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PubMed1996

Alteration of auditory cortex activity with a visual stimulus through conditioning: a 2-deoxyglucose analysis.

In two experiments, the 2-deoxyglucose metabolic mapping technique was used to examine the hypothesis that a stimulus of one modality (a light) will begin to activate the sensory cortex of a stimulus of another modality (a tone) with which it has been repeatedly paired. Adult gerbils received repeated presentations of either a light or the light paired with a tone known to affect 2DG labeling patterns in the auditory cortex. Intermittent footshock was included on a pseudo-random basis to maintain arousal in the subjects. One day after training, each gerbil was injected with 2DG and either received repeated presentations of the light only or was simply exposed to the training context. Analysis of the auditory cortex revealed no differences in overall metabolic activity of the auditory cortex between the groups. However, in both experiments, the light that was previously paired with the tone changed the relative activity of the cortical subfields compared to the light not previously paired with the tone. Specifically, the results indicate greater activity in the anterior auditory field (AAF-Experiments 1 and 2) and the posterior fields (DPVP-Experiment 2) relative to the primary field AI in response to the light that was previously paired with the tone during training. Gerbils either only placed in the context during the 2DG session or that received unpaired presentations of the light and tone during training did not show this shift in relative labeling between the subfields. Because no differences in overall activity of the auditory cortex were found, we conclude that the shift in relative labeling between the subfields reflects, on average, both an increase in activity of fields AAF and DPVP and a concomitant decrease in AI activity in response to the light stimulus. The results have implications for our understanding both of brain learning mechanisms in general and the potential functions of auditory cortex subfields in particular.

Animals↗

PubMed1996

Effect of carbamazepine, oxcarbazepine and lamotrigine on the increase in extracellular glutamate elicited by veratridine in rat cortex and striatum.

Lamotrigine, carbamazepine and oxcarbazepine inhibit veratrine-induced neurotransmitter release from rat brain slices in concentrations corresponding to those reached in plasma or brain in experimental animals or humans after anticonvulsant doses, presumably due to their sodium channel blocking properties. Microdialysis measurements of extracellular glutamate and aspartate were carried out in conscious rats in order to investigate whether corresponding effects occur in vivo Veratridine (10 microM) was applied via the perfusion medium to the cortex and the corpus striatum in the presence of the glutamate uptake inhibitor L-trans-pyrrolidine-2,4-dicarboxylic acid (1 mM in perfusion medium). Maximally effective anticonvulsant doses of carbamazepine (30 mg/kg), oxcarbazepine (60 mg/kg) and lamotrigine (15 mg/kg) were given orally. The uptake inhibitor increased extracellular glutamate and aspartate about 2-fold in striatum and about 7-fold and 3-fold, respectively, in cortex. Veratridine caused a further 2-3-fold increase in extracellular glutamate in striatum and cortex, respectively, but its effect on extracellular aspartate was less marked in both areas. None of the anticonvulsant compounds affected the veratridine-induced increases in extracellular glutamate or aspartate in the striatum which were, however, markedly inhibited by tetrodotoxin (1 microM) and thus are sensitive to sodium channel blockade. In the cortex the same drugs at the same doses did cause about 50% inhibition of the veratridine-induced increase in extracellular glutamate. Carbamazepine and to a lesser extent lamotrigine, but not oxcarbazepine, also inhibited the veratridine-induced increase in extracellular aspartate in the cortex. Although our results might seem to support the view that inhibition of glutamate and aspartate release is responsible for the anticonvulsant effects of lamotrigine, carbamazepine and oxcarbazepine, two complementary findings argue against this interpretation. First, as previously shown, inhibition of electrically induced released of glutamate requires 5 to 7 times higher concentrations of these compounds than release elicited by veratrine. Second, the present study indicates that doses totally suppressing convulsions caused no inhibition in the striatum and at best a 50% inhibition in the brain cortex. From this we conclude that the doses used here, although to some extent effective against veratridine, did not suppress the release of GLU and ASP elicited by the normal ongoing electrical activity of the glutamatergic and aspartatergic neurons and that the mechanism of the suppression of convulsions must be sought elsewhere.

