PubMed Health⌕ Search

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 1,657 records · Page 92Linked to original sources

Transcranial direct current stimulation applied over the somatosensory cortex - differential effect on low and high frequency SEPs.

OBJECTIVE: Transcranial direct current stimulation (tDCS) has an influence on the excitability of the human motor cortex measured by motor evoked potentials (MEPs) after transcranial magnetic stimulation. Low and high frequency (HFOs) components of somatosensory evoked potentials (SEPs) were studied questioning whether a comparable effect can be observed after applying tDCS to the human somatosensory cortex. METHODS: Multichannel median nerve SEPs were recorded before and after applying tDCS of 1mA over a period of 9min with the cathode placed over the somatosensory cortex and the anode over the contralateral forehead and vice versa in a second session. The source activity of the N20, N30 and HFOs was evaluated before and after application of tDCS. RESULTS: After cathodal tDCS to the somatosensory cortex we found a significant reduction of the N20 source amplitude while there was no effect after anodal stimulation. For the N30 component and HFOs no change in source activity was observed. CONCLUSIONS: Corresponding to the results for the motor cortex a sustained reduction of the excitability of the somatosensory cortex after cathodal tDCS was shown. SIGNIFICANCE: We demonstrated differential effects of tDCS on the high and low frequency components of SEPs confirming the hypothesis of locally and functionally distinct generators of these two components.

Adult↗

Remodeling of synaptic structures in the motor cortex following spinal cord injury.

After spinal cord injury (SCI), structural reorganization occurs at multiple levels of the motor system including the motor cortex, and this remodeling may underlie recovery of motor function. The present study determined whether SCI leads to a remodeling of synaptic structures in the motor cortex. Dendritic spines in the rat motor cortex were visualized by confocal microscopy in fixed slices, and their density and morphology were analyzed after an overhemisection injury at C4 level. Spine density decreased at 7 days and partially recovered by 28 days. Spine head diameter significantly increased in a layer-specific manner. SCI led to a higher proportion of longer spines especially at 28 days, resulting in a roughly 10% increase in mean spine length. In addition, filopodium-like long dendritic protrusions were more frequently observed after SCI, suggesting an increase in synaptogenic events. This spine remodeling was accompanied by increased expression of polysialylated neural cell adhesion molecule, which attenuates adhesion between the pre- and postsynaptic membranes, in the motor cortex from as early as 3 days to 2 weeks after injury, suggesting a decrease in synaptic adhesion during the remodeling process. These results demonstrate time-dependent changes in spine density and morphology in the motor cortex following SCI. This synaptic remodeling seems to proceed with a time scale ranging from days to weeks. Elongation of dendritic spines may indicate a more immature and modifiable pattern of synaptic connectivity in the motor cortex being reorganized following SCI.

Amino Acids↗

Detection of sequences in the cerebellar cortex: numerical estimate of the possible number of tidal-wave inducing sequences represented.

The two major cortices of the brain--the cerebral and cerebellar cortex--are massively connected through intercalated nuclei (pontine, cerebellar and thalamic nuclei). We suggest that the two cortices co-operate by generating precise temporal patterns in the cerebral cortex that are detected in the cerebellar cortex as temporal patterns assembled spatially in the mossy fibers. We will begin by showing that the tidal-wave mechanism works in the cerebellar cortex as a read-out mechanism for such spatio-temporal patterns due to the synchronous activity they generate in the parallel fiber system which drives the Purkinje cells--the output neurons of the cerebellar cortex--to fire action potentials. We will review the anatomy of the mossy fibers and show that within a "beam", or "row" of cerebellar cortex the mossy fibers in principle could embed a vast number of tidal-wave generating sequences. Based on anatomical data we will argue that the cerebellar mossy fiber-granule cell-Purkinje cell system can potentially detect and--through learning--select from an enormous number of spatio-temporal patterns.

Animals↗

Rapid eye movement sleep deprivation in post-critical period, adolescent rats alters the balance between inhibitory and excitatory mechanisms in visual cortex.

