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PubMed1999

Synaptic depression induced by pharmacological activation of metabotropic glutamate receptors in the perirhinal cortex in vitro.

The perirhinal cortex is crucially involved in various forms of learning and memory. Decrements in neuronal responsiveness occur in the perirhinal cortex with stimulus repetition during visual recognition performance. However, very little is known concerning the underlying mechanisms of synaptic transmission and plasticity in this cortical region. In this study, we provide evidence demonstrating the presence of functional group I, II and III metabotropic glutamate receptors in the rat perirhinal cortex in vitro. Furthermore, the results demonstrate long-lasting synaptic depression in the perirhinal cortex. Extracellular synaptic responses were recorded from superficial layers of the perirhinal cortex directly below the rhinal sulcus, in response to electrical stimuli delivered in the superficial or intermediate layers to the entorhinal or temporal cortex sides of the rhinal sulcus. Evoked synaptic potentials were depressed during bath perfusion of each of the following: the broad-spectrum metabotropic glutamate receptor agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid, the selective group I agonist (R,S)-3,5-dihydroxyphenylglycine, the group II agonist (2S,1'R,2'R,3'R)-(2',3'-dicarboxycyclopropyl)glycine and the group III agonist (S)-2-amino-4-phosphonobutanoate. Furthermore, there was a long-lasting depression of synaptic transmission following washout of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid, (R,S)-3,5-dihydroxyphenylglycine or (2S,1'R,2'R,3'R)-(2',3'-dicarboxy-cyclopropyl)glycine. Activation of group III metabotropic glutamate receptors by (S)-2-amino-4-phosphonobutanoate did not result in long-lasting changes in synaptic transmission. Thus, the pharmacological activation of metabotropic glutamate receptors can produce short- or long-term changes in synaptic transmission in the perirhinal cortex. It is possible therefore, that metabotropic glutamate receptors are involved in the decrement in neuronal responsiveness associated with visual recognition in the perirhinal cortex.

Animals↗

PubMed1998

Convergence of limbic input to the cingulate motor cortex in the rhesus monkey.

Limbic system influences on motor behavior seem widespread, and could range from the initiation of action to the motivational pace of motor output. Motor abnormalities are also a common feature of psychiatric illness. Several subcortical limbic-motor entry points have been defined in recent years, but cortical entry points are understood poorly, despite the fact that a part of the limbic lobe, the cingulate motor cortex (area 24c or M3, and area 23c or M4), contributes axons to the corticospinal pathway. Using retrograde and anterograde tracers in rhesus monkeys, we investigated the ipsilateral limbic input to area 24c and adjacent area 23c. Limbic cortical input to areas 24c and 23c arise from cingulate areas 24a, 24b, 23a, 23b, and 32, retrosplenial areas 30 and 29, and temporal areas 35, TF and TH. Areas 24c and 23c were also interconnected strongly. The dysgranular part of the orbitofrontal cortex and insula projects primarily to area 24c while the granular part of the orbitofrontal cortex and insula projects primarily to area 23c. Afferents from cingulate area 25, the retrocalcarine cortex, temporal pole, entorhinal cortex, parasubiculum, and the medial part of area TH target primarily or only area 24c. Our findings indicate that a variety of telencephalic limbic afferents converge on cortex lining the lower bank and fundus of the anterior part of the cingulate sulcus. Because it is known that this cortex gives rise to axons ending in the spinal cord, facial nucleus, pontine gray, red nucleus, putamen, and primary and supplementary motor cortices, we suggest that the cingulate motor cortex forms a strategic cortical entry point for limbic influence on the voluntary motor system.

Amino Acids↗

PubMed2003

Human motor cortex activity during mental rotation.

