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PubMed1976

Postcritical-period reversal of effects of monocular deprivation on striate cortex cells in the cat.

1. The possibility that effects of monocular deprivation on cat striate cortex could be reversed after the developmental critical period by removal of the normal eye was investigated. In addition, the time course of any postcriticalperiod reversal was studied. Single-unit recording was conducted in the striate cortex of kittens anesthetized with nitrous oxide.2. Six control kittens were raised with monocular lid suture until they were 4-8 mo old (group MD). In agreement with previous investigators, from 0-10% of the striate cortex cells could be driven by visual stimulation of the deprived eye in these kittens.3. Eleven kittens were raised with monocular lid suture until they were 4-5 mo old, at which time the normal eye was enucleated. In five of these (group MD-DE-immediate), recording was conducted in striate cortex on the day of the enucleation. In these animals, 29-39% of the striate cortex cells could be driven by the deprived eye. In four kittens (group MD-DE-3 mo), the deprived eye remained closed for an additional 3 mo before recording was conducted. In these animals, 17-45% of the striate cortex cells could be driven by the deprived eye. In two kittens (group MD-DE greater than 12 mo), the deprived eye remained closed for 14-15 mo after the normal eye was enucleated. In these kittens, 26-40% of the striate cortex cells could be driven by the deprived eye. Thus, removal of the normal eye after the critical period in monocularly drprived kittens results in a rapid increase in the percent of striate cortex cells that can be driven by visual stimulation of the deprived eye, and there is no further increase in responsiveness over a period of more than a year.4. The receptive-field properties of the cells which responded to the deprived eye following enucleation of the normal eye were usually abnormal; 61% of them had nonspecific receptive fields, 39% of the responsive cells were direction selective, and only 12% were both direction and orientation selective.5. The increase in responsive cells was observed in the striate cortex of both hemispheres. However, the increase was greater in the hemisphere contralateral to the deprived eye. The responsive cells tended to occur in clusters of two to four adjacent cells separated by regions containing nonresponsive cells. These clusters were not related to the horizontal cortical layers; however, they may be related to the ocular dominance columns in striate cortex.6. Several mechanisms were considered for the present findings, including neuronal sprouting, denervation supersensitivity, and release from inhibition. It was suggested that the increased responsiveness to the deprived eye was probably not the result of rapid sprouting in the 4- to 5-mo-old kittens. If this is so, then the results indicate that functional connections from the deprived layers of the DLG to the striate cortex remain following rearing with monocular deprivation...

Animals↗

PubMed1999

Carbachol induces fast oscillations in the medial but not in the lateral entorhinal cortex of the isolated guinea pig brain.

Fast oscillations at 25-80 Hz (gamma activity) have been proposed to play a role in attention-related mechanisms and synaptic plasticity in cortical structures. Recently, it has been demonstrated that the preservation of the entorhinal cortex is necessary to maintain gamma oscillations in the hippocampus. Because gamma activity can be reproduced in vitro by cholinergic activation, this study examined the characteristics of gamma oscillations induced by arterial perfusion or local intracortical injections of carbachol in the entorhinal cortex of the in vitro isolated guinea pig brain preparation. Shortly after carbachol administration, fast oscillatory activity at 25.2-28.2 Hz was observed in the medial but not in the lateral entorhinal cortex. Such activity was transiently associated with oscillations in the theta range that showed a variable pattern of distribution in the entorhinal cortex. No oscillatory activity was observed when carbachol was injected in the lateral entorhinal cortex. Gamma activity in the medial entorhinal cortex showed a phase reversal at 200-400 microm, had maximal amplitude at 400-500 microm depth, and was abolished by arterial perfusion of atropine (5 microM). Local carbachol application in the medial entorhinal cortex induced gamma oscillations in the hippocampus, whereas no oscillations were observed in the amygdala and in the piriform, periamygdaloid, and perirhinal cortices ipsilateral and contralateral to the carbachol injection. Hippocampal oscillations had higher frequency than the gamma activity recorded in the entorhinal cortex, suggesting the presence of independent generators in the two structures. The selective ability of the medial but not the lateral entorhinal cortex to generate gamma activity in response to cholinergic activation suggests a differential mode of signal processing in entorhinal cortex subregions.

Animals↗

PubMed1989

Removal and reimplantation of the parietal cortex of mice during the first nine days of life: consequences for the barrelfield.

