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 1,315 records · Page 73Linked to original sources

PubMed1986

The role of 3,3',5'-triiodothyronine in the regulation of type II iodothyronine 5'-deiodinase in the rat cerebral cortex.

Type II iodothyronine 5'-deiodinase (5'D-II) activity is the source of 75-80% of the cerebral cortex T3 content in euthyroid rats. The activity of this enzyme is increased in hypothyroidism and can be quickly suppressed by T4 and rT3 by mechanisms involving neither protein synthesis nor nuclear T3 receptors. We have examined the possibility that endogenous cerebrocortical rT3 levels play a physiological role in the regulation of this enzyme. Thyroidectomized rats were injected with graded doses of [125I]rT3, and cortex 5'D-II activity and rT3 content were determined at various times thereafter. Enzyme activity was reduced as early as 10 min after the injection of 0.75 microgram rT3/100 g BW, and 18 h after 25 micrograms/100 g BW remained 60% suppressed. Regardless of the time after the injection, 5'D-II activity was inversely related to the rT3 content in the cortex; nearly complete suppression was observed at 0.5 ng rT3/g tissue, 50% at 80 pg/g, and 20-30% at 30 pg/g, the euthyroid level. After the infusion of 0.75 microgram rT3/100 g, maximal inhibition occurred at 10 min, before the rT3 content reached maximum levels, and the 5'D-II activity started to recover after the rT3 level fell below 300 pg/g tissue. After increasing doses of T4 administered to thyroidectomized rats, serum and cerebrocortical T4 concentrations increased in a dose-dependent manner, but the increment in the latter was steeper than that in the former. Serum rT3 increments were also proportional to the dose of T4, but cerebrocortical rT3 increased to a greater extent, as evidenced by a 3-fold increment in the cerebrocortical rT3 to T4 ratio. With 1.6 microgram T4/100 g BW, cerebrocortical rT3 reached approximately 100 pg/g, about 3 times the euthyroid level, suggesting that at this T4 dose, the rT3 formed from T4 accounts for part of the inhibition of 5'D-II. With the half-maximal suppressive dose of T4, cortex T4 was about 400 pg/g, but rT3 was negligible. We conclude that: suppression of cortex 5'D-II by rT3 is rapid and requires the presence of rT3 in the tissue (i.e. no long-lived mediators); intracortical rT3 is about 5 times more potent than T4 in suppressing this enzyme; the cortex of rT3-5'D-II suppression relationships suggest that the euthyroid levels of cortex rT3 may be significant in the modulation of 5'D-II.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2001

Entorhinal cortex atrophy in epilepsy patients exhibiting normal hippocampal volumes.

OBJECTIVE: To determine whether MRI volumetric measurement of the entorhinal cortex could detect structural damage and lateralize the seizure focus in patients with temporal lobe epilepsy in whom no measurable hippocampal abnormalities were found. BACKGROUND: A reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with intractable temporal lobe epilepsy and hippocampal atrophy was recently shown. METHODS: MRI volumetric analysis of the entorhinal cortex was performed using a T1-weighted three-dimensional gradient echo sequence in 24 control subjects and 22 patients with temporal lobe epilepsy and normal hippocampal volumes. Thirteen patients underwent surgery, with a mean postoperative follow-up of 36 months. RESULTS: Group analysis (multivariate analysis of variance) showed a reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with left (p < 0.0001) and right temporal lobe epilepsy (p < 0.0001). Lateralization of the seizure focus could be done in 14 of 22 patients (64%) based on entorhinal cortex volumetry. CONCLUSION: Entorhinal cortex atrophy ipsilateral to the seizure focus supports the presence of structural damage in the mesial temporal lobe in patients with temporal lobe epilepsy and normal hippocampal volumes and emphasizes the participation of the entorhinal cortex in the pathogenesis of this disorder.

Adult↗

PubMed2006

Functional imaging reveals numerous fields in the monkey auditory cortex.