The functional role of human premotor and primary motor cortex during mental rotation has been studied using functional MRI at 3 T. Fourteen young, male subjects performed a mental rotation task in which they had to decide whether two visually presented cubes could be identical. Exploratory Fuzzy Cluster Analysis was applied to identify brain regions with stimulus-related time courses. This revealed one dominant cluster which included the parietal cortex, premotor cortex, and dorsolateral prefrontal cortex that showed signal enhancement during the whole stimulus presentation period, reflecting cognitive processing. A second cluster, encompassing the contralateral primary motor cortex, showed activation exclusively after the button press response. This clear separation was possible in 3 subjects only, however. Based on these exploratory results, the hypothesis that primary motor cortex activity was related to button pressing only was tested using a parametric approach via a random-effects group analysis over all 14 subjects in SPM99. The results confirmed that the stimulus response via button pressing causes activation in the primary motor cortex and supplementary motor area while parietal cortex and mesial regions rostral to the supplementary motor area are recruited for the actual mental rotation process.

Adult↗

PubMed2003

The anatomy of the cerebral cortex of the echidna (Tachyglossus aculeatus).

The cerebral cortex of the echidna is notable for its extensive folding and the positioning of major functional areas towards its caudal extremity. The gyrification of the echidna cortex is comparable in magnitude to prosimians and cortical thickness and neuronal density are similar to that seen in rodents and carnivores. On the other hand, many pyramidal neurons in the cerebral cortex of the echidna are atypical with inverted somata and short or branching apical dendrites. All other broad classes of neurons noted in therian cortex are also present in the echidna, suggesting that the major classes of cortical neurons evolved prior to the divergence of proto- and eutherian lineages. Dendritic spine density on dendrites of echidna pyramidal neurons in somatosensory cortex and apical dendrites of motor cortex pyramidal neurons is lower than that found in eutheria. On the other hand, synaptic morphology, density and distribution in somatosensory cortex are similar to that in eutheria. In summary, although the echidna cerebral cortex displays some structural features, which may limit its functional capacities (e.g. lower spine density on pyramidal neurons), in most structural parameters (e.g. gyrification, cortical area and thickness, neuronal density and types, synaptic morphology and density), it is comparable to eutheria.

Animals↗

PubMed2001

Hemispheric asymmetry of ipsilateral motor cortex activation during unimanual motor tasks: further evidence for motor dominance.

OBJECTIVES: To test to which extent the increase in ipsilateral motor cortex excitability during unimanual motor tasks shows hemispheric asymmetry. METHODS: Six right-handed healthy subjects performed one of several motor tasks of different complexity (including rest) with one hand (task hand) while the other hand (non-task hand) was relaxed. Focal transcranial magnetic stimulation was applied to the motor cortex ipsilateral to the task hand and the amplitude of the motor evoked potential (MEP) in the non-task hand was measured. In one session, the task hand was the right hand, in the other session it was the left hand. The effects of motor task and side of the task hand were analyzed. Spinal motoneuron excitability was assessed using F-wave measurements. RESULTS: Motor tasks, in particular complex finger sequences, resulted in an increase in MEP amplitude in the non-task hand. This increase was significantly less when the right hand rather than the left hand was the task hand. This difference was seen only in muscles homologous to primary task muscles. The asymmetry could not be explained by changes in F-wave amplitudes. CONCLUSIONS: Hemispheric asymmetry of ipsilateral motor cortex activation either supports the idea that, in right handers, the left motor cortex is more active in ipsilateral hand movements, or alternatively, that the left motor cortex exerts more effective inhibitory control over the right motor cortex than vice versa. We suggest that hemispheric asymmetry of ipsilateral motor cortex activation is one property of motor dominance of the left motor cortex.

Adult↗

PubMedDate not supplied

Contributions of cat posterior parietal cortex to visuospatial discrimination.

The purpose of the present study was to examine the contributions made by cat posterior parietal cortex to the analyses of the relative position of objects in visual space. Two cats were trained on a landmark task in which they learned to report the position of a landmark object relative to a right or left food-reward chamber. Subsequently, three pairs of cooling loops were implanted bilaterally in contact with visuoparietal cortices forming the crown of the middle suprasylvian gyrus (MSg; architectonic area 7) and the banks of the posterior-middle suprasylvian sulcus (pMS sulcal cortex) and in contact with the ventral-posterior suprasylvian (vPS) region of visuotemporal cortex. Bilateral deactivation of pMS sulcal cortex resulted in a profound impairment for all six tested positions of the landmark, yet bilateral deactivation of neither area 7 nor vPS cortex yielded any deficits. In control tasks (visual orienting and object discrimination), there was no evidence for any degree of attentional blindness or impairment of form discrimination during bilateral deactivation of pMS cortex. Therefore, we conclude that bilateral cooling of pMS cortex, but neither area 7 nor vPS cortex, induces a specific deficit in spatial localization as examined with the landmark task. These observations have significant bearing on our understanding of visuospatial processing in cat, monkey, and human cortices.