Vibrissal follicles on one side of the mouse whiskerpad are topologically connected to barrels in the contralateral somatosensory cortex. Barre's develop from postnatal day 3 to 6. Recently, I have observed that the barrelfields still develop in pieces of parietal cortex that were removed and reimplanted, in the same place and with the original orientation, on the day of birth, or on postnatal days 1 or 3. Now, two questions were asked: (i) Can the barrelfield form and/or remain in place after interrupting thalamocortical connections at different ages (from birth to postnatal day 9)? (ii) How does the cortex behave, in terms of cellular layers, after the interruption of thalamocortical connections? To answer these questions the parietal cortex was removed and reimplanted in the same place with the original orientation, in 79 mice from a C3H strain. Fifty-one mice survived and were processed for histology. Their brains were cut coronally to facilitate the identification of the limits of the reimplanted cortex and of its cellular layering. In 29 cases the reimplanted cortex could be identified, and in 17 cases barrel-like structures had developed. The "barrelfields" were obtained from coronal sections of each piece of reimplanted cortex, by means of a computer program which permitted reconstructing these pieces of cortex and rotating them in space. In this way, barrel-like structures and "barrelfields" could be visualized as if obtained from sections made tangential to the parietal cortex. "Barrelfields" were found in pieces of cortex reimplanted at different ages up to postnatal day 9. Cortical layers appeared to be more close to normal in cases operated after postnatal day 5.

Aging↗

PubMed1991

A comparison of neurotransmitter-specific and neuropeptide-specific neuronal cell types present in the dorsal cortex in turtles with those present in the isocortex in mammals: implications for the evolution of isocortex.

Although it seems highly likely that mammalian isocortex evolved from a structure resembling reptilian telencephalic cortex, it has been uncertain if this occurred by the laminar differentiation of three-layered reptilian cortex into six-layered mammalian isocortex without the addition of new cell types or by laminar differentiation with the addition of new cell types. To distinguish between these two possibilities, immunohistochemical techniques were used to study turtles to see if the same major neuronal cell types, as defined by neurotransmitter or neuropeptide content, present in mammalian isocortex are also present in the specific part of reptilian cortex thought to be the forerunner of at least parts of isocortex, namely the dorsal cortex. Neurons containing the following substances are the major transmitter-specific types of neurons known to be present in mammalian isocortex: cholecystokinin-8 (CCK8), vasoactive intestinal polypeptide (VIP), acetylcholine, substance P (SP), neuropeptide Y (NPY), somatostatin (SS), LANT6, enkephalin, GABA and glutamate (GLUT). In turtles, only those of the above substances that are found in large numbers of neurons in layers V-VI in mammalian isocortex, irrespective of whether they are also present in layers II-IV (i.e. SP, NPY, SS, LANT6, GABA and GLUT), were present in neurons in dorsal cortex. The neurons containing these substances in dorsal cortex in turtles were generally highly similar in morphology to their counterparts in mammalian isocortex. In contrast, neurons labeled for CCK8, VIP or acetylcholine, which are mainly found in neurons of layers II-IV of mammalian isocortex, were absent or extremely rare in dorsal cortex. The absence or paucity of neurons labeled for these latter substances in dorsal cortex in turtles did not reflect an overall staining failure of the antisera used since the same antisera yielded excellent labeling of neurons, fibers and terminals in many other brain regions in turtles. Thus, dorsal cortex in turtles appears to lack several of the major cell types characteristic of layers II-IV of mammalian isocortex, but possesses a number of the major cell types characteristic of layers V-VI of isocortex. The findings support and extend a previous suggestion by Ebner [1976], based on hodological data, that dorsal cortex in turtles may lack the types of neurons found in the more superficial layers of mammalian isocortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1997

Developmental and functional biology of the primate fetal adrenal cortex.