Anatomical studies propose that the primate auditory cortex contains more fields than have actually been functionally confirmed or described. Spatially resolved functional magnetic resonance imaging (fMRI) with carefully designed acoustical stimulation could be ideally suited to extend our understanding of the processing within these fields. However, after numerous experiments in humans, many auditory fields remain poorly characterized. Imaging the macaque monkey is of particular interest as these species have a richer set of anatomical and neurophysiological data to clarify the source of the imaged activity. We functionally mapped the auditory cortex of behaving and of anesthetized macaque monkeys with high resolution fMRI. By optimizing our imaging and stimulation procedures, we obtained robust activity throughout auditory cortex using tonal and band-passed noise sounds. Then, by varying the frequency content of the sounds, spatially specific activity patterns were observed over this region. As a result, the activity patterns could be assigned to many auditory cortical fields, including those whose functional properties were previously undescribed. The results provide an extensive functional tessellation of the macaque auditory cortex and suggest that 11 fields contain neurons tuned for the frequency of sounds. This study provides functional support for a model where three fields in primary auditory cortex are surrounded by eight neighboring "belt" fields in non-primary auditory cortex. The findings can now guide neurophysiological recordings in the monkey to expand our understanding of the processing within these fields. Additionally, this work will improve fMRI investigations of the human auditory cortex.

Animals↗

PubMed1992

Characterization of insulin receptors in the bovine adrenal cortex and medulla.

In order to identify insulin receptors in the bovine adrenal cortex and medulla, we have studied 125I-porcine insulin binding to the membrane preparations from the bovine adrenal cortex and medulla. 125I-porcine insulin bound not only to the bovine adrenal cortex but to the medulla in time-, temperature-, and pH-dependent manners. The maximum levels of 125I-porcine insulin binding in the two tissues were observed at 4 degrees C for 24 h of incubation, and its optimum pH ranged from 7.6 to 8.0. Under these conditions, at tracer concentration of porcine insulin (200 pg/ml), 10.4% and 6.6% of 125I-porcine insulin added to each reaction tube bound specifically to 10(5) x g-pellet fractions (microsomal membrane) from the cortical tissue (0.3 mg of protein) and from the medullary tissue (2 mg of protein), respectively. 125I-porcine insulin binding was observed predominantly in the microsomal membrane from the bovine adrenal cortex, and in a 15,000 x g- pellet fraction (synaptosomal membrane) from the bovine adrenal medulla. Scatchard analysis of binding data yielded curvilinear plots in each tissue. Analysis of curvilinear plots based on two sites model revealed similar affinity constant between the cortex and medulla. Receptor concentration of the cortex was several times higher than that of the medulla. In the two bovine adrenal tissues, human proinsulin and insulin-like growth factor I (IGF-I) had about 1/100 potency compared to porcine insulin in displacing 125I-porcine insulin binding. Porcine glucagon added with concentration up to 10(-6) M did not inhibit 125I-porcine insulin binding to both the cortex and the medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗

PubMed2005

Medial prefrontal cortex lesions abolish contextual control of competing responses.

There is much debate as to the extent and nature of functional specialization within the different subregions of the prefrontal cortex. The current study was undertaken to investigate the effect of damage to medial prefrontal cortex subregions in the rat. Rats were trained on two biconditional discrimination tasks, one auditory and one visual, in two different contexts. At test, they received presentations of audiovisual compounds of these training stimuli in extinction. These compounds had dictated either the same (congruent trials) or different (incongruent trials) responses during training. In sham-operated controls, contextual cues came to control responding to conflicting information provided by incongruent stimulus compounds. Experiment 1 demonstrated that this contextual control of responding was not evident in individual rats with large amounts of damage that included the prelimbic and cingulate subregions of the prefrontal cortex. Experiment 2 further dissociated the result of Experiment 1, demonstrating that lesions specific to the anterior cingulate cortex were sufficient to produce a deficit early on during presentation of an incongruent stimulus compound but that performance was unimpaired as presentation progressed. This early deficit suggests a role for the anterior cingulate cortex in the detection of response conflict, and for the medial prefrontal cortex in the contextual control of competing responses, providing evidence for functional specialization within the rat prefrontal cortex.

Animals↗

PubMed2000

Paracrine control of the adult adrenal cortex vasculature by vascular endothelial growth factor.