Animals↗

PubMedDate not supplied

Complete flatmounting of the macaque cerebral cortex.

The elaborate folding of the brain surface has posed a practical impediment to investigators engaged in mapping the areas of the cerebral cortex. This obstacle has been overcome partially by the development of methods to erase the sulci and gyri by physically flattening the cortex prior to sectioning. In this study, we have prepared a step-by-step atlas of the flatmounting process for the entire cerebral cortex in the macaque monkey. The cortex was dissected from the white matter, unfolded, and flattened in a single piece of tissue by making three relieving cuts. The flatmount was sectioned at 60-75 microm and processed for cytochrome oxidase (CO) or myelin. From animal to animal there was nearly a twofold variation in the surface area of individual cortical regions, and of the whole cortex. In each specimen, a close correlation was found between V1 surface area (mean = 1343 mm2), V2 surface area (mean = 1012 mm2), hippocampal area (mean = 181 mm2), and total cerebral cortex area (mean = 10,430 mm2). The complete pattern of CO stripes in area V2 was labeled clearly in several cases; the number of cycles of thick-pale-thin-pale stripes ranged from 26 to 34. Characteristic patterns of strong CO activity were encountered in areas V3, MT, auditory and somatosensory cortex. In some animals we made injections of a retrograde tracer, gold-conjugated cholera toxin B subunit, into area V2 to identify all sources of cortical input. In addition to previously described inputs, we identified three new regions in the occipitotemporal region that project to V2. Flatmounting the cerebral cortex is a simple, efficient method that can be used routinely for mapping areas and connections in the macaque brain, the most widely used primate model of the human brain.

Animals↗

PubMed2000

Craniotomy under local anesthesia and monitored conscious sedation for the resection of tumors involving eloquent cortex.

OBJECTIVE: Resection or even biopsy of an intra-axial mass lesion in close relationship to eloquent cortex carries a major risk of neurological deficit. We have assessed the safety and effectiveness of craniotomy under local anesthesia and monitored conscious sedation for the resection of tumors involving eloquent cortex. METHODS: We have performed a retrospective review of a consecutive series of 157 adult patients who underwent craniotomy under local anesthesia by one surgeon (P.M.B.) at Brigham and Women's Hospital in Boston. All patients had tumors in close proximity to eloquent cortex, including speech, motor, primary sensory, or visual cortex. In most cases the lesion was considered inoperable by the referring surgeon. All resection was verified by post-operative imaging approximately one month after surgery and all cases were reviewed by an independent neurosurgeon (A.D.). RESULTS: In 122 cases, brain mapping was performed to identify eloquent cortex and in the remainder neurological monitoring was maintained during the procedure. Radiological gross total resection was achieved in 57% of patients and greater than 80% resection was achieved in 23%. Thus 4 out of 5 of patients had major resection despite the close relationship of tumor to eloquent cortex. In 13%, less than 80% of tumor was removed because of danger of neurological deficit. In 7% of patients, only a biopsy could be done because of infiltration into eloquent cortex that could only be assessed at surgery. In 76 patients with pre-operative neurological deficits, there was complete resolution of these deficits in 33%, improvement in 32%, no change in 28%, and long-term worsening in 8%. Among 81 patients with no pre-operative neurological deficit, 1 patient suffered a major permanent neurological deficit, and 2 developed minor deficits. There was a transient post-operative deficit in one-third of cases, but this had resolved at one month in all but three patients. Monitored conscious sedation was performed without anesthetic complications using midazolam, sufentanyl and fentanyl with or without propofol. Only one case needed to be converted to general anesthesia. Patient satisfaction with the procedure has been good. Operating time and hospital stay were lower than the mean for brain tumor craniotomy at this hospital. CONCLUSIONS: Tumor surgery with conscious sedation is a safe technique that allows maximal resection of lesions in close anatomical relationship to eloquent cortex, with a low risk of new neurological deficit. Only 7% of intrinsic cortical tumors were ineligible for partial or complete resection with this technique.

