning of the air-exposure and thereafter administered as a drip infusion at the rate of 2 mg/kg/hour. In the untreated group, 12 hours after exposure, the cerebral water content measured by gravimetry in the cortex, white matter and thalamus increased by approximately 1.9, 4.1, 0.7%, respectively, compared to the control values. Local CBF measured by the hydrogen clearance method decreased to about 71, 57 and 56% of the control value, respectively. The latency of the N1 component of the somatosensory evoked response (SER) was prolonged significantly 6 hours after air-exposure. The amplitude of the direct cortical response (DCR) decreased significantly 6 hours after air-exposure, and became approximately 50% of the control 12 hours after exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Cortical hypoperfusion as a possible cause of 'subcortical aphasia'.

This study was designed to investigate whether aphasia in stroke patients with subcortical lesions ('subcortical aphasia') was due to the subcortical lesion itself or to dysfunction of cortical language zones. A consecutive series of 25 right-handed stroke patients with left hemisphere lesions verified by CT scanning were examined for aphasia in the acute stage, and two weeks, three months and six months after the insult. Cerebral angiography, CT scan and regional cerebral blood flow (rCBF) measurements with the 133Xe intracarotid method were performed in the acute stage. The CT scan was repeated six months later. Seven patients had lesions which involved cortical structures. All of these were severely aphasic in the acute stage and six months later. The rCBF studies showed severe reduction of flow in the infarcts; the perfusion was incompatible with tissue viability. Eighteen patients had subcortical lesions. Eight of these were midly to severely aphasic in the acute state. Recovery was always excellent. Five patients recovered completely, while 3 showed only discrete (clinically undetectable) aphasia after six months. The rCBF demonstrated low-flow areas in the cortex overlying the deep lesions, with a blood flow which was sufficient for tissue viability, but insufficient for normal tissue function (an 'ischaemic penumbra'). The blood flow was pressure dependent (showing impaired autoregulation) in these low flow areas. Ten patients with subcortical lesions were not aphasic. Their CBF was normal. The subcortical lesions were permanent on CT scan while aphasia was transient in these patients as recovery was seen within three months. It was therefore unlikely that the subcortical lesions as such were the cause of aphasia. The present findings indicate that aphasia in patients with subcortical lesions may be due to hypoperfusion and functional loss in cortical language zones. The cortical low-flow areas were invariably confined to occluded vascular territories. These territories were kept viable by collateral circulation characterized by penumbral flow and impaired autoregulation. The patients showed excellent recovery from aphasia. We suggest that the recovery of language is caused by spontaneous arterial recanalization or expansion of collaterals, giving rise to enhancement of flow in the hypoperfused cortical penumbra.

Adult↗

PubMed2000

Saccadic eye movement disturbances in whiplash patients with persistent complaints.

In order to analyse the possible basis of subjective complaints following whiplash injury, horizontal eye movements were examined in subjects with persistent complaints ('symptomatic group') and subjects who had completely recovered ('recovered group'). The results for the symptomatic and recovered groups were compared with those for age-matched, healthy volunteers (control group). A battery of different saccade paradigms was employed: two were reflexive saccade tasks including a gap and an overlap task, and two were intentional saccade tasks consisting of an antisaccade and a memory-guided saccade task. In addition, the symptomatic and recovered groups also underwent psychiatric evaluation in a structured clinical interview, and all groups were assessed for emotional functioning using the Beck Depression Inventory (BDI). The recovered group did not differ significantly from the control group in saccade performance and emotional functioning. The symptomatic group showed dissociation of their performances of reflexive and intentional saccade tasks: performance in reflexive saccade tasks was normal, but in intentional saccade tasks the symptomatic group showed significantly impaired inhibition of unwanted reflexive saccades, impaired saccade triggering (i.e. increased latency) and a higher percentage error in amplitude in memory-guided saccades. Based on clinical interviews, no signs of major depression or dysthymia were found in any of the groups. Compared with the other two groups, the symptomatic group had significantly higher overall BDI scores, but these resulted from BDI dimensions that were non-specific to depression, viz. 'physiological manifestations' (e.g. fatigue, sleep disturbance) or 'performance difficulty' (e.g. work inhibition). In summary, in the symptomatic group the pattern of eye movement disturbances together with normal performance in reflexive saccade tasks and impaired performance in the intentional saccade tasks, especially impaired inhibitory function, suggests dysfunction of prefrontal and frontal cortical structures.