Suppression of rapid eye movement sleep (REMS) in developing animals has both anatomical and physiological consequences. We have recently shown that initiating REMS deprivation (REMSD) prior to the end of the critical period in young rats delays termination of the critical period (CP) in visual cortex, and, consequently, the synaptic plasticity mechanisms that support a developmentally regulated form of long-term potentiation (LTP) are maintained in an immature state [J.P. Shaffery, C.M. Sinton, G. Bisset, H.P. Roffwarg, G.A. Marks, Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats, Neuroscience, 110 (2002) 431-443]. In CP animals, high-frequency, theta burst stimulation (TBS) directed at the white matter (WM) below visual cortex produces LTP in the post-synaptic cells in layer II/III (LTPWM-III). However, LTPWM-III can be induced in cortical tissue taken from REMS-deprived animals for up to a week beyond the usual end of the CP [J.P. Shaffery, C.M. Sinton, G. Bisset, H.P. Roffwarg, G.A. Marks, Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats, Neuroscience, 110 (2002) 431-443]. Further, in post-CP, adolescent animals (as late as postnatal day 60), REMSD appears to unmask synaptic plasticity mechanisms that allow for production of developmentally regulated LTPWM-III [J.P. Shaffery, J. Lopez, G. Bissette, H.P. Roffwarg, Rapid eye movement sleep deprivation revives a form of developmentally regulated synaptic plasticity in the visual cortex of post-critical period rats, Neurosci Lett., (2005), in press]. It has been proposed that REMSD's effects on production of LTPWM-III result from a reduction in efficiency of the inhibitory mechanisms thought to precipitate termination of the CP of brain development [J.P. Shaffery, J. Lopez, G. Bissette, H.P. Roffwarg, Rapid eye movement sleep deprivation revives a form of developmentally regulated synaptic plasticity in the visual cortex of post-critical period rats, Neurosci Lett., (2005), in press]. In this study we tested the hypothesis that low-frequency stimulation (LFS) of the fibers of the WM, which usually produces the related form of synaptic plasticity, long-term depression (LTD), will also reflect the reduction in inhibitory tone. We report here that LFS protocols, which in normally sleeping, adolescent rats usually produce either LTD or no change in response magnitude, in REMS-deprived, adolescent rats are more likely to produce LTP.

Age Factors↗

Effects of high dose of simvastatin on levels of dopamine and its reuptake in prefrontal cortex and striatum among SD rats.

Statins are increasingly being used for the treatment of a variety of conditions beyond their original indication for cholesterol lowering. We previously reported that simvastatin increased dopamine receptors in the rat prefrontal cortex [Q. Wang, W.L. Ting, H. Yang, P.T. Wong, High doses of simvastatin upregulate dopamine D(1) and D(2) receptor expression in the rat prefrontal cortex: possible involvement of endothelial nitric oxide synthase, Br. J. Pharmacol. 144 (2005) 933-939] and restored its downregulation in a model of Parkinson's disease (PD) [Q. Wang, P.H. Wang, C. McLachlan, P.T. Wong, Simvastatin reverses the downregulation of dopamine D1 and D2 receptor expression in the prefrontal cortex of 6-hydroxydopamine-induced Parkinsonian rats, Brain Res. 1045 (2005) 229-233]. Here we explore the effects of simvastatin treatment on tissue dopamine content and reuptake. Sprague-Dawley rats were given simvastatin (1 and 10 mg kg(-1)day(-1), p.o.) for 4 weeks. Brain tissue from prefrontal cortex and striatum were taken out for dopamine content and its reuptake. Using high-performance liquid chromatographic-mass spectrometer (HPLC-MS), simvastatin (10 mg kg(-1)day(-1)) was found to increase dopamine content by 110% in the striatum but decreased by 76% in the prefrontal cortex compared with the saline treated group. Dopamine (DA) reuptake was unchanged in both brain regions. These results suggest that chronic treatment with high dose of simvastatin may affect DA tissue level in prefrontal cortex and striatum without changing on DA reuptake. This may have important clinical implications in psychiatric and striatal dopaminergic disorders.

Analysis of Variance↗

Vestibular projection to the periarcuate cortex in the monkey.

Vestibular inputs to the cerebral cortex are important for spatial orientation, body equilibrium, and head and eye movements. We examined vestibular input to the periarcuate cortex in the Japanese monkey by analyzing laminar field potentials evoked by electrical stimulation of the vestibular nerve. Laminar field potential analysis in the depths of the cerebral cortex showed that vestibular-evoked potentials consisted of early-positive and late-negative potentials and early-negative and late-positive potentials in the superficial and deep layers of the periarcuate cortex, respectively, with latencies of 4.8-6.3 ms, suggesting that these potentials were directly conveyed to the cortex through the thalamus. These potentials were distributed continuously in the fundus, dorsal and ventral banks of the spur and the bottom of the junctional part of the arcuate sulcus and spur. This vestibular-projecting area overlapped the cortical distribution of corticovestibular neurons that were retrogradely labeled by tracer injection into the vestibular nuclei (previously reported area 6 pa), and also the distribution of smooth pursuit-related neurons recorded in the periarcuate cortex including area 8 in a trained monkey. These results are discussed in relation to the function of vestibular information in control of smooth pursuit and efferents of the smooth pursuit-related frontal eye field.

