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PubMed1987

Plasticity of the synaptic contact zone following loss of synapses in the cerebral cortex of aging humans.

Quantitative ultrastructural analyses of ethanolic phosphotungstic acid-stained human layer 1 precentral motor cortex (Brodmann's area 4) and layer 1 postcentral somatosensory cortex (Brodmann's area 3) were undertaken to determine the nature of synaptic changes occurring over a series of ages (45-84 years) of a normal aging human population. In the precentral cortex, a significant decrease in the number of synapses was accompanied by an increase in mean length of the postsynaptic contact zone and a decrease in the mean width of the presynaptic paramembranous density. The frequency of mature type A and immature type E synaptic profiles decreased with age. There were no changes in the width of the postsynaptic paramembranous density, cleft width or the number of presynaptic dense projections per synapse. In the postcentral cortex there were no significant changes in synaptic number or in any of the synaptic parameters measured. The present study demonstrates that age-related synapse loss in the human cerebral cortex may be confined to specific cortical regions. The data suggest that in the precentral cortex the plasticity of the synaptic contact zone may be a compensatory response by the remaining synapses to age-related synapse loss.

Aged↗

PubMed1987

Ultrastructural localization of beta-adrenergic receptor-like immunoreactivity in the cortex and neostriatum of rat brain.

We sought to quantitatively examine the processes containing beta-adrenergic receptor-like immunoreactivity (beta-AR-LI) in the cerebral cortex and neostriatum using a previously characterized rabbit antiserum to frog erythrocyte beta-ARs under optimized immunolabeling conditions. Quantitative assessments of the laminar distribution of beta-AR-LI in the cortex was achieved by computer-assisted image analysis of immunoautoradiographs and by quantitative electron microscopic analysis of peroxidase-antiperoxidase (PAP) labeling in aldehyde-fixed sections and unfixed synaptosomes. In the somatosensory and anterior cingulate cortical areas, light microscopy of aldehyde-fixed sections immunolabeled by the PAP method revealed small (0.5-1.0 micron) punctate processes in all layers. In the deeper layers, rims of immunoreactivity around the plasmalemma of a population of neuronal perikarya and processes were also observed. By immunoautoradiography, labeling was seen in distinct, laminar distributions resembling the reported autoradiographic patterns using radioligands. By electron microscopy, the immunoreactive profiles in all cortical layers were primarily thick and thin postsynaptic densities (PSDs), comprising 4% of all identifiable PSDs in fixed sections and 12% in unfixed synaptosomal preparations. Also labeled were saccules of smooth endoplasmic reticulum and pinocytotic vesicles in dendrites, glial processes and lightly myelinated axons. In the neostriatum, the density of autoradiographic immunoreactivity was equivalent to the heavily labeled laminae of the cerebral cortex. Immunoreactivity detectable by light microscopy included punctate processes and rims of perikarya, as was seen in the cerebral cortex. The PAP reaction was shown by electron microscopy to be localized to the cytoplasmic surface of plasmalemma of a few proximal dendrites, but was most prominently associated with PSDs of dendritic spines. Preadsorption of the antiserum with a partially purified beta-AR preparation abolished all detectable immunoreactivity. These results provide further support for the specificity of the antiserum for beta-ARs, and are the first quantitative ultrastructural evidence for association of beta-AR-LI with PSDs in the cerebral cortex. The neostriatum, whose major catecholaminergic innervation is dopaminergic, and not noradrenergic, is also confirmed to exhibit high levels of beta-AR-LI within subcellular structures analogous to those seen in the cerebral cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Somatosensory neurons in partially deafferented rat hindlimb granular cortex subsequent to transection of the sciatic nerve: effects of glutamate and acetylcholine.