Animals↗

PubMed1990

Formation of new synapses in the cat motor cortex following lesions of the deep cerebellar nuclei.

The effects of unilateral lesions of the deep cerebellar nuclei on the corticocortical (CC) projection from the somatosensory to the motor cortex were studied in adult cats, utilizing electrophysiological and electron microscopical methods. Axon terminals in the motor cortex belonging to CC afferents were labeled by degeneration induced by lesions of the somatosensory cortex; neurons in the motor cortex were labeled by the Golgi/EM method. In each cat, data from the motor cortex (MCx) contralateral (experimental) and ipsilateral (control) to the cerebellar lesion were compared. Cerebellar lesions produced marked motor deficits, which receded gradually and disappeared after 30 to 40 days. Subsequent lesions of the somatosensory cortex (area 2) contralateral to the cerebellar lesions resulted in the reappearance of the cerebellar symptoms. The number of CC synapses per unit area in experimental MCx was significantly higher than in control MCx. The increase in the number of CC synapses was apparent throughout layers II-V of the MCx, but was most prominent in layers II/III. The increase in the number of CC synapses in experimental MCx was due mainly to an increase of axon terminals synapsing with dendritic spines belonging to pyramidal neurons. In comparison, the numbers and spatial distribution of CC synapses with aspinous, nonpyramidal neurons from both experimental and control MCx were similar. Field potentials in the experimental MCx, evoked by stimulation of area 2, were altered following cerebellar lesions. In experimental MCx, the polarity of the early component of the field potentials reversed at cortical depths corresponding to layers II-III, whereas this reversal was not observed in control MCx. These findings suggest that lesions of the cerebellar nuclei induced sprouting of axon terminals in the MCx to establish a new function. The results provide the first anatomical evidence for the generation of new synapses in the adult CNS which is not induced by elimination of existing synapses.

Animals↗

PubMed1996

Steroid hormonal regulation of calcium-binding protein regucalcin mRNA expression in the kidney cortex of rats.

The effect of various steroid hormones on the expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the kidney cortex but not the medulla. Rats received a single subcutaneous administration of steroid; the animals were sacrificed 60 min after the treatment of aldosterone (2.5, 5.0 and 10 micrograms/100 g body weight) or 6 h after the treatment of estrogen (17 beta-estradiol; 0.05, 0.1 and 0.2 mg/100 g), hydrocortisone (0.5, 1.0 and 3.0 mg/100 g) and dexamethasone (50, 100 and 150 micrograms/100 g). Regucalcin mRNA levels in the kidney cortex were clearly diminished by the administration of aldosterone or estrogen, while hydrocortisone administration had no effect. The administration of dexamethasone (100 micrograms/100 g) caused a remarkable increase of regucalcin mRNA levels in the kidney cortex. The dexamethasone-induced increase in regucalcin mRNA levels was completely blocked by the simultaneous administration of cycloheximide (150 micrograms/100 g), although the drug administration had no effect on the mRNA levels in control rats. Meanwhile, the dexamethasone administration did not cause an appreciable alteration of calcium content in the kidney cortex. The present study demonstrates that, of the various steroid hormones used, dexamethasone uniquely has a stimulatory effect on regucalcin mRNA expression in the kidney cortex of rats. The steroid effect may be mediated through a newly synthesized protein.

Aldosterone↗

PubMed1991

Topographical projections from the cerebral cortex to the nucleus of the solitary tract in the cat.