The unique characteristics of the primate (particularly human) fetal adrenal were first realized in the early 1900s when its morphology was examined in detail and compared with that of other species. The unusual architecture of the human fetal adrenal cortex, with its unique and disproportionately enlarged fetal zone, its compact definitive zone, and its dramatic remodeling soon after birth captured the interest of developmental anatomists. Many detailed anatomical studies describing the morphology of the developing human fetal adrenal were reported between 1920 and 1960, and these morphological descriptions have not changed significantly. More recently, it has become clear that fetal adrenal cortical growth involves cellular hypertrophy, hyperplasia, apoptosis, and migration and is best described by the migration theory, i.e. cells proliferate in the periphery, migrate centripetally, differentiate during their migration to form the functional cortical zones, and then likely undergo apoptosis in the center of the cortex. Consistent with this model, cells of intermediate phenotype, arranged in columnar cords typical of migration, have been identified between the definitive and fetal zones. This cortical area has been referred to as the transitional zone and, based on the expression of steroidogenic enzymes, we consider it to be a functionally distinct cortical zone. Elegant experiments during the 1950s and 1960s demonstrated the central role of the primate fetal adrenal cortex in establishing the estrogenic milieu of pregnancy. Those findings were among the first indications of the function and physiological role of the human fetal adrenal cortex and led Diczfalusy and co-workers to propose the concept of the feto-placental unit, in which DHEA-S produced by the fetal adrenal cortex is used by the placenta for estrogen synthesis. Tissue and cell culture techniques, together with improved steroid assays, revealed that the fetal zone is the primary source of DHEA-S, and that its steroidogenic activity is regulated by ACTH. In recent years, function of the human and rhesus monkey fetal adrenal cortical zones has been reexamined by assessing the localization and ontogeny of steroidogenic enzyme expression. The primate fetal adrenal cortex is composed of three functionally distinct zones: 1) the fetal zone, which throughout gestation does not express 3 beta HSD but does express P450scc and P450c17 required for DHEA-S synthesis; 2) the transitional zone, which early in gestation is functionally identical to the fetal zone but late in gestation (after 25-30 weeks) expresses 3 beta HSD, P450scc, and P450c17, and therefore is the likely site of glucocorticoid synthesis, and 3) the definitive zone, which lacks P450c17 throughout gestation but late in gestation (after 22-24 weeks) expresses 3 beta HSD and P450scc, and therefore is the likely site of mineralocorticoid synthesis. Indirect evidence, based on effects of P450c21 deficiency and maternal estriol concentrations, indicate that the fetal adrenal cortex produces cortisol and DHEA-S early in gestation (6-12 weeks). However, controversy exists as to whether cortisol is produced de novo or derived from the metabolism of progesterone, as data regarding the expression of 3 beta HSD in the fetal adrenal cortex early in gestation are conflicting. During the 1960s, Liggins and colleagues demonstrated that in the sheep, cortisol secreted by the fetal adrenal cortex late in gestation regulates maturation of the fetus and initiates the cascade of events leading to parturition. Those pioneering discoveries provided insight into the mechanism underlying the timing of parturition and therefore were of particular interest to obstetricians and perinatologists confronted with the problems of preterm labor. However, although cortisol emanating from the fetal adrenal cortex promotes fetal maturation in primates as it does in sheep, its role in the regulation of primate parturition, unlike that in sheep

Adrenal Cortex↗

PubMed1987

Brain cortex reverse triiodothyronine (rT3) and triiodothyronine concentrations under steady state infusions of thyroxine and rT3.

T4 and reverse T3 (rT3) can inhibit 5'-deiodinase type II activity in rat brain cortex, pituitary, and brown adipose tissue, raising the possibility that T4 may act in vivo after conversion to rT3. The aim of this study was to measure in hypothyroid (Tx) rats the content of brain cortex rT3 during a constant 7-day infusion of either [125I]T4 alone, corresponding to 12 pmol T4/day X 100 g body weight (BW), or together with 400 pmol T4/day. [125I]T4, rT3, and T3 were extracted from brain cortex, pituitary, kidney, and liver with a combination of adsorption chromatography on Sephadex G-25, HPLC, and immunoprecipitation. [131I]T4, T3, or rT3 were used as internal standards. [125I]rT3 could be detected in brain cortex, liver, and kidney in Tx rats infused with [125I]T4 (12 pmol T4/day X 100 g BW) and in those infused with 400 pmol T4/day X 100 g BW. The highest rT3 concentrations were found in brain cortex, where it represented 6% to 10.5% of the local T4 concentration. During an infusion of 400 pmol T4/day X 100 g BW, brain cortex T3 concentration was 6 times higher in the brain cortex than in serum, and even exceeded that of T4. In Tx rats receiving [125I]T4 alone the brain cortex to serum T3 ratio was 3:1, but the total serum T3 concentration, measured by RIA, was much higher than that due to conversion [0.50 +/- (SE) 0.1 pmol/ml vs. 0.018 +/- 0.002 pmol T3/ml], indicating thyroidal secretion. The effect of the blood-brain barrier on rT3 was measured by infusing [125I]rT3 over 4 days. After killing, rT3 was isolated as above. Approximately 3% of serum rT3 was retrieved from the brain cortex, whereas during the T4 infusion 40-50% of serum rT3 was found demonstrating that brain cortex rT3 is locally produced.