The effects of drugs administered iontophoretically were studied on 302 neurons isolated from partially deafferented hindlimb granular cortex of the rat and were compared to a previously studied sample from normal granular cortex. The proportions of cells affected by glutamate and acetylcholine (ACh) were not markedly different after partial deafferentation, but the cells were more readily depolarized by glutamate and their responses to a fixed dose of glutamate were larger. Fewer cells were excited strongly by ACh (up to the point of depolarization block) and the amplitudes of responses to test pulses of ACh were reduced in infragranular layers after partial deafferentation. Fifteen cells (5.9%) were inhibited by ACh administration, whereas in normal cortex this value was less than 1%. Fewer receptive fields were uncovered by glutamate after partial deafferentation, but more receptive fields were enlarged by this substance after nerve transection. These data were interpreted to mean that the cells from deafferented cortex had fewer excitatory inputs and as well, were apparently under a comparatively weaker degree of inhibitory control after deafferentation. The administration of ACh uncovered fewer somatic inputs than in normal animals. Responses were enhanced by ACh less frequently, and repeated treatments with ACh often led to a reduction in the effectiveness of the afferent stimulus. Increases in neuronal thresholds for somatic stimuli also were observed. The laminar distribution of the effects of ACh was similar to the distribution observed in normal animals. The responses to iontophoretically administered ACh and its agonists appeared to be mediated through both nicotinic and muscarinic receptor processes after partial deafferentation. Often the time course of the effects of ACh was abnormal, being characterized by oscillations between silence and very high rates of discharge with a period of 6-12 s. These observations are consistent with the hypothesis that after a major deafferentation (i) there is a reduction of the inhibitory controls normally present in the somatosensory cortex, and (ii) neuronal responses to ACh are modified in partially deafferented cortex. The magnitude of the responses of cells to ACh in the supragranular layers are larger after deafferentation whereas the magnitude of responses in the infragranular layers are reduced by this procedure. These changes may be related to changes induced by deafferentation in the distribution of receptors and/or in their pharmacological properties.

Acetylcholine↗

PubMed1988

D1 dopamine receptors in human putamen, frontal cortex and calf retina: differences in guanine nucleotide regulation of agonist binding and adenylate cyclase stimulation.

High-affinity binding sites for the D1 dopamine receptor antagonist [3H]SCH 23390 were identified in membranes from human putamen, frontal cortex and calf retina. In frontal cortex binding not only occurred to D1 but also to 5-HT2 receptors. In retina and putamen no binding to 5-HT2 receptors was detected. All further binding experiments in frontal cortex were carried out in the presence of 20 nM mianserin to prevent binding to 5-HT2 receptors. In the 3 tissues, antagonist competition curves were monophasic, whereas competition curves with the agonist dopamine revealed the presence of two binding sites, one having high affinity (RH) (32% in retina, 28% in putamen, and 15% in frontal cortex) and the other having low affinity (RL). In retina, the addition of 100 microM GTP caused a full conversion of RH into RL. In contrast, in frontal cortex, RH sites were not altered by 400 microM GTP or 100 microM 5'-guanylyl-imidodi-phosphate (Gpp(NH)p). In putamen, both guanine nucleotides provoked only a partial conversion of RH into RL. Dopamine (100 microM) produced a 220% and 56% increase in cAMP production in respectively retina and putamen homogenates, while no increase was observed in frontal cortex homogenate. These data may suggest that not all D1-receptors are coupled to the adenylate cyclase system.

Adenylyl Cyclases↗

PubMed1990

Neurotensin innervation of the human cerebral cortex: lack of colocalization with catecholamines.