The distribution of cerebral cortical neurons sending projection fibers to the nucleus of the solitary tract (NST), and the topographical distribution of axon terminals of cortico-NST fibers within the NST were examined in the cat by two sets of experiments with horseradish peroxidase (HRP) and HRP conjugated with wheat germ agglutinin (WGA-HRP). First, HRP was injected into the NST. In the cerebral cortex of these cats, neuronal cell bodies were labeled retrogradely in the deep pyramidal cell layer (layer V): After HRP injection centered on the rostral or middle part of the NST, HRP-labeled neuronal cell bodies were distributed mainly in the orbital gyrus and caudal part of the infralimbic cortex, and additionally in the rostral part of the anterior sylvian gyrus. After HRP injection centered on the caudal part of the NST, labeled neuronal cell bodies were seen mainly in the caudoventral part of the infralimbic cortex, and additionally in the orbital gyrus, posterior sigmoid gyrus and rostral part of the anterior sylvian gyrus. The labeling in the infralimbic cortex, orbital gyrus and anterior sylvian gyrus was bilateral with a predominantly ipsilateral distribution, while that in the posterior sigmoid gyrus was bilateral with a clear-cut contralateral dominance. In the second set of experiments, WGA-HRP was injected into the cerebral cortical regions where neuronal cell bodies had been retrogradely labeled with HRP injected into the NST: After WGA-HRP injection into the orbital gyrus, presumed axon terminals in the NST were labeled in the rostral two thirds of the nucleus bilaterally with an ipsilateral predominance. After WGA-HRP injection into the rostral part of the anterior sylvian gyrus, a moderate number of presumed axon terminals were labeled throughout the whole rostrocaudal extent of the NST bilaterally with a slight ipsilateral dominance. After WGA-HRP injection into the middle and caudal parts of the anterior sylvian gyrus, no labeling was found in the NST. After WGA-HRP injection into the caudal part of the infralimbic cortex, presumed terminal labeling in the NST was seen throughout the whole rostrocaudal extent of the nucleus bilaterally with a dominant ipsilateral distribution. After WGA-HRP injection into the posterior sigmoid gyrus, however, no terminal labeling was found in the NST. The results indicate that cortico-NST fibers from the orbital gyrus terminate in the rostral two thirds of the NST, while those from the infralimbic cortex and the rostral part of the anterior sylvian gyrus project to the whole rostrocaudal extent of the NST.

Animals↗

PubMed1993

In vivo tracing of pathways and spatio-temporal activity patterns in rat visual cortex using voltage sensitive dyes.

We monitored optical signals from cortex stained with a voltage sensitive dye to study activity evoked by intracortical electrical stimulation. The objectives were to study the spatial and temporal spread of activity from intrinsic connections near the stimulating electrode and to develop a new technique to study extrinsic projections from striate cortex to extrastriate target areas. Various measures were made of the time course of the optical signal (latency, rise time, decay time, temporal summation, facilitation versus depression, and presence or absence of a slow undershoot); in general, these measures were found to vary significantly across different response positions, different experiments, and even different runs within the same experiment. The spatial distribution of responses near the stimulating electrode in striate cortex was usually elliptical and was most often elongated along the anterior-posterior axis, with a typical size (full width at 75% max) of 1.3 mm (anterior-posterior axis) by 0.75 mm (medio-lateral axis). In some cases, complex spatio-temporal patterns were observed, in which the position of the maximum optical signal shifted with time or split into multiple peaks. In eight experiments, a response focus was found in extrastriate cortex at an expected location within the lateromedial area (LM). The response focus in LM was typically about half the size of that in striate cortex. In some experiments we observed additional focal responses in the anterolateral visual area (AL). The extrastriate responses showed a significant delay (3-10 ms) in onset and time to peak relative to the striate response. The validity of this technique for determining extrinsic projections was tested in two types of experiments. In the first, stimulation from two electrodes in striate cortex generated response foci consistent with the known topographic organization of area LM. In the second, the optically measured response focus was shown to correlate with the histologically reconstructed projection of a chemical tracer injected near the site of stimulation. We discuss the chain of neurophysiological events that occur during and after focal electrical stimulation and how they relate to the observed optical signal. We conclude that direct passive responses were a small component of our signal, that the component due to action potentials in directly stimulated neurons should have occurred in the first 1-2 ms post stimulus and is small compared to the peak signal, and that overall our signals were probably dominated by a combination of asynchronously occurring action potentials and excitatory and inhibitory synaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1985

Efferent fibers from the motor cortex terminate bilaterally in the thalamus of rats and cats.