Adult↗

PubMed1988

Dendritic pattern formation involves both oriented regression and oriented growth in the barrels of mouse somatosensory cortex.

The dendritic structure of neurons in the inner one-third of the wall of the barrels of somatosensory cortex was examined in animals at 10, 15, 20, 25, and 30 days of age. In adults, dendrites of these neurons project largely towards the barrel hollow. The amount of dendrite in the hemifield towards the barrel hollow, in which thalamic afferents terminate, increased with age, while the amount in the hemifield away from the hollow decreased, as measured by dendritic intersections with concentric rings. Loss of primary dendritic branches across these ages occurred both for dendrites arising on the side of the soma oriented away from the barrel hollow and for dendrites on the side of the soma nearest to the hollow. The loss of primary branches was much greater on the side away from the hollow. The amount of dendrite per primary branch increased for branches oriented towards the hollow, whereas it did not change or was somewhat reduced for those branches that remained on the side of the soma opposite the hollow. Thus both the selective loss of entire branches and the selective embellishment of others occur during the development of these somatosensory cortical structures.

Aging↗

PubMed1995

Relationship between the organization of the forepaw barrel subfield and the representation of the forepaw in layer IV of rat somatosensory cortex.

We studied the organization of the forepaw barrel subfield (FBS) in layer IV of adult rat somatosensory cortex using the mitochondrial marker cytochrome oxidase and related this organization to the representation of the forepaw. The FBS is an ovoid structure consisting of barrels and barrel-like structures, the most conspicuous of which form four centrally located medio lateral running bands. Each band contains three to four barrels. These centrally located bands are bordered along their entire lateral side by a nebulous zone of undifferentiated labeling. At the anterior border, two small barrels are located laterally and one or two larger barrels are located medially. Medial to the central zone are three well-defined barrels. The posterior border consists of a nebulous field of labeling and occasional barrel-like structures. The results from our electrophysiological recording and mapping revealed that the forepaw representation was topographically organized into a single map and that the forepaw map matches almost precisely with individual barrels and barrel-like structures in the FBS. Each of the four central bands is associated with the representation of a single glabrous digit. Digit two (D2) is represented anteriorly and followed posteriorly by D3 through D5. Within each digit band the digit is somatotopically organized, with the skin over the distal phalanx represented in the two lateral barrels and the middle and proximal phalanges represented in the medial barrel(s). The dorsal hairy digit skin and dorsal hand are represented in the lateral zone. D1 is represented by two small anteriorly located barrels. Medial to the representation of the glabrous digits is the representation of the palmar pads. The representation of these pads, in turn, lies between the representations of the thenar (located anteriorly) and hypothenar (located posteriorly) pads. Posterior to the hypothenar pad representation lie the representations of the wrist and forearm. While the present results support the conclusion that individual barrels are associated with discrete locations on the forepaw, examples were found where the recording site was not precisely located within the predicted barrel. Some of these errors may be accounted for by limitations in the mapping techniques; nevertheless, the FBS offers an excellent model system to study relationships between cortical structure and function.

Animals↗

PubMed2004

Cortical-area specific block of genetically determined absence seizures by ethosuximide.

Absence epilepsy is characterised by a paroxysmal loss of consciousness, of abrupt onset and termination, and is associated with a bilateral synchronous spike and wave discharge (SWD) on the electroencephalogram. Absence seizures involve an interplay between thalamic and cortical structures, although most research has so far focussed on sensory thalamic nuclei and the reticular thalamic nucleus (RTN). Thus, microinfusion of ethosuximide (ETX), a first choice anti-absence drug, into either the ventrobasal thalamus or RTN of the genetic absence epilepsy rat from Strasbourg (GAERS), a validated rat model of absence epilepsy, does not produce immediate cessation of seizure activity, as is seen following systemic administration. As recent evidence indicates a seizure initiation site within the peri-oral region of the primary somatosensory cortex (S1po), we have now applied ETX into S1po as well as the somatosensory cortex forelimb region (S1FL) and the motor cortex (M1) of freely moving GAERS. Microinfusion of 10 or 20 nmol/side of ETX into S1po produced an immediate cessation of seizure activity. A less marked response was produced when even a higher dose (200 nmol/side) was infused into S1FL. No reduction of SWD was seen when ETX was infused into M1. Microinfusion of CGP 36742 (5 nmol/side), a GABA(B) antagonist, produced immediate cessation of seizure activity in both S1po and M1 and a delayed effect in S1FL. These data suggest that the ability of ETX to abolish genetically determined absence seizures is cortical-area specific and support the involvement of S1po in the initiation of SWDs.