Animals↗

PubMed2004

Motor skill learning depends on protein synthesis in motor cortex after training.

The role of protein synthesis in memory consolidation is well established for hippocampus-dependent learning and synaptic plasticity. Whether protein synthesis is required for motor skill learning is unknown. We hypothesized that skill learning is interrupted by protein synthesis inhibition (PSI). We intended to test whether local protein synthesis in motor cortex or cerebellum is required during skill acquisition and consolidation. Anisomycin (ANI; 100 microg/microl in 1 microl of PBS) injected into motor cortex, posterior parietal cortex, or cerebellum produced 84.0 +/- 1.44% (mean +/- SEM), 85.9 +/- 2.31%, and 87.3 +/- 0.17% of PSI 60 min after administration, respectively. In motor cortex, protein synthesis was still reduced at 24 hr (72.0 +/- 4.68% PSI) but normalized at 48 hr after a second injection given 24 hr after the first. To test for the effects of PSI on learning of a skilled reaching task, ANI was injected into motor cortex contralateral to the trained limb or into ipsilateral cerebellum immediately after daily training sessions 1 and 2. Two control groups received motor cortex injections of vehicle or ANI injections into contralateral parietal cortex. Control and cerebellar animals showed a sigmoid learning curve, which plateaued after day 4. PSI in motor cortex significantly reduced learning during days 1-4. Thereafter, when protein synthesis normalized, learning was reinitiated. ANI injections into motor cortex did not induce a motor deficit, because animals injected during the performance plateau did not deteriorate. This demonstrates that motor skill learning depends on de novo synthesis of proteins in motor cortex after training.

Animals↗

PubMed2001

Effects of changes in power setting of an ultrasonic aspirator on amount of damage to the cerebral cortex of healthy dogs.

OBJECTIVE: To determine the minimal ultrasonic aspirator pressure necessary to damage the cerebral cortex of healthy dogs. ANIMALS: 9 mixed-breed dogs. PROCEDURE: The study comprised 2 parts. In part A, 6 dogs were euthanatized immediately prior to the experiment. In part B, 3 dogs were anesthetized for recording of physiologic variables. In both parts, craniectomy and durotomy were performed to bilaterally expose the lateral aspect of the cerebral cortex. An ultrasonic aspirator was placed in contact with various areas of the cerebral cortex, and aspirator power was altered (10, 20, 30, and 40%). Duration of contact at each power was 5 and 10 seconds. Subsequently, gross morphologic and histologic damage was assessed in the cortex. RESULTS: Gross observations for all dogs were similar. At 10% power, visible or histologic damage was not evident in the cortex. At 20% power, the cortex was slightly indented from contact with the hand piece; however, cortical disruption was not evident. Cortical disruption was initially detectable at 30% power in some dogs and was consistently evident at 40% power in both sets of dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Ultrasonic aspirator power of < 20% created minimal acute morphologic damage to the cortex. Power settings between 20 and 30% may superficially damage the cerebral cortex in healthy dogs, whereas 40% power consistently damages the cerebral cortex. Knowledge of the degree of damage to cerebral cortex caused by various amounts of power for ultrasonic aspirators will allow surgeons to avoid damaging normal brain tissues during surgery.

Animals↗

PubMed2001

Loss and atrophy of layer II entorhinal cortex neurons in elderly people with mild cognitive impairment.