We have localized neurotensin (NT) with immunocytochemical methods in the normal human cerebral cortex. Extensive areas of the frontal cortex, the hippocampal formation, and selected areas of the parietal, temporal and occipital lobes, were examined using post-mortem brain tissue. The peptidergic innervation was characteristically restricted to the limbic belt and to the dorsally contiguous regions. NT-labeled perikarya were found throughout the subiculum, including its dorsal supra-callosal continuation. NT terminal plexuses were particularly abundant in layers I-VI of the anterior cingulate cortex, in layer I of area 32 and of medical areas 9, 8, 6 and in layers II-III of area 29, of the presubiculum and entorhinal cortex. Elsewhere, NT fibers were scarce being more frequent in layer I. This regional and laminar pattern differed significantly from that of tyrosine hydroxylase (TH), which was used to label catecholaminergic axons, and preferentially the dopaminergic ones. Even in zones where TH and NT innervations were abundant, such as the anterior cingulate cortex or area 32, double-labeling procedures disclosed no colocalized fibers. The lack of NT-TH colocalization in human, contrasts with previous findings in the rodent cortex, where a contingent of the DA cortical afferents contains NT. The DA mesocortical neuronal population, labeled by TH antisera, thus seems to change its chemical phenotype, by losing the expression of an associated peptidergic neurotransmitter; this could be related to the predominant extension in the ascent of the phylogenetic scale of the non-colocalized, type of cortical DA innervation which is also found in rodents. The possible origins of the cortical, non-dopaminergic NT innervation in human are discussed: thalamo-cortical, subiculo-cortical or intrinsic. Such cortical NT innervation could be very important in limbic circuitry as a regulatory peptide in affective processes and could be involved in the physiology of pain and memory.

Adult↗

PubMed1991

Morphological heterogeneity within the cingulate cortex in rat: a horseradish peroxidase transport study.

We compared the connections of two areas within rat cingulate cortex, the Cg1/Cg2 area vs the Cg3 area, by iontophoresing small quantities of wheatgerm agglutinin-horseradish peroxidase (WGA-HRP) into either of these two divisions and identifying afferent and efferent connections. Cortical projections were more widespread for the cingulate cortex (Cg3) area than for the Cg1/Cg2 area and included the dysgranular and agranular insular cortex, and perirhinal cortex. The Cg3 area received input from the CA1 layer of the hippocampus while the Cg1/Cg2 area was interconnected primarily with retrosplenial cortex. In the brainstem, both received input from Barrington's nucleus however, many of the subcortical connections of the two areas differed and supported the hypothesis that the Cg3 area is part of the limbic and visceral motor system while the Cg1/Cg2 area is more closely allied with somatic motor control. The Cg3 area received input from the basolateral nucleus of the amygdala, the supramammillary hypothalamic nucleus, the laterodorsal tegmental nucleus, and the lateral parabrachial nucleus. The Cg1/Cg2 area received input from the substantia nigra and targeted deep layers of the superior colliculus. Thus, rat cingulate cortex is a heterogeneous area that can be further subdivided into separate limbic/autonomic (Cg3) and somatic motor areas (Cg1/Cg2).

Animals↗

PubMed1991

Efferent projections of the infralimbic (area 25) region of the medial prefrontal cortex in the rat: an anterograde tracer PHA-L study.

The efferent projections of the infralimbic region (IL) of the medial prefrontal cortex of the rat were examined by using the anterograde transport of Phaseolus vulgaris leucoagglutinin (PHA-L). Major targets of the IL were found to include the agranular insular cortex, olfactory tubercle, perirhinal cortex, the whole amygdaloid complex, caudate putamen, accumbens nucleus, bed nucleus of the stria terminalis, midline thalamic nuclei, the lateral preoptic nucleus, paraventricular nucleus, supramammillary nucleus, medial mammillary nucleus, dorsal and posterior areas of the hypothalamus, ventral tegmental area, central gray, interpeduncular nucleus, dorsal raphe, lateral parabrachial nucleus and locus coeruleus. Previously unreported projections of the IL to the anterior olfactory nucleus, piriform cortex, anterior hypothalamic area and lateroanterior hypothalamic nucleus were observed. The density of labeled terminals was especially high in the agranular insular cortex, olfactory tubercle, medial division of the mediodorsal nucleus of the thalamus, dorsal hypothalamic area and the lateral division of the central amygdaloid nucleus. Several physiological and pharmacological studies have suggested that the IL functions as the 'visceral motor' cortex, involved in autonomic integration with behavioral and emotional events. The present investigation is the first comprehensive study of the IL efferent projections to support this concept.