The extensive vascular network that irrigates the adult adrenal cortex is essential for both the delivery of oxygen and nutrients to glandular steroidogenic cells and for the rapid and efficient export of corticosteroid products from these cells into the blood flow. During experimental and pathological changes in adrenal cortex size caused by ACTH overproduction or deficiency, the vasculature evolves in a coordinated manner with the mass of glandular cells so that blood vessel formation/regression and cortical gowth/atrophy are respectively synchronized. In addition to its previously reported expression in human fetal adrenocortical cells, the angiogenic factor VEGF-A appears also to be strongly expressed by both glomerulosa and fasciculata cells of the adult bovine adrenal cortex, when the endothelium is quiescent. Moreover, the expression of the two major transcripts encoding the 121 and the 165 amino acid-long isoforms of VEGF-A was observed to be rapidly (within 2-4 h) up-regulated (2-3 fold) by ACTH in primary cultures of bovine fasciculata and glomerulosa cells. The expression of the signalling VEGF receptors R1 (flt-1) and R2 (flk-1) was restricted to the endothelial cells of the cortex whereas neuropilin-1 was expressed by both endothelial and steroidogenic cells. This suggests that, under the control of the pituitary hormone ACTH, VEGF exerts a paracrine control over the vasculature of the adult adrenal cortex. Given its known effects as an anti-apoptotic agent and an inducer of endothelial fenestration, VEGF is likely to play a role in the maintenance of the dense and fenestrated vascular bed of the adrenal cortex. The vasculature thus appears as an important secondary target of ACTH action in the physiological control of adrenal cortex homeostasis.

Adrenal Cortex↗

PubMed1992

Neuronal response properties within subregions of raccoon somatosensory cortex 1 week after digit amputation.

Multiple penetrations in the somatosensory cortex of three anesthetized raccoons 1 week following amputation of the fourth digit provided detailed information about somatotopy and neuronal responsiveness in the deafferented cortex. Recordings in a total of 601 penetrations (292 in deafferented cortex and 309 in the surrounding cortex) were compared with those from intact control animals described previously (Rasmusson et al., 1991). The level of spontaneous activity increased within the deafferented cortex, with 42% of the sites having high or moderate levels of spontaneous activity, in comparison with 18% in control animals. There was also an increase in the incidence of inhibitory responses to stimulation of adjacent digits (26% of the penetrations vs. 10% in control animals), confirming previous findings. These two variables, increased spontaneous activity and the presence of strong lateral inhibition, were highly correlated in individual penetrations. An unexpected finding was that the cortex representing the intact parts of forepaw was also disrupted with respect to these two measures, suggesting that amputation had an effect outside the deafferented region. In contrast, response properties that are more clearly a reflection of information processing in the dorsal column-medial lemniscal pathway (adaptation and threshold) were altered only within the deafferented region. The deafferented region was not homogeneous immediately after amputation, but consisted of a radically affected core region and a slightly affected fringe adjacent to the intact representations. This inhomogeneity had also been apparent with partial digit deafferentation, reported previously. The fringe, approximately 1 mm in width, may reflect overlapping projections from adjacent digits at one or more levels of the somatosensory pathway. Since the size of the fringe is similar to the maximum extent of reorganization found in other models of reorganization, the mechanisms of plasticity within this region may involve an unmasking of pre-existing synapses with slight modification in synaptic strength. However, the plasticity within the core region of the raccoon seen in these experiments, which may be 5 mm from nondeafferented cortex, requires more extensive changes, perhaps via polysynaptic pathways.

Afferent Pathways↗

PubMed1999

Gliomas in rodent whisker barrel cortex: a new tumor model.