Afferent Pathways↗

Geometric atlas: modeling the cortex as an organized surface.

Recent atlases of the cortical surface are based on a modelization of the cerebral cortex as a topological sphere. This captures effectively its organization as a regular bidimensional sheet of layers parallel to the surface and with perpendicular cortical columns. Yet, while in the vertical direction cortices are almost the same throughout phylia, in the sense of its surface the cerebral cortex is one of the most variable and distinctive parts of the nervous system. Indeed, gyri and sulci appear to have a crucial organizing role in an architectonic, connectional, and functional sense. This organization is not explicitly captured by the surface model of the cortex. We propose a geometric model of the cortical anatomy based on flat representations of principal sulci obtained from surface reconstructions of MRI data, and on neuroanatomical and theoretical considerations concerning the folding patterns of the cortex. The cortex is modeled by a sphere where primary sulci are included as axes. The arrangement of the axes is a simplification of the arrangement of principal sulci observed in flat stereographic representations of the whole cortical surface. The position of secondary and tertiary sulci is then defined by a field of orientations parallel and orthogonal to the axes. We consider the use of the geometric model as a synthetic reference cortex for addressing reconstructions of cortical surfaces. We present a method which establishes a bijection between the geometric model and a cortical surface reconstruction by using the axes of the model as boundary conditions for a set of partial differential equations solved over both surfaces. Using the geometric model as atlas provides a natural parameterization of the cortical surface that, unlike angular coordinates, allows for a localization based on the surface distance to its main organizing landmarks and folding patterns.

Algorithms↗

Modulation of motor-cortex oscillatory activity by painful Adelta- and C-fiber stimuli.

Spontaneous approximately 20-Hz oscillations, arising predominantly from the primary motor cortex (MI), are readily observed by magnetoencephalography (MEG). Prior studies have indicated that the level of the approximately 20-Hz rhythm reflects the functional state of the MI cortex: increased 20-Hz level is associated with increased inhibition and suppression of the rhythm with excitation of MI. Close interaction is suggested between pain and the motor system by the association of chronic pain with motor dysfunction and by the alleviation of pain by motor-cortex stimulation. We therefore explored the effect of noxious input on motor-cortex functions by recording MEG signals from nine healthy subjects during selective laser stimulation of Adelta- and C-fibers of the hand. The approximately 20-Hz level was suppressed in the contralateral MI cortex in all nine subjects after painful Adelta- and C-fiber stimuli (P < 0.001). The suppression started 180 +/- 10 ms (mean +/- SEM) after Adelta-fiber stimuli and 820 +/- 30 ms after C-fiber stimuli, and peaked 160-170 ms later. Similar, but about 50% weaker, suppression of the approximately 20-Hz oscillations occurred in seven out of nine subjects in the ipsilateral MI. These results suggest automatic, lateralized, excitation of the MI cortex by noxious Adelta- and C-fiber input.

Adult↗

Estimating linear cortical magnification in human primary visual cortex via dynamic programming.

Human primary visual cortex is organized retinotopically, with adjacent locations in cortex representing adjacent locations on the retina. The spatial sampling in cortex is highly nonuniform: the amount of cortex devoted to a unit area of retina decreases with increasing retinal eccentricity. This sampling property can be quantified by the linear cortical magnification factor, which is expressed in terms of millimeters of cortex per degree of visual angle. In this paper, we present a new method using dynamic programming and fMRI retinotopic eccentricity mapping to estimate the linear cortical magnification factor in human primary visual cortex (V1). We localized cortical activity while subjects viewed each of seven stationary contrast- reversing radial checkerboard rings of equal thickness that tiled the visual field from 1.62 to 12.96 degrees of eccentricity. Imaging data from all epochs of each ring were contrasted with data from fixation epochs on a subject-by-subject basis. The resulting t statistic maps were then superimposed on a local coordinate system constructed from the gray/white matter boundary surface of each individual subject's occipital lobe, separately for each ring. Smoothed maps of functional activity on the cortical surface were constructed using orthonormal bases of the Laplace-Beltrami operator that incorporate the geometry of the cortical surface. This allowed us to stably track the ridge of maximum activation due to each ring via dynamic programming optimization over all possible paths on the cortical surface. We estimated the linear cortical magnification factor by calculating geodesic distances between activation ridges on the cortical surface in a population of five normal subjects. The reliability of these estimates was assessed by comparing results based on data from one quadrant to those based on data from the full hemifield along with a split-half reliability analysis.