Adolescent↗

PubMed1984

Effects of inferior temporal lesions on visual discrimination performance in monkeys with complete and incomplete striate cortex ablations.

In order to determine whether inferior temporal cortex participates in the relearning of visual discriminations following striatectomy, monkeys were retrained to perform two preoperatively acquired discriminations (brightness-flux and brightness-area) after receiving bilateral striate cortex lesions and then retested in the same tasks after bilateral inferior temporal surgery. After inferior temporal surgery, the monkeys with histologically verified total ablation of striate cortex showed little or no impairment in relearning the discriminations, whereas the monkeys with remnants of intact striate cortex were severely impaired. These findings suggest that inferior temporal cortex is, at most, of minor importance in relearning brightness-flux and brightness-area discriminations in the absence of striate cortex. This interpretation is consistent with the view that the contribution of inferior temporal cortex to visual discrimination performance depends on input from striate cortex.

Animals↗

PubMed2000

Functional connections and epileptic spread between hippocampus, entorhinal cortex and amygdala in a modified horizontal slice preparation of the rat brain.

The hippocampus, the entorhinal cortex and the amygdala are interconnected structures of the limbic system that are implicated in memory and emotional behaviour. They demonstrate synaptic plasticity and are susceptible to development of temporal lobe epilepsy, which may lead to emotional and psychological disturbances. Their relative anatomical disposition has limited the study of neurotransmission and epileptic spread between these three regions in previous in vitro preparations. Here we describe a novel, modified-horizontal slice preparation that includes in the same plane the hippocampus, entorhinal cortex and amygdala. We found that, following application of bicuculline, each region in our preparation could generate spontaneous bursts that resembled epileptic interictal spikes. This spontaneous activity initiated in the hippocampal CA3/2 region, from where it propagated and controlled the activity in the entorhinal cortex and the amygdala. We found that this spontaneous bursting activity could spread via two different pathways. The first pathway comprises the well-known subiculum-entorhinal cortex-perirhinal cortex-amygdala route. The second pathway consists of a direct connection between the CA1 region and perirhinal cortex, through which the hippocampal bursting activity can spread to the amygdala while bypassing the entorhinal cortex. Thus, our experiments provide a new in vitro model of initiation and spread of epileptic-like activity in the ventral part of the limbic system, which includes a novel, fast and functional connection between the CA1 region and perirhinal cortex.

Action Potentials↗

PubMed1972

Mitochondrial autonomy. Sialic acid residues on the surface of isolated rat cerebral cortex and liver mitochondria.