OBJECT: Surgical treatment of gliomas is difficult because they are invasive. Invasion of essential cortex often limits or precludes surgical resection. A tumor model was developed in which the rodent whisker barrel cortex was used to examine how gliomas affect cortical function and structure. METHODS: Both DBT (mouse) and C6 (rat) glioma cell lines were grown in culture and labeled with the fluorescent marker Dil in vitro. Labeled tumor cells were then injected into the whisker barrel cortex of adult mice and rats. Neurological assessments were made daily and magnetic resonance (MR) images were obtained. Animals were killed by perfusion 6 to 14 days after injection, and histological sections were prepared and studied. Tumors were found in all 20 rats and 10 mice that had been injected with the C6 and DBT cell lines, respectively. The animal cells had been labeled with Dil in vitro, and all in vivo tumors proved to be Dil positive. The MR images revealed the tumor locations and serial MR images demonstrated tumor growth. Histological evaluation confirmed the location of the tumor and the disruption of barrel cortex architecture. CONCLUSIONS: Both DBT and C6 glioma cell lines can be used to generate malignant glial tumors reproducibly in the whisker barrel cortex. Fluorescent labeling and cytochrome oxidase staining permit visualization of tumor growth patterns, which disrupt the barrel cortex by microscopic invasion and by gross tissue deformation. Magnetic resonance imaging demonstrates the anatomical extension of these tumors in live rodents. Using this model for further studies on the effects of malignant glioma growth on functional cerebral cortex should advance our understanding of the neurological issues and management of patients with these tumors.

Animals↗

PubMed1999

Comparison of effects of haloperidol administration on amphetamine-stimulated dopamine release in the rat medial prefrontal cortex and dorsal striatum.

Research has shown that there are important neurochemical differences between the mesocortical and mesostriatal dopamine systems. The work reported in this paper has sought to compare the regulation of dopamine release in the medial prefrontal cortex and the anterior caudate-putamen. In vivo microdialysis was used to recover dialysate fluid for subsequent assay for dopamine concentrations. The responses to D2 antagonist (haloperidol) administration, which has been shown to increase impulse-dependent dopamine release, were compared. Results demonstrated a diminished effect of systemic haloperidol administration on dopamine efflux in the prefrontal cortex. The responses to systemic administration of a nonimpulse-dependent, transporter-mediated, dopamine releaser (d-amphetamine) were also contrasted. Results again demonstrated a diminished pharmacological effect in the cortex. The potential interaction of stimulation of these two types of dopamine release was examined by coadministration of these compounds. Haloperidol pretreatment dramatically potentiated the dopamine-releasing effect of amphetamine administration. This effect was observed in both the cortex and the striatum. Subsequent work demonstrated that this effect of haloperidol was mediated by D2-like receptors in the prefrontal cortex. These results are discussed in relation to other neurochemical and neuroanatomical studies demonstrating sparse densities of dopamine transporter sites and dopamine D2 receptors in the cortex compared with the striatum. They demonstrate a functional correlate to the recently reported, largely extrasynaptic localization of dopamine transporter sites in the prefrontal cortex. Furthermore, they demonstrate the existence of cortical D2-like autoreceptors that may normally be "silent" under basal conditions.

Animals↗

PubMed1999

Localization of the first and second somatosensory areas in the human cerebral cortex with functional MR imaging.

BACKGROUND AND PURPOSE: Our objective was to map by means of a conventional mid-field (1.0 T) MR imaging system the somatosensory areas activated by unilateral tactile stimulation of the hand, with particular attention to the areas of the ipsilateral hemisphere. METHODS: Single-shot echo-planar T2*-weighted imaging sequences were performed in 12 healthy volunteers to acquire 10 contiguous 7-mm-thick sections parallel to the coronal and axial planes during tactile stimulation of the hand. The stimulation paradigm consisted of brushing the subjects' palm and fingers with a rough sponge at a frequency of about 1 Hz. RESULTS: Stimulation provoked a signal increase (about 2% to 5%) that temporally corresponded to the stimulus in several cortical regions of both hemispheres. Contralaterally, activation foci were in the anterior parietal cortex in an area presumably corresponding to the hand representation zone of the first somatosensory cortex, in the posterior parietal cortex, and in the parietal opercular cortex forming the upper bank of the sylvian sulcus and probably corresponding to the second somatosensory cortex. Activation foci were also observed in the frontal cortex. Ipsilaterally, activated areas were in regions of the posterior parietal and opercular cortices roughly symmetrical to those activated in the contralateral hemisphere. The same activation pattern was observed in all subjects. CONCLUSION: The activated areas of the somatosensory cortex described in the present study corresponded to those reported in other studies with magnetoelectroencephalography, positron emission tomography, and higher-field functional MR imaging. An additional area of activation in the ipsilateral parietal operculum, unnoticed in other functional MR imaging studies, was also observed.