Brain Mapping↗

Stimulation of adenosine A2A receptors elicits zif/268 and NMDA epsilon2 subunit mRNA expression in cortex and striatum of the "weaver" mutant mouse, a genetic model of nigrostriatal dopamine deficiency.

Interaction between basal ganglia and cerebral cortex is critical for normal goal-directed behavior. In the present study we have used the immediate early gene zif/268, as functional marker to investigate how the stimulation of adenosine A2A receptors, i.e. of the "indirect" striatal output pathway, affects striatal and cortical function in "weaver" mouse, a genetic model of dopamine deficiency. Furthermore, we have examined the effect of A2A receptor stimulation on glutamate receptor expression in the "weaver" brain. A single injection of CGS21680 (A2A receptor agonist), induced strong expression of zif/268 mRNA, detected by in situ hybridization, not only in striatum but also in the motor cortex of the "weaver" mutant. This cortical response seems to be elicited through the basal-ganglia-thalamo-cortical circuit, rather than through a direct cortical effect, since A2A receptors are not detectable in cortex according to our autoradiographic study. Co-administration of CGS21680 and quinpirole (D2 receptor agonist) attenuated the expression of zif/268 mRNA in dorsal striatum but not in motor cortex, indicating that the cortical response is dopamine-D2-receptor-independent. However, this co-administration induced an increase in zif/268 mRNA expression in somatosensory cortex, which could rely on disinhibition of the thalamo-cortical pathway. The motor cortical response could be of clinical interest, as it would further stimulate the "indirect" striatal pathway in a feed forward circuit, thus worsening the parkinsonian symptoms. Furthermore, the up-regulation of epsilon2 subunit mRNA of the NMDA receptor, induced by CGS21680 administration, seen in striatum and cortex of the "weaver" mouse, would lead to overactivity of these receptors worsening dyskinesias. These results suggest adenosine to play a significant role in regulating striatal and cortical neurochemistry in a dopamine-depleted mouse. Blockade of these receptors by specific A2A antagonists could ameliorate parkinsonian symptoms.

Adenosine↗

Tonotopic and heterotopic projection systems in physiologically defined auditory cortex.

Combined physiological and connectional studies show significant non-topographic extrinsic projections to frequency-specific domains in the cat auditory cortex. These frequency-mismatched loci in the thalamus, ipsilateral cortex, and commissural system complement the predicted topographic and tonotopic projections. Two tonotopic areas, the primary auditory cortex (AI) and the anterior auditory field (AAF), were electrophysiologically characterized by their frequency organization. Next, either cholera toxin beta subunit or cholera toxin beta subunit gold conjugate was injected into frequency-matched locations in each area to reveal the projection pattern from the thalamus and cortex. Most retrograde labeling was found at tonotopically appropriate locations within a 1 mm-wide strip in the thalamus and a 2-3 mm-wide expanse of cortex (approximately 85%). However, approximately 13-30% of the neurons originated from frequency-mismatched locations far from their predicted positions in thalamic nuclei and cortical areas, respectively. We propose that these heterotopic projections satisfy at least three criteria that may be necessary to support the magnitude and character of plastic changes in physiological studies. First, they are found in the thalamus, ipsilateral and commissural cortex; since this reorganization could arise from any of these routes and may involve each, such projections ought to occur in them. Second, they originate from nuclei and areas with or without tonotopy; it is likely that plasticity is not exclusively shaped by spectral influences and not limited to cochleotopic regions. Finally, the projections are appropriate in magnitude and sign to plausibly support such rearrangements; given the rapidity of some aspects of plastic changes, they should be mediated by substantial existing connections. Alternative roles for these heterotopic projections are also considered.

Animals↗

PSA-NCAM expression in the rat medial prefrontal cortex.