Layer II of the entorhinal cortex contains the cells of origin for the perforant path, plays a critical role in memory processing, and consistently degenerates in end-stage Alzheimer's disease. The extent to which neuron loss in layer II of entorhinal cortex is related to mild cognitive impairment without dementia has not been extensively investigated. We analyzed 29 participants who came to autopsy from our ongoing longitudinal study of aging and dementia composed of religious clergy (Religious Orders Study). All individuals underwent detailed clinical evaluation within 12 months of death and were categorized as having no cognitive impairment (n = 8), mild cognitive impairment (n = 10), or mild or moderate Alzheimer's disease (n = 11). Sections through the entorhinal cortex were immunoreacted with an antibody directed against a neuron-specific nuclear protein (NeuN). Stereological counts of NeuN-immunoreactive stellate cells, their volume, and the volume of layer II entorhinal cortex were estimated. Cases exhibiting no cognitive impairment averaged 639,625 +/- 184,600 layer II stellate neurons in the right entorhinal cortex. Individuals with mild cognitive impairment (63.5%; p < 0.0003) and mild or moderate Alzheimer's disease (46.06%; p < 0.0017) displayed significant losses of layer II entorhinal cortex neurons relative to those with no cognitive impairment but not relative to each other (p > 0.33). There was also significant atrophy of layer II entorhinal cortex neurons in individuals with mild cognitive impairment (24.1%) and Alzheimer's disease (25.1%). The volume of layer II was also reduced in individuals with mild cognitive impairment (26.5%), with a further reduction in those with Alzheimer's disease (46.4%). The loss and atrophy of layer II entorhinal cortex neurons significantly correlated with performance on clinical tests of declarative memory. Atrophy of layer II entorhinal cortex and the neurons within this layer significantly correlated with performance on the Mini Mental Status Examination. These data indicate that atrophy and loss of layer II entorhinal cortex neurons occur in elderly subjects with mild cognitive impairment prior to the onset of dementia and suggests that these changes are not exacerbated in early Alzheimer's disease.

Aged↗

PubMed1989

Patterns of connections in rat visual cortex.

The definition of visual areas is one of the central problems in visual cortex research. Rodent extrastriate cortex offers a striking example of the complexity of this issue, in that different parcelation schemes identify within it from 2 to as many as 13 separate visual areas. In the experiments reported here, patterns of connections within rat visual cortex were studied in an effort to better define its organizational layout. The experimental paradigm used consisted of the following steps: first, the pattern of callosal connections was revealed in vivo with the fluorescent tracer bisbenzimide. Then, using the callosal pattern as a landmark, single injections of WGA-HRP were placed at various sites in striate and extrastriate cortex. Subsequently, the relation between the tangential distribution of ipsilateral corticocortical connections, the callosal connections, and the borders of striate cortex were examined in the flattened cortex preparation. The experiments revealed widespread, patchy connections within rat visual cortex. These connections appeared to reflect 3 organizational trends. First, neighboring sites were more extensively connected than distant ones. Second, extrastriate sites receiving common striate cortex inputs tended to be interconnected. Finally, projections from opposite poles in striate cortex tended to form interdigitating patterns of connections in regions of overlap. Altogether these trends suggest that the extrastriate band adjoining striate cortex has a single, global map organization. However, within the global map, a clear modular organization was evident, which appeared to correspond to the multiple visuotopic representations reported for this region. Based on its location, and some organizational similarities. it is suggested that the global map may constitute the rat homolog of area V2 in cat and monkey.

Animals↗

PubMed1989

Neuropeptide Y in the cerebral cortex and the caudate-putamen nuclei: ultrastructural basis for interactions with GABAergic and non-GABAergic neurons.