Adult↗

PubMed1999

Zinc inhibition of gamma-aminobutyric acid(A) receptor function is decreased in the cerebral cortex during pilocarpine-induced status epilepticus.

Functional modulation of gamma-aminobutyric acid(A) (GABA(A)) receptors by Zn(2+), pentobarbital, neuroactive steroid alphaxalone, and flunitrazepam was studied in the cerebral cortex and cerebellum of rats undergoing status epilepticus induced by pilocarpine. Under control conditions, Zn(2+) dose-dependently inhibited muscimol-stimulated uptake of (36)Cl(-) in cortical and cerebellar membranes. However, Zn(2+) inhibition of stimulated (36)Cl(-) uptake was selectively decreased in the cortex (but not in the cerebellum) 1 to 2 h after the onset of status epilepticus. This loss of Zn(2+) response in the cortex appeared to be selective to Zn(2+) only, because pentobarbital-, alphaxalone-, or flunitrazepam enhancement of muscimol-stimulated (36)Cl(-) uptake did not change in this brain region either at 1 or 2 h after seizures. Because this loss of Zn(2+) response in the cortex was apparent only about 1 h after the onset of status epilepticus but not earlier, we tested whether status epilepticus was critical for the development of the loss of Zn(2+) response. We found that, in rats where status epilepticus was terminated by diazepam within 30 min after seizure onset, Zn(2+) response was preserved in the cortex. These findings suggest that continuous seizures of pilocarpine-induced status epilepticus caused a rapid and selective decrease in Zn(2+) inhibition of GABA(A) receptor function in the cortex. The possible relevance of such rapid seizure-induced GABA(A) receptor plasticity in the cerebral cortex is discussed.

Animals↗

PubMed1999

Cerebellar cortex lesions prevent acquisition of conditioned eyelid responses.

We have used aspiration and electrolytic lesions to investigate the contributions of cerebellar cortex to the acquisition and expression of conditioned eyelid responses. We show that lesions of the anterior lobe of rabbit cerebellar cortex disrupt the timing of previously learned conditioned eyelid responses. These short-latency responses were used as an indication that the cerebellar cortex was sufficiently damaged and that the underlying pathways necessary for the expression of responses were sufficiently intact to support responses. Rabbits were subsequently trained for 15 daily sessions using a new conditioned stimulus. Whereas rabbits in which lesions had no significant effect on response timing showed rapid acquisition of appropriately timed eyelid responses to the new conditioned stimulus, animals with lesions that disrupt timing showed no significant increases in either amplitude or probability of responses. Histological analysis suggests that damage to the anterior lobe of the cerebellar cortex is necessary and sufficient to abolish timing and prevent acquisition. These data indicate that the cerebellar cortex is necessary for the acquisition of conditioned eyelid responses and are consistent with the hypotheses that (1) eyelid conditioning results in plasticity in both the anterior lobe of the cerebellar cortex and in the anterior interpositus nucleus and (2) induction of plasticity in the interpositus requires intact input from the cerebellar cortex.

Animals↗

PubMed2000

Hydroxyl radical production in the cortex and striatum in a rat model of focal cerebral ischemia.

BACKGROUND: Increases in hydroxyl radical production have been used as evidence of oxidative stress in cerebral ischemia/ reperfusion. Ischemia can also induce increased dopamine release from the striatum that may contribute to hydroxyl radical formation. We have compared hydroxyl radical production in the cortex and striatum as an index of oxidative stress in a rat model of focal cerebral ischemia with cortical infarction. METHODS: Using a three vessel occlusion model of focal cerebral ischemia combined with bilateral microdialysis, hydroxylation of 4-hydroxybenzoate (4HB) was continuously monitored in both hemispheres in either the lateral striatum or frontoparietal cortex. The ischemia protocol consisted of one hour equilibration, 30 min of three vessel occlusion, then release of the contralateral common carotid artery (CCA) for 2.5 h. RESULTS: Induction of ischemia resulted in a 30-fold increase in dopamine release in the lateral striatum. Compared to the nonischemic striatum, the ratio of the hydroxylation product 3,4-dihydroxybenzoate (34DHB) to 4HB (trapping agent) in the ipsilateral striatum increased significantly 30 min after ischemia induction. In contrast, during the 30 min of three vessel occlusion there was no increase in the ratio in the cortex. Following the release of the contralateral CCA, the ratio from the ischemic cortex increased significantly compared to sham-operated animals. However, under all circumstances, the 34DHB/4HB ratio was greater in the striatum than in the cortex. CONCLUSION: The increase in the 34DHB/4HB ratio in the lateral striatum coincides with the increased dopamine release suggesting a role for dopamine oxidation in the increased production of hydroxyl radicals. The significant increase in the ratio from the ischemic cortex compared to that from the sham-operated animals is consistent with increased oxidative stress induced by ischemia. However, the lower 34DHB/4HB ratio in the cortex which does not receive dopaminergic innervation compared to the striatum suggests a different mechanism for hydroxyl radical production. Such an alternate mechanism may represent a more toxic oxidative insult that contributes to infarction.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2000