The anterograde transport of lectin-conjugated horseradish peroxidase (WGA-HRP) was here employed in order to visualize crossed corticothalamic efferents of the motor cortex in rats and cats. After WGA-HRP cortical injections in the rat retrogradely labeled cells were observed in the ipsilateral thalamus, and heavy anterograde labeling was observed both in the ipsi- and contralateral thalamus. The contralateral anterograde labeling was less intense than the ipsilateral one and it was distributed in the anterior intralaminar structures, in the parafascicular nucleus, in the ventromedial, ventrolateral and ventrobasal nuclei and in the posterior complex, symmetrically to the labeling observed on the ipsilateral side. Further experiments were made in the rat in order to ascertain that the bilateral anterograde labeling in the thalamus derived unilaterally from the cortex. To this purpose, kainic acid was injected unilaterally either into the frontal cortex or into the thalamus, and WGA-HRP was later injected on the same side in the frontal cortex. Moreover, WGA-HRP was injected into the frontal cortex after splitting of the corpus callosum. The results obtained in these experiments confirmed that cortical neurons projected bilaterally upon the thalamus. Further, these experiments indicated that at least the majority of the contralateral fronto-thalamic fibers crossed the midline in the thalamic massa intermedia. WGA-HRP injections into the pericruciate cortex in the cat confirmed the presence of anterogradely labeled terminals in the contralateral anterior and posterior intralaminar, ventral anterior, ventromedial and ventrolateral nuclei. The labeling was in all cases heavier in the intralaminar nuclei than in the other structures, but it was less intense than that observed in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Input-output organization of the rat vibrissal motor cortex.

The afferent and efferent connections of the vibrissal area of the rat motor cortex (VMCx) were investigated by injecting Phaseolus vulgaris leucoagglutinin (PHA-L) or wheat germ agglutinin-horseradish peroxidase into the physiologically defined VMCx. The VMCx formed reciprocal connections with the primary and secondary somatosensory cortex, lateral and ventrolateral orbital cortex, retrosplenial cortex, and perirhinal cortex. These corticocortical afferents originated from cell bodies in layers II-III and V, and some afferents originated from cell bodies in layer VI of the primary sensory cortex. All of the VMCs efferents terminated in layers I and V or layers I-III and V. The VMCx also formed reciprocal connections with the ventrolateral, ventromedial and centrolateral nucleus, the lateral portion of the mediodorsal nucleus and the posterior complex of the thalamus. It projected bilaterally to the caudate putamen, primarily ipsilaterally to the superior colliculus, anterior pretectal nucleus, and pontine nucleus, and mainly contralaterally to the oral part of the spinotrigeminal nucleus and the reticular formation around the facial nerve nucleus. Finally, injections of PHA-L into the superior colliculus demonstrated that this structure projected contralaterally to the lateral part of the facial nerve nucleus. These data suggest that the VMCx plays a key role in sensorimotor integration, through its extensive interconnectivity with numerous brain structures, and may modulate orientation behaviors by relaying processed information to the superior colliculus.

Animals↗

PubMed1994

Inhibitory actions of motor cortex following unilateral brain lesions as studied by magnetic brain stimulation.