The rat medial prefrontal cortex, an area considered homologous to the human prefrontal cortex, is a region in which neuronal structural plasticity has been described during adulthood. Some plastic processes such as neurite outgrowth and synaptogenesis are known to be regulated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). Since PSA-NCAM is present in regions of the adult CNS which are undergoing structural remodeling, such as the hypothalamus or the hippocampus, we have analyzed the expression of this molecule in the medial prefrontal cortex of adult rats using immunohistochemistry. PSA-NCAM immunoreactivity was found both in cell bodies and in the neuropil of the three divisions of the medial prefrontal cortex. All cell somata expressing PSA-NCAM corresponded to neurons and 5' bromodeoxyuridine labeling after long survival times demonstrated that these neurons were not recently generated. Many of these PSA-NCAM immunoreactive neurons in the medial prefrontal cortex could be classified as interneurons on the basis of their morphology and glutamate decarboxylase, isoform 67 expression. Some of the PSA-NCAM immunoreactive neurons also expressed somatostatin, neuropeptide Y and calbindin-D28K. By contrast, pyramidal neurons in this cortical region did not appear to express PSA-NCAM. However, some of these principal neurons appeared surrounded by PSA-NCAM immunoreactive puncta. Some of these puncta co-expressed synaptophysin, suggesting the presence of synapses. Since the etiology of some psychiatric disorders has been related to alterations in medial prefrontal cortex structural plasticity, the study of PSA-NCAM expression in this region may open a new approach to the pathophysiology of these mental disorders.

Animals↗

Transhemispheric functional reorganization of the motor cortex induced by the peripheral contralateral nerve transfer to the injured arm.

Peripheral nerve injury in a limb usually causes functional reorganization of the contralateral motor cortex. However, a dynamic process of the novel transhemispheric functional reorganization in the motor cortex was found in adult rats after transferring the seventh cervical nerve root from the contralateral healthy side to the injured limb. Initially the ipsilateral motor cortex activated the injured forepaw for 5 months after the operation. Then, both hemispheres of the cortex activated the injured forepaw, and finally the contralateral cortex exclusively controlled the injured forepaw. It is concluded an extensive functional shift occurred between two hemispheres based on neural plasticity in the CNS. The experimental results of the later lesions of the ipsilateral cortex suggest that maintaining transhemispheric functional reorganization does not depend on the corpus callosum, but depends on mechanisms involving central axonal sprouting. Possible mechanisms underlying the alternative changes in cortical functions were discussed in rats and in patients having similar operations.

Animals↗

Gene expression in the rat cerebral cortex: comparison of recovery sleep and hypnotic-induced sleep.

Most hypnotic medications currently on the market target some aspect of GABAergic neurotransmission. Although all such compounds increase sleep, these drugs differentially affect the activity of the cerebral cortex as measured by the electroencephalogram. Whereas benzodiazepine medications such as triazolam tend to suppress slow wave activity in the cortex, the GABA(B) ligand gamma-hydroxybutyrate greatly enhances slow wave activity and the non-benzodiazepine, zolpidem, which binds to the omega1 site on the GABA(A) receptor/Cl(-) ionophore complex, is intermediate in this regard. Our previous studies have demonstrated that a small number of genes exhibit increased expression in the cerebral cortex of the mouse and rat during recovery sleep after sleep deprivation: egr-3, fra-2, grp78, grp94, ngfi-b, and nr4a3. Using these genes as a panel of biomarkers associated with sleep, we asked whether hypnotic medications induce similar molecular changes in the rat cerebral cortex to those observed when both sleep continuity and slow wave activity are enhanced during recovery sleep. We find that, although each drug increases the expression of a subset of genes in the panel of biomarkers, no drug fully replicates the molecular changes in the cortex associated with recovery sleep. Furthermore, high levels of slow wave activity in the cortex are correlated with increased expression of fra-2 whereas the expression of grp94 is correlated with body temperature. These results demonstrate that sleep-related changes in gene expression may be affected by physiological covariates of sleep and wakefulness rather than by vigilance state per se.

Analysis of Variance↗

Postnatal alterations in dopaminergic markers in the human prefrontal cortex.