In the cerebral cortex and caudate-putamen (CP) nuclei, neuropeptide Y (NPY) immunoreactivity is detectable within 1-2% of all neurons. The NPY-immunoreactive neurons are interneuronal and are believed to be mostly GABAergic in the cerebral cortex but not in the CP nuclei. Thus NPY and GABA may play different roles in the circuitry within these 2 regions. We tested this possibility by comparing the ultrastructure of NPY-containing neurons between (1) cortex (somatosensory and anterior cingulate areas) versus dorsolateral CP; and (2) GABAergic versus non-GABAergic NPY neurons within each area. Single coronal sections through the rat forebrain were dually labeled for GABA and NPY by combining immunoautoradiography with the immunoperoxidase method. NPY-containing neurons with or without GABA occurred throughout the rostrocaudal portions of CP and all laminae of somatosensory and anterior cingulate cortex. Comparisons between the areas confirmed that somata and terminals dually labeled for GABA and NPY were more prevalent in the cortex. NPY terminals lacking detectable GABA immunoreactivity also were found within the cortex, thus suggesting additional heterogeneity in cortical NPY innervation. The ultrastructural features of NPY perikarya in both regions were morphologically similar regardless of whether the cells also contained GABA. Most synaptic inputs to NPY neurons occurred at distal dendrites. In comparison to neighboring neurons, synaptic inputs to proximal dendrites and somata of NPY neurons of cortex and CP were rare, suggesting that fewer and weaker inputs may modulate the excitability of NPY-containing neurons. In both regions, nearly all NPY- and NPY-GABA-labeled terminals formed symmetric junctions suggestive of inhibitory action. The majority of these junctions were with dendrites containing neither NPY nor GABA. NPY terminals formed few contacts on proximal dendrites and somata of GABAergic neurons (8% of 179 contacts in cortex; 12% of 73 contacts in CP) which, unlike most singly-labeled GABAergic neurons, were sparsely innervated. Thus, NPY may play a more prominent role in modulation of certain GABAergic neurons than would be predicted by the observed frequency of NPY-to-GABA contacts in the two regions. One notable regional difference was the greater prevalence in cortex of axoaxonic associations between NPY-immunoreactive terminals and other terminals, some of which also contained NPY. These nonsynaptic associations may be involved in the modulation of (1) the release of NPY by another transmitter or (2) NPY's modulation of release of other transmitters in cortex.

Animals↗

PubMed1997

Atrophy of the hippocampus, parietal cortex, and insula in Alzheimer's disease: a volumetric magnetic resonance imaging study.

The hippocampus, parietal cortex, and insula were measured on volumetric magnetic resonance imaging to determine whether patients with early Alzheimer's disease had significantly more atrophy than healthy controls. To determine whether the atrophy is limited to certain cortical regions, the striate cortex was measured because this area is not usually neuropathologically involved early in Alzheimer's disease. Eight mildly to moderately impaired patients who met National Institute of Neurological Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for probable Alzheimer's disease and eight controls who matched for age, gender, and educational level were studied. Atrophy was quantified in the following regions: hippocampus, parietal cortex, insular cortex, and striate cortex. The authors found significantly more atrophy of the hippocampus (p < 0.0001), parietal cortex (p < 0.025), and insula (p < 0.003) in the Alzheimer's patients. Measures of the striate cortex did not differ between the groups. There were no significant left-right differences in any of the regions measured. Their findings show that mildly to moderately impaired Alzheimer's patients have significantly more atrophy of the hippocampus, parietal cortex, and insula than healthy age-matched controls. Furthermore, this atrophy is probably discrete because the groups did not differ on measures of the striate cortex. Selective atrophy of the parietal and insular cortices has not previously been reported using the authors' methodology on volumetric magnetic resonance imaging. Their data suggest that the insula may be involved early in Alzheimer's disease and that atrophy of the insular cortex may contribute to the cognitive deficits typical of early Alzheimer's disease.

Aged↗

PubMed1998

Dopaminergic regulation of extracellular gamma-aminobutyric acid levels in the prefrontal cortex of the rat.

Dopaminergic axons in the prefrontal cortex synapse with interneurons as well as pyramidal cells. Electrophysiological data suggest that dopamine depolarizes certain gamma-aminobutyric acid (GABA)-containing interneurons in the cortex. We investigated the dopaminergic regulation of extracellular GABA levels in the prefrontal cortex using in vivo microdialysis. Systemic administration of the mixed D1/D2 dopamine receptor agonist apomorphine increased extracellular GABA levels in the prefrontal cortex, but did not increase levels of glycine; the apomorphine-elicited increase in GABA levels was blocked by tetrodotoxin infusion into the prefrontal cortex. Local administration of the D2 agonist quinpirole into the cortex via the dialysis probe resulted in a dose-dependent increase in extracellular GABA levels. In contrast, administration of the D1 agonist SKF 38393 did not alter GABA levels. The ability of systemic apomorphine to increase extracellular GABA levels in the prefrontal cortex was blocked by local administration of the D2-like antagonist sulpiride to the cortex, but was not attenuated significantly by local perfusion of the D1 antagonist SCH 23390. Similarly, the ability of local infusion of the D2 agonist quinpirole to enhance extracellular GABA levels was blocked by sulpiride but not by SCH 23390. These data suggest that dopamine agonists increase the release of GABA in the prefrontal cortex through a D2-like receptor. In view of posited changes in prefrontal cortical dopamine and GABA systems in schizophrenia, it is possible that changes in GABAergic function in the cortex in schizophrenia are secondary to changes in cortical dopamine function.