N-acetylneuraminic acid at the surfaces of rat cerebral cortex and liver mitochondria and derived mitoplasts (inner membrane plus matrix particles) was studied biochemically and electrokinetically. Rat cerebral cortex mitochondria in 0.0145 M NaCl, 4.5% sorbitol, pH 7.2 +/- 0.1, 0.6 mM NaHCO(3), had an electrophoretic mobility of - 2.88 +/- 0.01 micro/sec per v per cm. In the same solution the electrophoretic mobility of rat liver mitochondria was - 2.01 +/- 0.02, of rat liver mitoplasts was - 1.22 +/- 0.07, and of rat cerebral cortex mitoplasts - 0.91 +/- 0.04 micro/sec per v per cm. Treatment of these particles with 50 microg neuraminidase/mg particle protein resulted in the following electrophoretic mobilities in micro/sec per v per cm: rat cerebral cortex mitochondria, - 2.27; rat liver mitochondria, - 1.40; rat cerebral cortex mitoplasts, - 0.78; and rat liver mitoplasts, - 1.10. Rat liver mitochondria, mitoplasts, and outer mitochondrial membranes contained 2.0, 1.1, and 4.1 nmoles of sialic acid/mg protein, respectively. 10% of the liver mitochondrial protein and 27.5% of the sialic acid was solubilized in the mitoplast and outer membrane isolation procedure. Rat cerebral cortex mitochondria, mitoplasts, and outer mitochondrial membranes contained 3.1, 0.8, and 6.2 nmoles sialic acid/mg protein, respectively; 10% of the brain mitochondrial protein and 49 % of the sialic acid was solubilized in the mitoplast and outer membrane isolation solution procedure. Treatment of both the rat liver and cerebral cortex mitochondria with 50 microg neuraminidase (dry weight) /mg protein resulted in the release of about 50% of the available outer membrane sialic acid residues. Treatment of all of the particles with trypsin caused release of sialic acid but did not greatly affect the particle electrophoretic mobility. In each instance, curves of pH vs. electrophoretic mobility indicated that the particle surface contained an acid dissociable group, most likely a carboxyl group of sialic acid with pK(a) approximately 2.7. Treatment of either the rat liver or the cerebral cortex mitochondria with trypsinized concanavalin A did not affect the particle electrophoretic mobility but did cause a decrease in the electrophoretic mobility of L5178Y mouse leukemic cells.

Animals↗

PubMedDate not supplied

The topographical and neuroanatomical distribution of neurofibrillary tangles and neuritic plaques in the cerebral cortex of patients with Alzheimer's disease.

The distribution of neurofibrillary tangles (NFTs) and neuritic plaques (NPs) was mapped in 39 cortical areas of 11 brains of patients with Alzheimer's disease (AD). Whole hemisphere blocks were embedded in polyethylene glycol (Carbowax), sectioned coronally, and stained with thioflavin S and thionin. The densities of NFTs and NPs were assessed using a numerical rating scale for each area. Scores were grouped by type of cortex and by lobe for statistical analysis. Highly significant differences were obtained. For example, limbic periallocortex and allocortex had more NFTs than any other type of cortex. In descending order, the density of NFTs was as follows: periallocortex (area 28) greater than allocortex (subiculum/CA1 zones of hippocampal formation, area 51) greater than corticoid areas (accessory basal nucleus of amygdala, nucleus basalis of Meynert) greater than proisocortex (areas 11, 12, 24, 23, anterior insula, 38, 35) greater than nonprimary association cortex (32, 46, superior temporal sulcus, 40, 39, posterior parahippocampal cortex, 37, 36) greater than primary sensory association cortex (7, 18, 19, 22, 21, 20) greater than agranular cortex (44-5, 8, 6, 4) greater than primary sensory cortex (41-2, 3-1-2, 17). The laminar distribution of NFTs tended to be selective, involving primarily layers III and V of association areas and layers II and IV of limbic periallocortex. There were far more NFTs in both limbic and temporal lobes than in frontal, parietal, and occipital lobes. In general, NPs were more evenly distributed throughout the cortex, with the exceptions of limbic periallocortex and allocortex, which had notably fewer NPs than other cortical areas. Temporal and occipital lobes had the highest NP densities, limbic and frontal lobes had the lowest, and parietal lobe was intermediate. No significant left-right hemispheric differences for NFT or NP densities were found across the population, and there was no relationship between duration of illness and densities of NFTs or NPs. The regional and laminar distribution of NFTs (and, to a lesser degree, that of NPs) suggests a consistent pattern of vulnerability within the cerebral cortices that seems correlated to the hierarchies of cortico-cortical connections. The higher-order association cortices, especially those in the anterior and ventromedial sectors of temporal lobe, are the most vulnerable, while other cortices appear less vulnerable to a degree commensurate with their connectional "distance" (i.e., synapses removed) from the limbic areas.

Aged↗

PubMed2003

Increase in reelin-positive cells in the marginal zone of Pax6 mutant mouse cortex.