Dopamine in the prefrontal cortex plays a critical role in normal cognition throughout the lifespan and has been implicated in the pathophysiology of neuropsychiatric disorders such as schizophrenia and attention deficit disorder. Little is known, however, about the postnatal development of the dopaminergic system in the human prefrontal cortex. In this study, we examined pre- and post-synaptic markers of the dopaminergic system in postmortem tissue specimens from 37 individuals ranging in age from 2 months to 86 years. We measured the levels of tyrosine hydroxylase, the rate limiting enzyme in dopamine biosynthesis, using Western immunoblotting. We also examined the gene expression of the three most abundant dopamine receptors (DARs) in the human prefrontal cortex: DAR1, DAR2 and DAR4, by in situ hybridization. We found that tyrosine hydroxylase concentrations and DAR2 mRNA levels were highest in the cortex of neonates. In contrast, the gene expression of DAR1 was highest in adolescents and young adults. No significant changes across age groups were detected in mRNA levels of DAR4. Both DAR1 and DAR2 mRNA were significantly lower in the aged cortex. Taken together, our data suggest dynamic changes in markers of the dopamine system in the human frontal cortex during postnatal development at both pre-and post-synaptic sites. The peak in DAR1 mRNA levels around adolescence/early adulthood may be of particular relevance to neuropsychiatric disorders such as schizophrenia in which symptoms manifest during the same developmental period.

Adolescent↗

The involvement of the orbitofrontal cortex in learning under changing task contingencies.

Previous investigations examining the rat prefrontal cortex subregions in attentional-set shifting have commonly employed two-choice discriminations. To better understand how varying levels of difficulty influence the contribution of the prefrontal cortex to learning, the present studies examined the effects of orbitofrontal cortex inactivation in a two- or four-choice odor reversal learning test. Long-Evans rats were trained to dig in cups that contained distinct odors. In the two-choice odor discrimination, one odor cup was always associated with a cereal reinforcement in acquisition while the opposite odor cup was associated with a cereal reinforcement in reversal learning. In the four-choice odor discrimination, an additional two cups containing distinct odors were used that were never associated with reinforcement in acquisition or reversal learning. Bilateral infusions of the GABA-A agonist, muscimol (0.5 microg) into the orbitofrontal cortex did not impair acquisition of either the two- or four-choice discrimination task. However, muscimol infusions into the orbitofrontal cortex impaired two- and four-choice reversal learning. In the two-choice odor reversal, muscimol treatment selectively increased perseverative errors. In the four-choice odor reversal, muscimol treatment increased perseverative, regressive, as well as irrelevant errors. These findings suggest that the orbital prefrontal cortex not only enables task switching by supporting the initial inhibition of a previously relevant choice pattern, but under increasing task demands also enables the reliable execution of a new choice pattern and reduction of interference to irrelevant stimuli.

Animals↗

Effects of pre- or post-training entorhinal cortex AP5 injection on fear conditioning.

Fear conditioning is one of the most studied paradigms to assess the neural basis of emotional memory. The circuitry involves NMDA receptor activation in the amygdala and, in the case of contextual conditioning, in the hippocampus. Entorhinal cortex is one of the major input/output structures to the hippocampus and also projects to the amygdala, both through glutamatergic transmission. Other learning tasks involving hippocampus and amygdala, such as inhibitory avoidance, require entorhinal cortex during acquisition and consolidation. However, the involvement of NMDA receptors mediated transmission in entorhinal cortex in fear conditioning acquisition and consolidation is not clear. To investigate that issue, rats were trained in fear conditioning to both contextual and tone conditioned stimulus. Immediately before, immediately, 30 or 90 min after training they received NMDA antagonist AP5 or saline injections bilaterally in the entorhinal cortex (AP-6.8 mm, L +/-5.0 mm DV-6.8 mm). Contextual fear conditioning was measured 24 h after training, and tone fear conditioning 48 h after training. AP5 injections selectively impaired contextual fear conditioning only when injected pre-training. Post-training injections had no effect. These findings suggest that entorhinal cortex NMDA receptors are necessary for acquisition, but not for consolidation, of contextual fear conditioning. On the other hand, both acquisition and consolidation of tone fear conditioning seem to be independent of NMDA receptors in the entorhinal cortex.

2-Amino-5-phosphonovalerate↗

Bilateral volume reduction of the insular cortex in patients with schizophrenia: a volumetric MRI study.

The morphologic changes of the insular cortex have been described in schizophrenia, but with inconsistencies between reports. We investigated the insular cortex volume by magnetic resonance imaging in 59 schizophrenia patients (31 males, 28 females) and 62 age- and gender-matched healthy controls (31 males, 31 females). The insular cortex volume was measured on consecutive coronal 1-mm slices. Volumes of the left and right insular cortex were significantly reduced in schizophrenia patients compared with control subjects. There were no effects of gender on the insular cortex volume in the patient group or control subjects. Bilateral insular cortex volumes were correlated negatively with illness duration in the patient group. The findings of this study suggest that there is a possible progressive loss of the gray matter volume of the bilateral insular cortices subsequent to the onset of schizophrenia.

Adolescent↗