Animals↗

PubMed1994

Intensity dependence of auditory evoked dipole source activity.

The spatio-temporal approach of dipole source analysis represents a crucial methodological progress in research on individual differences in the dependence of auditory evoked potential amplitude on stimulus intensity (augmenting/reducing) because overlapping subcomponents of the N1/P2-component can be separated and can be related to their generating cortical structures. Basic aspects of the intensity dependence of auditory evoked dipole source activity were analysed in 40 healthy subjects. The evoked responses to binaural 1000-Hz tones at five levels of intensity (60, 70, 80, 90, 100 dB sound pressure level) were recorded at 33 sites across the scalp. The dipole source analysis of the grand average data confirms the reports in the literature that the N1/P2 potentials at the scalp can be explained by two dipoles per hemisphere: a tangential dipole, representing activity of the superior temporal cortex (including primary auditory cortex), and a radial dipole, representing activity of the lateral temporal cortex (secondary auditory areas). The intensity dependence of the tangential dipole activity was significantly more pronounced than that of the radial dipoles, supporting the assumption that radial and tangential dipoles represent different physiological processes. A high reliability of the intensity dependence of the tangential dipole (Pearson correlation: r = 0.88) was found when retesting the subjects after three weeks. Age was negatively correlated with the intensity dependence of the tangential dipole. Dipole source analysis proved to be a reliable method which allows, at least in part, to study separately the intensity dependence of the evoked responses from primary and secondary auditory cortices. This is of importance with regard to the hypothesis that the central serotonergic system modulates the intensity dependence of the evoked N1/P2-response of primary auditory cortex.

Adult↗

PubMed2000

Neocortical neurons lacking the protein-tyrosine kinase B receptor display abnormal differentiation and process elongation in vitro and in vivo.

The spatial and temporal expression of the protein-tyrosine kinase B (TrkB) receptor and its ligands has been correlated with the development of the neocortex. Activation of the receptor has been associated with neocortical neuronal survival, differentiation, connectivity and neurotransmitter release. Although such findings suggest an important role for TrkB signaling in corticogenesis, conclusive evidence from targeted gene deletion ("knockout"; TrkB -/-) mice has been limited, due in part to the neonatal lethality of most of these mutant mice and the confounding variables associated with the poor health of those few surviving slightly longer postnatally. In the present study, the effects of TrkB signaling on the survival, differentiation and integration of neocortical neurons was directly investigated in vitro and in vivo. First, we conducted a neuron-specific immunocytochemical analysis of TrkB -/- mice to determine whether early cortical structure and patterns of histogenesis were normal or perturbed. We then employed in vitro and in vivo approaches to extend the life of TrkB -/- neocortical neurons beyond the period possible in TrkB -/- mutant mice themselves: (i) dissociated cell culture to directly compare the developmental potential of TrkB -/-, +/- and +/+ neurons; and (ii) neural transplantation into homochronic wild-type recipients to investigate the cell-autonomous effects of the receptor knockout on the differentiation, growth and integration of neocortical neurons. These latter experiments allowed, for the first time, study of the survival and differentiation potential of TrkB -/- neocortical neurons beyond the initial stages of corticogenesis. Direct comparison of brains of TrkB -/-, +/- and +/+ littermates immunocytochemically labeled with antibodies to microtubule-associated protein-2, neurofilament and beta-tubulin III revealed subtle anatomical anomalies in the mutant mice. These anomalies include abnormally diffuse microtubule-associated protein-2 positive neurons just dorsal to the corpus callosum, and heterotopic aggregations of postmitotic neurons in the subventricular zones of the ganglionic eminences, both suggesting delayed neuronal migration and differentiation. Cell culture experiments revealed substantially reduced survival by TrkB -/- neocortical neurons, and a significant reduction in neurite outgrowth by surviving TrkB -/- neurons. In experiments where prelabeled embryonic or neonatal TrkB -/- neocortical neurons were transplanted into the cerebral cortices of neonatal wild-type recipients, a similar quantitatively significant defect in the formation of dendrites, as well as reduced integration of TrkB -/- neocortical neurons, was also evident. These findings demonstrate cell-autonomous abnormalities in the development of neocortical neurons from TrkB -/- mice, and the subtle, but potentially critical, role of protein-tyrosine kinase B signaling in neocortical neuronal survival, differentiation and connectivity.

Animals↗