Amygdala↗

PubMed1992

Do forebrain structures compete for behavioral expression? Evidence from amphetamine-induced behavior, microdialysis, and caudate-accumbens lesions in medial frontal cortex damaged rats.

The neurochemical basis of behavioral changes following medial frontal cortex damage were investigated. Experiment 1 examined locomotion in response to D-amphetamine (1.5 and 5 mg/kg) in rats that had received bilateral aspirative lesions of the medial frontal cortex alone or in combination with 6-hydroxydopamine (6-OHDA) lesions of the nucleus accumbens or caudate-putamen. Relative to controls, medial frontal cortex rats were initially hypoactive (day 1 postoperative) but rapidly became hyperactive (days 5-15 postoperative). Locomotor-time profiles and stereotypy ratings showed that amphetamine produced a selective enhancement of locomotion at the expense of stereotyped behavior. Nucleus accumbens lesions blocked the locomotion but enhanced stereotyped behavior in the medial frontal cortex damaged rats, suggesting that amphetamine-enhanced locomotion is dependent upon the integrity of the nucleus accumbens. In Experiment 2, intracerebral microdialysis was used to examine whether alterations in dopamine (DA) or monoamine metabolites in the nucleus accumbens or caudate-putamen accompanied the lesion-induced changes in locomotion. There were no differences in extracellular DA or monoamine levels between control rats and medial frontal cortex rats when tested on day 1 or day 15 postsurgery, either when they were at rest, while they walked on a motor-driven belt, or after amphetamine treatment. Therefore, it seems unlikely that changes in amphetamine-induced locomotion following medial frontal cortex lesions are related to underlying modifications in dopaminergic activity in the nucleus accumbens. It is suggested that neural structures compete for behavioral expression and that postlesion behavioral alterations reveal the competitive advantage of remaining intact neural systems.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Kindling in the perirhinal cortex.

In vitro experiments have indicated that the perirhinal cortex is highly excitable and its relationship to the basolateral amygdala and piriform cortex is altered by previous amygdala or dorsal hippocampal kindling. As a result, we felt it was important to assess the excitability of the perirhinal cortex in vivo by comparing its kindling profile to that of the basal amygdala, piriform cortex or dorsal hippocampus. We observed that the after-discharge (AD) threshold of the perirhinal cortex was higher than the other 3 structures but the AD duration was not different. Subsequently, the perirhinal cortex kindled more rapidly than the other 3 structures, and with extremely short latencies to onset of forelimb clonus. With the view that synchronized discharge in the perirhinal-piriform area provides the critical trigger for limbic kindled convulsions, the relationship of kindling rate and convulsion latencies and durations between the 4 structures was discussed.

Amygdala↗

PubMed1995

Lateralized effect of unilateral somatosensory cortex contusion on behavior and cortical reorganization.

Previous studies have shown that rats recover function after unilateral somatosensory cortex lesions, possibly by transfer of information processing to other brain areas not normally involved in those functions. In the present study, adult rats underwent unilateral contusions of the somatosensory cortex with ablation of the barrel receptor field. Behavioral testing with modified beam-walking and sensory neglect tasks demonstrated persistent somatosensory deficits in rats with left contusions but no apparent deficits in right injured animals. After 2 months, the [14C]2-deoxyglucose (2-DG) method was used to show the metabolic activity produced by unilateral stimulation of the facial vibrissae. In left injured animals, cortical metabolic activity rostral and caudal to the injury site was depressed both under basal conditions and during right vibrissal stimulation. On the other hand, comparison of the pattern of [14C]2-DG uptake in the intact, right cortex revealed changes in the pattern of glucose utilization associated with left injury combined with right vibrissal stimulation. Pattern changes were quantified by measuring the area in which glucose utilization was within the highest 25% of this range (high activity area; HAA). Right vibrissal stimulation in left injured rats caused an expansion of this HAA in the intact occipital/temporal cortex. Also, in the intact somatosensory cortex of left injured rats, there was an enlarged HAA whether or not vibrissal stimulation was performed. Thus, a combination of depressed peri-injury metabolic activity and aberrant activity in remote brain areas occurs following unilateral somatosensory cortex injury. It remains to be shown whether these factors ameliorate or contribute to persistent behavioral deficits.