Noninvasive transcranial magnetic stimulation (TMS) of the motor cortex not only induces short-latency, motor-evoked potentials (MEP) in contralateral muscles, but also inhibitory phenomena. One type of inhibitory action appears directly after the MEP in contralateral muscles and can be visualized by blockade of tonic, voluntary electromyographic (EMG) activity (postexcitatory inhibition, PI). Evidence for a cortical origin of PI, especially in its later part, was derived from double cortical stimulation in previous studies and is further supported by examination of PI in patients with focal hemispheric unilateral brain lesions in the present study. Thirty patients with different sites of vascular or tumour lesions were studied by TMS. In 6 patients with circumscribed lesions of the primary sensorimotor cortex a significant shortening of PI to contralateral muscles was observed. In 7 patients with focal lesions of the thalamus or internal capsule, in 6 patients with lesions of the premotor cortex and in 5 patients with lesions restricted to the parietal or temporal lobe, a significant prolongation of PI to the contralateral muscles was detected. Six patients with transient ischemic attacks showed either prolongation or shortening of PI. We conclude that PI is predominantly generated in the primary motor cortex, correspondingly its damage causes shortening of PI. In contrast, damage to brain areas that project to the primary motor cortex is followed by prolongation of PI. This remote effect on the primary motor cortex may result from disinhibition of cortical interneurones.

Adult↗

PubMed1988

Organization of feedback and feedforward projections of the barrel cortex: a PHA-L study in the mouse.

In order to analyze the organization of the efferent projections of single barrel columns (BC, i.e. a barrel in layer IV of parietal cortex plus the cortical tissue above and below it), we made small iontophoretic injections of the anterograde tracer Phaseolus vulgaris leucoagglutinin in the barrel cortex of 20 adult mice. On the basis of reconstructions of the sites of terminal labelling, the brain regions receiving projections from the barrel cortex could be identified and classified in five groups. Each group is characterized by the topography of the distribution of efferents arising from a single BC. The projections to the trigeminal sensory complex are point to point: i.e. one BC projects only to the site of termination of the primary sensory neurons innervating the corresponding whisker follicle. In the ventrobasal thalamic nucleus BC projections are not restricted to the corresponding barreloid; instead they contract parts of barreloids belonging to one arc. In the reticular and posterior thalamic nuclei the projections from a row of BC's converge to a collective termination site, whereas in the superior colliculus the projections from an arc of BC's converge to a common termination site. There is a complete overlap of BC projections in restricted zones within SII, motor cortex, perirhinal cortex, contralateral barrelfield, caudoputamen and pons. The organization of the efferents from the barrel cortex demonstrates a contrast between feedback and feedforward projections from this important area of neocortex.

Animals↗

PubMed1983

Structural organization of the human cerebral cortex prior to the appearance of the cortical plate.

The early development and the structural organization of the human cerebral cortex, prior to the appearance of the cortical plate (Carnegie stage 22, ca. 54 days), was studied in two embryos: 43 (stage 18) and 50 day old (stage 20), respectively. It has been shown that the human cerebral cortex begins its ontogenetic development around the sixth rather than around the eighth week of gestation as it has been previously assumed. The human cerebral cortex starts to develop soon after the cerebral vesicles have been formed (stage 15) and a primitive internal capsule has been established (stage 17, ca. 41 days). By stage 18 of human development fibres from this primitive internal capsule have reached and probably have penetrated into the developing cerebral vesicle, through its more superficial zone. Fibres from this primitive internal capsule have been traced backward through the ventral thalamus to the mesencephalic tegmentum. The possible existence of primitive ascending fibres from the mid-brain which terminate in the superficial zone of the developing cerebral cortex (tegmento-thalamostriato-cortical tract) is suggested. The arrival of these primitive corticipetal fibres establishes in the outer zone of the cerebral cortex a primordial plexiform lamina or an external white matter. Horizontal-bipolar cells (embryonic Cajal-Retzius neurons) begin to differentiate by stage 18 of human development (43 days in our case). By stage 20 (50 days in our case), the primordial plexiform lamina is well established, extends throughout the entire surface of the developing cerebral cortex, and is considered to be functionally active. It is, by this age, a superficial, 40 micrometers thick, complex fibrillar neuronal organization composed of numerous horizontal corticipetal fibres (demonstrable with silver methods), horizontal-bipolar Cajal-Retzius neurons and a few other, less defined, cellular elements. This primordial plexiform lamina is considered to represent a primitive "premammalian" cortical organization. The next event in cortical ontogenesis is the appearance of the cortical plate or the mammalian neocortical grey at stage 22 (ca. 54 days). Migrating neuroblasts attracted toward the preexisting primordial plexiform lamina and guided by glial fibres start to accumulate within it.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell Movement↗