The extracellular matrix molecule reelin is a crucial molecule in CNS development, in particular in the cerebellum and cerebral cortex. In the cerebral cortex, reelin is provided by a small number of neurons located in the marginal zone (MZ). These neurons belong to the earliest neurons generated, but little is known about the molecular mechanisms of their specification. Here we describe that reelin-positive cells are strongly increased in the developing cortex of the Pax6 mutant mice Small eye. Shortly after the onset of reelin expression, the number of reelin- and calretinin-positive cells is doubled in the cortex of Pax6 mutants and this increase is further enhanced during development. In contrast, calbindin-positive cells in the MZ do not co-express reelin and are not altered in the Pax6 mutant cortex. The split of the preplate cells was also defective in the Pax6 mutant cortex, suggesting that the amount of reelin is crucial for positioning of the cortical plate between the MZ and subplate. We further show that Pax6 mutant cortical cells isolated in vitro do not develop an increase in reelin-positive cells, while cells isolated from the entire telencephalon do. Consistent with non-cell-autonomous mechanisms contributing to the increase in reelin-positive cells in the Pax6-deficient cortex, tangential migration of diverse cell types from the ventral telencephalon into the cortex is enhanced in the Pax6 mutant mice. Taken together, these experiments further elucidate how patterning of the forebrain by the transcription factor Pax6 regulates the specification of distinct neuronal subtypes in the cortical MZ.

Animals↗

PubMed2004

GABAA receptors reorganize when layer 4 in ferret somatosensory cortex is disrupted by methylazoxymethanol (MAM).

We established a model of cortical development that arrests the birth of layer 4 cells by injecting methylazoxymethanol (MAM) on embryonic day 33 (E33) in ferrets. This leads to adult somatosensory cortex with a very thin layer 4. Earlier, we determined the relative absence of layer 4 changed the growth and differentiation of the somatosensory cortex and the growth of thalamic afferents into the cortical plate. To identify other features of cortical organization that might be altered after MAM treatment, we assessed the distribution of selected excitatory and inhibitory receptors in area 3b of ferret somatosensory cortex. Initial screening revealed the distribution of several excitatory receptors (NMDA, AMPA, kainate) in E33 MAM-treated cortex was similar to that in normal adult animals. In contrast, the binding pattern of inhibitory GABAA receptors was altered in MAM-treated cortex. Normally, GABAA receptors densely locate in central layers of cortex. In E33 MAM-treated animals, GABAA receptor binding extended superficially, covering a broader area of cortex. Further experiments using antibodies directed against GABAAalpha receptors disclosed that pan alpha GABAA receptors strongly localize to layer 4 in normal area 3b. In E33 MAM-treated cortex, however, GABAAalpha receptors extend outside and are located above and below the very thin layer 4. The redistribution of inhibitory receptors suggests that layer 4 plays an important role in regulating thalamic terminations and also in the resulting ability to refine processing of incoming stimuli.

Animals↗

PubMed2004

Thinning of the cerebral cortex in aging.

The thickness of the cerebral cortex was measured in 106 non-demented participants ranging in age from 18 to 93 years. For each participant, multiple acquisitions of structural T1-weighted magnetic resonance imaging (MRI) scans were averaged to yield high-resolution, high-contrast data sets. Cortical thickness was estimated as the distance between the gray/white boundary and the outer cortical surface, resulting in a continuous estimate across the cortical mantle. Global thinning was apparent by middle age. Men and women showed a similar degree of global thinning, and did not differ in mean thickness in the younger or older groups. Age-associated differences were widespread but demonstrated a patchwork of regional atrophy and sparing. Examination of subsets of the data from independent samples produced highly similar age-associated patterns of atrophy, suggesting that the specific anatomic patterns within the maps were reliable. Certain results, including prominent atrophy of prefrontal cortex and relative sparing of temporal and parahippocampal cortex, converged with previous findings. Other results were unexpected, such as the finding of prominent atrophy in frontal cortex near primary motor cortex and calcarine cortex near primary visual cortex. These findings demonstrate that cortical thinning occurs by middle age and spans widespread cortical regions that include primary as well as association cortex.