Dissociable roles of mid-dorsolateral prefrontal and anterior inferotemporal cortex in visual working memory.

Functional neuroimaging in human subjects and studies of monkeys with lesions limited to the mid-dorsolateral (MDL) prefrontal cortex have shown that this specific region of the prefrontal cortex is involved in visual working memory, although its precise role remains a matter of debate. The present study compared the effect on visual working memory of lesions restricted to the mid-dorsolateral prefrontal cortex of the monkey with that of lesions to the anterior inferotemporal cortex, a region of the temporal cortex specialized for visual memory. Increasing the delay during which information had to be maintained in visual working memory impaired performance after lesions of the anterior inferotemporal cortex, but not after mid-dorsolateral prefrontal lesions. By contrast, increasing the number of stimuli that had to be monitored impaired the performance of animals with mid-dorsolateral prefrontal lesions, but not that of animals with anterior inferotemporal lesions. This demonstration of a double dissociation between the effects of these two lesions provides strong evidence that the role of the mid-dorsolateral prefrontal cortex in visual working memory does not lie in the maintenance of information per se, but rather in the executive process of monitoring this information. In addition, the present study demonstrated that lesions limited to area 9, which constitutes the superior part of the mid-dorsolateral prefrontal region, give rise to a mild impairment in the monitoring of information, whereas lesions of the complete mid-dorsolateral prefrontal region yield a very severe impairment.

Analysis of Variance↗

PubMed2000

The role of the insular cortex in temporal lobe epilepsy.

The role of the insular cortex in the genesis of temporal lobe epileptic (TLE) seizures has been investigated in 21 patients with drug-refractory TLE using chronic depth stereotactic recordings of the insular cortex activity and video recordings of ictal symptoms during 81 spontaneous electroclinical seizures. All of the recorded seizures were found to invade the insula, most often after a relay in the ipsilateral hippocampus (19/21 patients). However, 2 patients had seizures that originated in the insular cortex itself. Ictal symptoms associated with the insular discharges were similar to those usually attributed to mesial temporal lobe seizures, so that scalp video-electroencephalographic monitoring does not permit making any difference between ictal symptoms of temporo-mesial and insular discharges. A favorable outcome was obtained after a temporal cortectomy sparing the insular cortex in 15 of 17 operated patients. Seizures propagating to the insular cortex were found to be fully controlled by surgery, whereas those originating in the insular cortex persisted after temporal cortectomy. The fact that seizures originating in the insular cortex are not influenced by temporal lobectomy is likely to explain some of the failures of this surgical procedure in TLE.

Adolescent↗

PubMed2001

Amygdala regulation of nucleus accumbens dopamine output is governed by the prefrontal cortex.