PubMed1975

Fine structure of labelled axons in the cerebellar cortex and nuclei of rodents and primates after intraventricular infusions with tritiated serotonin.

The cerebellar cortex and deep cerebellar nuclei in rats and rhesus monkey were studied after treatment with monoamine oxidase inhibitor and continuous intraventricular infusion with 10(-5) M serotonin-3H. Autoradiographs were prepared for light and electron microscopy. The cerebellum contained no labelled cells. Labelled unmyelinated axons arrive from the brain stem via the periventricular zones of the aqueduct and fourth ventricle. In the parafloccular cortex about 1 per cent of the mossy fibers are labelled, together with a small number of fine varicose axons in the molecular layer that run parallel to the folial axes (less than 0.1%). In the paravermal and vermal cortex there are few labelled fibers in the granular layer and a five-fold greater number of labelled axons in the molecular layer (about 0.5%). Apparently three systems of serotonin-containing axons are present in the cortex: mossy fibers, parallel fiber-like, and a diffuse system in granular and molecular layers. The fastigial (medial), interpositus, and dentate (lateral) nuclei, lateral vestibular and other vestibular nuclei all have numerous labelled axons. The dentate and interpositus nuclei receive labelled fibers which arrive through the superior cerebellar peduncle as well as from the periventricular area. Six morphologically different classes of labelled axon terminals have been differentiated. Class 1a, the mossy fiber rosettes, and class 1b, the CAT2 axons, have small, round, clear synaptic vesicles and large granular vesicles (lgv); class 2 axons have a distinctive collection of round granular vesicles; class 3 boutons have numerous tubular profiles, a few containing dense dots, packed in a dark axoplasmic matrix; class 4 axons have tiny 250 A granular vesicles, clear tubular profiles and occasional LGV; class 5 terminals have numerous LGV, both round and elongated, with clear round and tubular profiles; class 6 terminals have LGV, clear and granular synaptic vesicles and clear tubular profiles. All these axons have LGV 900 A in diameter with 500-600 A variably dense centers that do not fill the vesicle, and Gray's type 1 axodendritic or axasomatic synapses on postsynaptic locations in the cortex and nuclei. Labelled axons in the cortex end as mossy fibers upon granule cell dendrites in glomeruli (Class 1a) or upon dendrites of cortical interneurons, e.g. Golgi cells, basket and stellate cells, and not on Purkinje cells. ...

Animals↗

PubMed1982

Noradrenergic neurotransmission in the brain of a convulsive mutant mouse, differences between the cerebral cortex and the brain stem.

The Quaking mouse is a genetically determined model of convulsive disorders. We investigated the modulation of noradrenergic neurotransmission through alpha 2-adrenoceptors in the occipital cortex and the brain stem of this mutant. The endogenous levels of noradrenaline were similar in the cerebral cortex of the Quaking mice and their corresponding controls, while a significant increase of endogenous noradrenaline was found in the brain stem of the mutants. The rate of disappearance of noradrenaline in the cerebral cortex and the brain stem after injection of FLA 63 was identical in control and Quaking mice. The calcium-dependent electrically evoked overflow of 3H-noradrenaline from slices of occipital cortex was inhibited by clonidine and enhanced by yohimbine in Quaking as well as in normal mice. The negative feed-back mechanism mediated by presynaptic alpha 2-adrenoceptors operates to a similar extent in both strains of mice. In contrast to the occipital cortex, in the brain stem, the amount of neurotransmitter released by electrical stimulation was significantly increased in Quaking mice when compared with controls. However, in the brain stem, the negative feed-back regulation of noradrenaline release operates to a similar extent in both strains of mice. When the endogenous levels of MOPEG were determined in the brain stem, they were found to be significantly higher in the Quaking mice when compared to the controls. The results suggest that an increase in noradrenergic neurotransmission in the brain stem, rather than in the cerebral cortex, could contribute to the behavioural abnormalities exhibited by the Quaking mice.