Adolescent↗

PubMed1998

Immunocytochemical study on the distribution of NOS-immunoreactive neurons in the cerebral cortex of aged rats.

Nitric oxide (NO) involvement has been demonstrated in mechanisms of synaptic plasticity, particularly in hippocampal long-term potentiation, a mechanism that underlies certain forms of learning and memory. Several findings suggest that NO production may be decreased in the aged rats. Changes in the nNOS-containing neurons with ageing were demonstrated by immunocytochemistry. NOS-immunoreactive (IR) cells in aged rats were present in all cortical areas and the hippocampus, and the pattern of distribution was similar to that of the control group. The number of NOS-IR cells in the cerebral cortex was significantly decreased in the aged rats, but the extent of changes was variable in each area, and ranged from mild decrease (< 30%) to severe decrease (> 50%). Severely decreased areas were the cingulate cortex, parietal cortex area 1, temporal cortex area 1, 2, 3, medial part of occipital cortex area 2, monocular and binocular part of occipital cortex area 1, entorhinal cortex, hippocampus proper, dentate gyrus and subiculum. Morphologically, the number of dendritic branches seemed to be decreased in aged group and the length of dendrites of NOS-IR neurons showed a tendency to shorten. These results indicate the involvement of neuronal system containing NOS in the ageing brain, and provide the first morphological evidence for the loss of NOS neurons in the cerebral cortex of the aged rats by immunocytochemistry.

Aging↗

PubMed1996

Effects of entorhinal cortex lesion on learning behavior and on hippocampus in the rat.

The initial stage of Alzheimer's disease is characterized by a neuropathological change in the entorhinal cortex. In a previous study it was shown that rats with excitotoxic lesion of entorhinal cortex showed an impaired acquisition of passive and active avoidance responses. In this study a rat with excitotoxic lesion of the entorhinal cortex was tested for 'more operant' behavioral learning (i.e., positive reinforcement operant learning). The hippocampus was also examined histologically as acetylcholinesterase-stained sections, and as synaptophysin immunostained sections and examined biochemically by liquid chromatography. Eight weeks after operation, the bilateral entorhinal cortex lesioned rats showed an impaired acquisition of positive reinforcement operant learning. The lesioned side of unilateral entorhinal cortex lesioned rats showed a decrease of acetylcholinesterase-positive fibers in the CA3, the dentate gyrus, and of synaptophysin-positive substances in the CA3. Biochemical study showed a decreased level of acetylcholine in the CA3, and in the dentate gyrus. The histological and biochemical findings are interpreted as indicating that the entorhinal cortex of the rat provides the major extrinsic synaptic input to the hippocampal formation via the circuit which serves as a relay passage through the dentate gyrus and via direct projections into the hippocampus. Behavioral findings confirmed the importance of the entorhinal cortex in memory acquisition and indicated that rats with a partial neuronal loss in the entorhinal cortex may be a useful model for the memory disturbance of Alzheimer's disease.

Acetylcholine↗

PubMed2005

Removal of cholinergic input to perirhinal cortex disrupts object recognition but not spatial working memory in the rat.

The perirhinal cortex of the temporal lobe has a crucial role in object recognition memory. Cholinergic transmission within perirhinal cortex also seems to be important for this function, as the muscarinic receptor antagonist scopolamine disrupts object recognition performance when administered systemically or directly into perirhinal cortex. In the present study, we directly assessed the contribution of cholinergic basal forebrain input to perirhinal cortex in object recognition. Selective bilateral removal of the cholinergic basal forebrain inputs to perirhinal cortex was accomplished by injecting the immunotoxin 192 IgG-saporin directly into perirhinal cortex in rats. These animals were significantly impaired relative to vehicle-injected controls in a spontaneous object recognition task despite intact spatial alternation performance. These results are consistent with recent reports of object recognition impairment following acute cholinergic receptor blockade and extend these findings by demonstrating that chronic removal of cholinergic basal forebrain input to an otherwise intact perirhinal cortex causes a severe object recognition deficit similar to that associated with more extensive cell body lesions of perirhinal cortex.

Animals↗