A dynamic interaction between the prefrontal cortex (PFC), amygdala, and nucleus accumbens (NAc) may be fundamental to regulation of goal-directed behavior by affective and cognitive processes. This study demonstrates that a mechanism for this triadic relationship is an inhibitory control by prefrontal cortex on accumbal dopamine release during amygdala activation. In freely moving rats, microstimulation of basolateral amygdala at intensities that produced mild behavioral activation produced an expected rapid increase in glutamate efflux in the prefrontal cortex and the nucleus accumbens shell region of the ventral striatum. However, during the stimulation, dopamine release increased only in the prefrontal cortex, not in the nucleus accumbens. An increase in accumbal dopamine release was observed during the stimulation if glutamate activation in the prefrontal cortex was inhibited at either presynaptic or postsynaptic levels. Some behaviors expressed during the stimulation were intensified in animals in which prefrontal cortex glutamate activation was blocked. In addition, these animals continued to express stimulus-induced behaviors after the termination of stimulation, whereas normal poststimulus behaviors such as ambulation and grooming were not displayed as frequently. Considering that dopamine neurotransmission in the nucleus accumbens is thought to play an integral role in goal-directed motor behavior, these findings suggest that the prefrontal cortex influences the behavioral impact of amygdala activation via a concomitant active suppression of accumbal dopamine release. Absence of this cortical influence appears to result in an aberrant pattern of behavioral expression in response to amygdala activation, including behavioral perseveration after stimulus termination.

Amygdala↗

PubMed2001

MR imaging of the human brain at 1.5 T: regional variations in transverse relaxation rates in the cerebral cortex.

BACKGROUND AND PURPOSE: Heterogeneity in cortical signal intensity on T2-weighted MR images has been recently documented. Using a whole-brain, multiecho MR imaging technique, we sought to determine the T2 relaxation times of nine predefined regions in the cerebral cortex and one region in the deep gray matter. METHODS: Ten adult volunteers (nine men and one woman; age range, 18-40 y; average age, 30.8 y) underwent whole-brain imaging with an oblique coronal multiecho 3D Carr-Purcell-Meiboom-Gill MR sequence at 1000/25, 50, 75, 100, 125, and 150 (TR/TE). T2 measurements were obtained, with variably sized regions of interest, from the primary auditory cortex, primary visual cortex, caudate nucleus, superior frontal gyrus, inferior temporal gyrus, middle temporal gyrus, superior temporal gyrus, insula cortex, cingulate gyrus, and hippocampus. Repeated-measures analysis of variance was used to assess the existence of differences in T2 measurements among the anatomic locations. RESULTS: On the basis of T2 measurements, the gray matter structures examined could be divided into four statistically different groups. In ascending order of T2 measurements, the first group consisted of the primary auditory cortex and primary visual cortex; the second group, the caudate nucleus, superior frontal gyrus, inferior temporal gyrus, middle temporal gyrus, and superior temporal gyrus; the third group, the insula cortex; and the fourth group, the cingulate gyrus and hippocampus. CONCLUSION: Significant variation in T2 values among the cortical gray matter of the human brain exists.

Adolescent↗

PubMed2001

Regional differences in neurotrophin availability regulate selective expression of VGF in the developing limbic cortex.

Gene and protein expression patterns in the cerebral cortex are complex and often change spatially and temporally through development. The signals that regulate these patterns are primarily unknown. In the present study, we focus on the regulation of VGF expression, which is limited to limbic cortical areas early in development but later expands into sensory and motor areas. We isolated neurons from embryonic day 17 rat cortex and demonstrate that the profile of VGF expression in perirhinal (expressing) and occipital (nonexpressing) populations in vitro is similar to that in the perinatal cortex in vivo. The addition of neutralizing neurotrophin antibodies indicates that endogenous brain-derived neurotrophic factor (BDNF) is necessary for the normal complement of VGF-expressing neurons in the perirhinal cortex, although endogenous neurotrophin-3 (NT-3) regulates the expression of VGF in a subpopulation of cells. ELISA analysis demonstrates that there is significantly more BDNF present in the perirhinal cortex compared with the occipital cortex in the perinatal period. However, the total amount of NT-3 is similar between the two regions and, moreover, there is considerably more NT-3 than BDNF in both areas, a finding seemingly in conflict with regional VGF expression. Quantification of the extracellular levels of neurotrophins in perirhinal and occipital cultures using ELISA in situ analysis indicates that perirhinal neurons release significantly more BDNF than the occipital population. Furthermore, the amount of NT-3 released by the perirhinal neurons is significantly less than the amount of BDNF. Local injection of BDNF in vivo into a normally negative VGF region results in robust ectopic expression of VGF. These data suggest that the local availability of specific neurotrophins for receptor occupation, rather than the total amount of neurotrophin, is a critical parameter in determining the selective expression of VGF in the developing limbic cortex.

Animals↗