Animals↗

PubMed1999

Primary motor cortex involvement in Alzheimer disease.

In Alzheimer disease (AD) the involvement of entorhinal cortex, hippocampus, and associative cortical areas is well established. Regarding the involvement of the primary motor cortex the reported data are contradictory. In order to determine whether the primary motor cortex is involved in AD, the brains of 29 autopsy cases were studied, including, 17 cases with severe cortical AD-type changes with definite diagnoses of AD, 7 age-matched cases with discrete to moderate cortical AD-type changes, and 5 control cases without any AD-type cortical changes. Morphometric analysis of the cortical surface occupied by senile plaques (SPs) on beta-amyloid-immunostained sections and quantitative analysis of neurofibrillary tangles (NFTs) on Gallyas-stained sections was performed in 5 different cortical areas including the primary motor cortex. The percentage of cortical surface occupied by SPs was similar in all cortical areas, without significant difference and corresponded to 16.7% in entorhinal cortex, 21.3% in frontal associative, 16% in parietal associative, and 15.8% in primary motor cortex. The number of NFTs in the entorhinal cortex was significantly higher (41 per 0.4 mm2), compared with those in other cortical areas (20.5 in frontal, 17.9 in parietal and 11.5 in the primary motor cortex). Our findings indicate that the primary motor cortex is significantly involved in AD and suggest the appearance of motor dysfunction in late and terminal stages of the disease.

Adult↗

PubMed2000

Chronic ethanol administration alters immunoreactivity for GABA(A) receptor subunits in rat cortex in a region-specific manner.

BACKGROUND: Chronic ethanol administration has a plethora of physiological effects. Among the most consistently observed findings is a change in the expression pattern of gamma-aminobutyric acid type A (GABA(A)) receptor subunits in the rat brain cortex. These findings led to the hypothesis of "subunit substitution" to account for changes in receptor function without changes in receptor number. METHODS: We used subunit (alpha1 and alpha4) specific antibodies and a combination of immunohistochemistry and immunoblotting to examine subregions of cortex (prefrontal, cingulate, motor, parietal, and piriform) for their response to 2 weeks of forced ethanol administration. RESULTS: Overall, cortical immunoreactivity for the alpha1 subunit was decreased and for the alpha4 subunit increased whether measured immunohistochemically or by immunoblotting. Piriform cortex exhibited a bidirectional change in GABA(A) receptor alpha1 and alpha4 immunoreactivity, similar to that previously observed in preparations of whole cortex. However, in parietal cortex, declines in alpha1 immunoreactivity (55 +/- 12% control value [CV] and 88.3 +/- 4.3% CV; immunohistochemistry and immunoblotting, respectively) were not accompanied by concomitant increases in alpha4 immunoreactivity (104 +/- 8% CV and 116 +/- 9.3% CV; immunohistochemistry and immunoblotting, respectively). Conversely, alpha4 immunoreactivity increased in cingulate cortex (210 +/- 30% CV and 134 +/- 9.5% CV; immunohistochemistry and immunoblotting, respectively) without a decline in alpha1 immunoreactivity (90 +/- 4% CV and 91.3 +/- 3.9% CV; immunohistochemistry and immunoblotting, respectively). Prefrontal and motor cortex exhibited GABA(A) receptor subunit peptide alterations, but these changes varied with the method of analysis. CONCLUSIONS: These findings demonstrate that ethanol dependence results in nonuniform changes in GABA(A) receptor subunit peptide levels across the rat brain cortex and suggest that mechanisms which subserve functional changes in receptor activity may vary in accordance with anatomic or cellular differences within the cortex.

Cerebral Cortex↗

PubMed1990

[A new approach to the quantitative analysis of the vascular architecture and its application to the cerebral cortex of the reeler mouse].