Animals↗

PubMed1995

Localized alterations in pre- and postsynaptic serotonin binding sites in the ventrolateral prefrontal cortex of suicide victims.

Altered serotonin indices have been reported in the brain of suicide victims. We sought to localize the changes in presynaptic and postsynaptic serotonin receptors and identify an area of prefrontal cortex that may influence suicide risk. Quantitative autoradiography was performed in coronal sections of prefrontal cortex to determine whether serotonin 5-HT1A receptor (postsynaptic in cortex) and serotonin transporter (presynaptic) binding are different in suicide victims compared to matched controls. 5-HT1A receptor binding was higher in 85 of the 103 sampled areas in the suicide group (n = 18 pairs; P < 0.0001). The increase ranged from 17 to 30%. The increase was more pronounced in the ventrolateral prefrontal cortex. Serotonin transporter binding was found to be lower in the suicide group in all but one of the 43 sampled regions (n = 22 pairs; P < 0.0001). The reduction in binding was most pronounced in the ventrolateral prefrontal cortex, where the difference between suicides and controls ranged between 15 and 27%. Serotonin transporter and 5-HT1A binding were negatively correlated (r = -0.35 to -0.44, P = 0.04 to 0.007) within the same brain areas, suggesting common regulatory factors with opposite effects on binding to the two receptors. We conclude that suicide victims have an abnormality in the serotonin system involving predominantly the ventrolateral prefrontal cortex, and hypothesize that the serotonergic dysfunction in this brain region contributes to the risk for suicidal behavior.

Adult↗

PubMed1996

Coexistence of parvalbumin and GABA in nonpyramidal neurons of the rat entorhinal cortex.

The possible coexistence of the calcium-binding protein, parvalbumin, with the major inhibitory neurotransmitter, gamma-aminobutyric acid (GABA), and its synthesizing enzyme, glutamate decarboxylase (GAD), was studied in nonpyramidal cells of the rat medial and lateral entorhinal cortex. The material was analyzed by two different methods, the first of which was a mirror techniques where the possible coexistence of two different antigens was analyzed from cells cut in half at the surface of the adjacent section. The other method consisted of analyzing double immunofluorescent-stained sections with a confocal microscope. The colocalization analysis revealed that all parvalbumin-immunoreactive neurons (mirror technique n = 688 and confocal microscopy n = 644) in all layers of the medial and lateral entorhinal cortex were also immunopositive for GABA or GAD. Parvalbumin-cells made up 52% of the GABA cells in most of the layers in the medial and lateral entorhinal cortex. In layer III of the entorhinal cortex, the proportion was about 40%. Thus, parvalbumin-containing neurons in the entorhinal cortex represent a large GABAergic cell population, which is likely to play an important role in controlling both the input and the output of the entorhinal cortex.

Animals↗

PubMed1993

Neurotensin participates in self-stimulation of the medial prefrontal cortex in the rat.

The effects of intracerebral microinjections of neurotensin and xenopsin on self-stimulation of the medial prefrontal cortex of the rat were studied. Unilateral microinjections into the medial prefrontal cortex of neurotensin at doses of 0.625, 1.25, 2.5, 5 and 10 nmol produced a dose-related decrease of self-stimulation in the ipsilateral medial prefrontal cortex. Self-stimulation of the contralateral medial prefrontal contex, used as control, was not affected by the microinjections. Similar results were found with the neurotension-like octapeptide, xenopsin. Unilateral microinjections of xenoposin into the medial prefrontal cortex, at doses of 1.8, 3.6, 7.2 and 14.4 nmol produced a dose-related decrease of self-stimulation of the ipsilateral medial prefrontal cortex. Self-stimulation of the contralateral medial prefrontal cortex was not affected. These results suggest that neurotensin is part of the neurochemical substrate of self-stimulation in this cortical area.