(1) A new method for morphometric studies on the vascular architecture of the mouse brain was developed. The method was as follows: the cerebral vascular images of the arteries, capillaries and veins, which were visualized by injection with gelatinized India-ink, were entirely entered into a personal computer system from a digitizer through light-microscopic photographs (X250). Thus the vessels were transformed into consecutive lines composed of short straight "line segments". The parameters obtained from these "line segments" were the total vascular length per unit area and volume ("length density"), the direction of the "orientation axis" and the "intensity of orientation" of the blood vessels. The three-dimensional properties of the vascular vessels were calculated from these data. The frontal and sagittal vascular patterns of the occipital cortex, thalamus, hippocampus, piriform cortex, internal capsule and corpus callosum were entered and the parameters described above were calculated. The calculated three-dimensional "length densities" of the blood vessels in the occipital cortex and thalamus were about twice as great as those of the corpus callosum and internal capsule, and those of the hippocampus and piriform cortex had intermediate values. The "orientation axis" of the occipital cortex was approximately perpendicular to the cerebral surface, while those of the corpus callosum and internal capsule were parallel to the course of the nerve fibers. The axis of the thalamus was parallel to the horizontal plane, and that of the hippocampus was perpendicular to its surface. The "intensity of orientation" of the piriform cortex, however, was very small. (2) In order to investigate the factors defining the vascular pattern in the cerebral cortex, the reeler mutant mouse, in which the lamination of the cortex is reversed and the neurons distributed more homogeneously than in normal mice, was investigated by the above-mentioned method. The vascular pattern of the reeler mutant mouse revealed a difference from that of the normal mouse in that the "length density" of the reeler mouse was apparently equal in different layers, and the degree of vascular orientation was not as intensive as that of the normal cortex, in which the blood vessels tended to be perpendicular to the pial surface.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1985

Extent and organization of opossum prefrontal cortex defined by anterograde and retrograde transport methods.

Prefrontal cortex is commonly defined as cortex which receives afferents from the thalamic mediodorsal nucleus (MD). The extent of opossum prefrontal cortex was mapped with anterograde and retrograde axonal transport methods. The prefrontal field was found to include not only cortex on the lateral convexity of the frontal lobe as reported in earlier studies, but, in addition, cortex within the rhinal fissure and cortex on the rostral medial wall of the hemisphere. The organization of the thalamic input to the medial wall was analyzed in some detail and compared with that of the rat. The reason for this emphasis stemmed from earlier observations which suggested that a lateral, nonolfactory segment of MD, prominent in the rat and other species, may not be present in opossum MD. In the rat, the lateral segment, which constitutes approximately one-third of MD, projects to a relatively large expanse of rostral medial cortex which is also projected upon by the anteromedial nucleus. The main projection field of the lateral one-third of opossum MD is to cortex on the lateral convexity of the frontal lobe which has no input from the anteromedial nucleus and has no counterpart in the rat. Only the most lateral edge of opossum MD projects to medial cortex, to a very small field, which is also projected upon by the anteromedial nucleus. In other respects, the organization of the rostral medial cortex is similar in rat and opossum. These results suggest that, rather than being absent, an equivalent of a nonolfactory segment may be present in opossum MD but is markedly reduced in size, compared to that in rat and other species.

Animals↗

PubMed1992

Parvalbumin and calbindin D-28K in the human entorhinal cortex. An immunohistochemical study.

Research is here reported on the distribution of immunoreactivities of the calcium-binding proteins parvalbumin and calbindin D-28K in the entorhinal cortex of normal human brains. Topographically, parvalbumin immunoreactive neurons were only seen in the lateral portion of the rostral entorhinal cortex, in continuity with the adjacent perirhinal cortex. The intermediate and caudal portions gave positive results along the mediolateral extension of the entorhinal cortex. The laminar distribution of parvalbumin immunoreactive neurons was similar throughout the entorhinal cortex. Heavy immunostaining, largely coincident with cell islands, was observed in cells and fibers in layer II, being densest in the deep half of layer III and more sparsely distributed in layers V and VI. Calbindin D-28K immunoreactivity was found throughout the entorhinal cortex. In contrast to parvalbumin immunoreactivity, calbindin D-28K was present from layer I up to upper layer III, the neurons being most numerous in the cell islands of layer II. These results show that rostromedial portions of the human entorhinal cortex contain calbindin immunoreactivity, but not parvalbumin, while the lateral, intermediate and caudal portions of the entorhinal cortex contain both calcium-binding proteins. As it is known that these two proteins belong to a subset of GABAergic neurons, we suggest that a topographical diversity in some of the cells may be responsible for inhibitory effects in the human entorhinal cortex. This proposed diversity might be relevant to the processing of information that the entorhinal cortex conveys to the dentate gyrus and receives from various components of the hippocampus, the subicular complex and other cortical and subcortical sources.

Calbindins↗