Animals↗

PubMed1995

Possible involvement of medial prefrontal cortex in amphetamine-induced sensitization of mesolimbic dopamine function.

We examined the role of the dopamine projection to the medial prefrontal cortex in amphetamine-induced sensitization of meso-nucleus accumbens dopamine function. In the first experiment, male rats received bilateral microinfusions either of 6-hydroxydopamine or of vehicle (sham) into prefrontal cortex. Six weeks later animals from both groups were injected once daily for 5 consecutive days with either amphetamine or saline. Two days after the last daily injection, all the animals were each implanted with a voltammetric electrode into nucleus accumbens. Increases in dopamine-dependent electrochemical signals elicited by amphetamine were monitored 3-4 days later using chronoamperometry. The results showed that amphetamine stimulates dopamine efflux to a greater extent in the nucleus accumbens of lesioned than of sham-lesioned animals. Furthermore, of the animals with prefrontal cortical lesions, amphetamine-induced dopamine efflux was greater in animals previously treated with the drug than in animals with no prior drug experience. In a second experiment, sensitization to the acute locomotor-stimulant effect of amphetamine was examined in prefrontal cortex-lesioned and sham-lesioned animals. The locomotor response of all animals to a test dose of amphetamine was first monitored and then on each of the subsequent 5 days, lesioned and sham-lesioned animals received an injection either of amphetamine or of saline. Five and then 13 days later, the locomotor response of all animals to the test dose of amphetamine was again measured. The results of this study showed that prefrontal cortex-lesioned animals were less responsive to the first amphetamine injection than sham-lesioned animals. However, after repeated daily administration, the acute locomotor response of lesioned animals to amphetamine was significantly greater than that of sham-lesioned animals with the same drug history. These findings are generally consistent with evidence from other sources suggesting that the dopamine input to medial prefrontal cortex exerts an indirect, inhibitory influence on mesolimbic dopamine transmission. They also suggest that long-term changes to a dopamine-sensitive mechanism in prefrontal cortex may contribute to the development of stimulant-induced sensitization of mesolimbic dopamine function.

Amphetamine↗

PubMed1995

Excitatory responses evoked in prefrontal cortex by mediodorsal thalamic nucleus stimulation: influence of anaesthesia.

The prefrontal cortex and the mediodorsal thalamic nucleus are reciprocally connected through excitatory amino acid pathways. Cortical excitatory responses resulting from activation of either the mediodorsal thalamic nucleus-prefrontal cortex pathway (short latency) or the recurrent collaterals of prefrontal cortex-mediodorsal thalamic nucleus neurons (long latency) can be discriminated mainly by their latency. The present study was undertaken to compare the effects of halothane and ketamine anaesthesia on these cortical excitatory responses and to establish their pharmacological characteristics using microiontophoretic application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D,L-2-amino-5-phosphonovaleric acid (APV), the specific antagonists of D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptors respectively. The number of prefrontal cortex cells which presented short or long latency excitatory responses was smaller in halothane- than in ketamine-anaesthetized rats. Whatever the anaesthetic used, short latency responses were blocked by CNQX and not affected by APV. Long latency responses were mainly blocked by APV and occasionally by CNQX in halothane-anaesthetized rats, while they were only blocked by CNQX in ketamine-anaesthetized animals. Therefore, halothane seems to preferentially reduce evoked responses mediated by AMPA receptors while ketamine completely abolishes evoked responses involving NMDA receptors. Moreover, the present data confirm that excitatory responses resulting from the activation of the mediodorsal thalamic nucleus-prefrontal cortex pathway are mainly mediated by AMPA receptors. In addition, they demonstrate that cortical responses linked to the activation of recurrent collaterals from prefrontal cortex-mediodorsal thalamic nucleus neurons involve both AMPA and NMDA receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1985

Comparative effects of topical perfusions of pentylenetetrazol in the mesencephalon and cerebral cortex of cats.

Push-pull perfusions of pentylenetetrazol (PTZ) were carried out in the mesencephalon and cerebral cortex (orbitofrontal, motor, and suprasylvian) of "encéphale isolé" cats, while EEG recordings from motor cortices and EMG of facial muscles were obtained. There were significant differences between perfusions in the mesencephalic reticular formation (MRF) and in the cerebral cortex: (i) EEG spikes not accompanied by muscular contractions occurred during perfusion of cerebral cortex (motor cortex included), but never with perfusions in MRF. (ii) In some instances muscular tonic and clonic contractions occurred in the absence of EEG spikes when perfusing the mesencephalon, but never with cortical perfusions. (iii) Both MRF and cortical perfusions induced EEG spikes accompanied by myoclonic seizures; however, muscular seizures were practically of the same amplitude in both sides after perfusion of the MRF and were predominant in the contralateral side after cortical perfusions. In addition, significantly less perfusion time (total dose) of PTZ was needed to induce such events in the MRF than in the cerebral cortex. (iv) Generalized seizures induced by cortical perfusions showed a clear predominance of contractions in the muscles contralateral to the perfusion site, whereas perfusions in the MRF induced generalized seizures indistinguishable from those produced by i.v. administration of PTZ. Results suggest that PTZ generalized seizures, closely resembling the so called "primary generalized seizures," result from activation of the MRF, whereas PTZ acting in the cerebral cortex produces a model of focal convulsions that may become secondarily generalized.

Administration, Topical↗

PubMed1981

The short-term toxicity of ethanol to neurons in rat cerebral cortex tested by topical application in vivo, and a note on a problem in estimating ethanol concentrations in tissue.

In rats anesthetized with ethanol 4.0 g/kg i.p. the dura overlying the parietal cortex was exposed and superfused with 100% ethanol for 1 h. After 6 days survival the underlying cortex was stained with a silver method that is selective for degenerating axons and their terminals. No degeneration was found in the superfused cortex, although heat-lesioned tissue stained concurrently showed axonal degeneration and so validated the technique. Electron microscopy after 3-20 days survival did not show any degeneration, and synapses of normal appearance were present immediately beneath the cortical surface. In other rats the ethanol concentration in the superfused tissue was assayed in 0.4 mm thick discs sectioned with a vibratome from a 4-mm diameter core cut with a trocar from the cortex immediately after 1 h of superfusion. The ethanol was eluted in 2% TCA, and an aliquot assayed enzymatically. A second elution of the tissue disc contributed a further 5% of the ethanol content indicating a partition coefficient for ethanol between wet brain tissue and 2% TCA of about 10. The total concentration of ethanol in the superficial cortex was found to be about 0.82 M or 3.8%. This estimation was confirmed by superfusion with 14C-labelled ethanol and scintillation counting. Thus neurons in the cerebral cortex did not degenerate after exposure for 1 h to a concentration of ethanol that was 3 times greater than the concentration that causes death in a rat by paralysis of the respiratory centre (1.2%).

Administration, Topical↗

PubMed1996

Histological evidence for cholinergic alteration in the hippocampus following entorhinal cortex lesion.

The initial stage of Alzheimer's disease is characterized by neuropathological alteration in the entorhinal cortex. To model one aspect of the neurodegeneration observed and to investigate anatomical changes of the hippocampus associated with unilateral entorhinal cortex lesion, excitotoxin ibotenic acid was used to produce selective unilateral neuronal loss in rat entorhinal cortex. Histological and morphometrical analyses confirmed excitotoxic lesion of the entorhinal cortex after 3 months and showed a decrease of acetylcholineste-rase-stained fibers in the stratum moleculare of the dentate gyrus and the stratum radiatum of the CA3 field. This study demonstrates the importance of the entorhinal cortex in the hippocampal cholinergic function which appears to be important to memory and learning, and raises the possibility that memory deficit in Alzheimer's disease may be associated with partial neuronal loss in the entorhinal cortex.

Acetylcholinesterase↗