Animals↗

PubMed1990

Functional organization of the direct and indirect projection via the reticularis thalami nuclear complex from the motor cortex to the thalamic nucleus ventralis lateralis.

The projection systems which arise from the motor cortex to reach the nucleus ventralis lateralis (VL) were investigated in the rat. They included a direct as well as an indirect projection via the reticularis thalami nuclear complex (RT). The investigation was performed in two steps: i) the former concerned the projection to the VL as well as to the RT from individual cortical foci electrophysiologically identified by the motor effects evoked by electrical stimulation; the second step concerned the projection from the RT to functionally defined regions of the VL. The direct projection from the motor cortex to the VL is somatotopically arranged. The projection reciprocates the fiber system directed from the VL to the motor cortex. Thus cortical zones controlling the motor activity of the proximal segments of the limbs project onto the regions of the VL that project back to these same cortical areas. With regard to cortical zones controlling the motor activity of the distal segments of the limbs, they not only project to the region of the VL specifically related to them, but also to the region of the VL associated with the cortical areas responsible for movements of the proximal parts of the same limb. In that case fiber terminals were more dense in the VL region controlling the proximal segment than in the region controlling the distal segment of the same limb. This organization suggests that proximal adjustments may be automatically provided by the motor activity of the distal segments of the same limb. The motor cortex projects to the rostral region of the RT with a precise topographical organization. In particular, the projection shows a dorsoventral organization in the RT in relation to the caudorostral body representation in the motor cortex. The projection which arises from the rostral region of the RT also reaches the VL with a topographical arrangement. It discloses a rostrocaudal organization in the VL in relation to a dorsoventral displacement in the RT. Comparing the projection from the motor cortex to the RT and that from this nuclear complex to the VL it was shown that the regions of the VL and their receptive cortical areas were associated with the same regions of the RT. It was therefore concluded that the motor cortical projection to the VL relayed by the RT is somatotopically organized. In both direct and relayed pathways the projections from "hind-" and "forelimb" motor area are segregated, whereas the "head" projection overlaps, at least partially, the "forelimb" terminal field.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Factors affecting human autopsy kidney-cortex and kidney-medulla platinum concentrations after cisplatin administration.

The objective of this study was to determine factors that affect cisplatin concentrations in human kidney cortex. We used flameless atomic absorption spectrophotometry to assay platinum in autopsy specimens of kidney cortex obtained from 83 cisplatin-treated patients. Concentrations were correlated with pretreatment factors and treatment conditions using univariate nonparametric statistics. Hierarchical stepwise multiple regression analyses of transformed (to normalize) data were then used to assess which factors were most important, controlling for other factors. Kidney-cortex platinum concentrations varied from 0 to 14.8 micrograms/g (median, 2.04 micrograms/g). The cumulative lifetime dose of cisplatin ranged from 10 to 1120 mg/m2 (median, 112 mg/m2). The time from the last cisplatin dose to death was < 1-609 days (median, 38 days). According to univariate statistics, factors that correlated (P < 0.05) with kidney-cortex platinum concentrations were the cisplatin dose per course, the pretreatment serum urea level, metoclopramide use (positive correlations), the time from the last cisplatin treatment to death, and the pretreatment serum albumin value (negative correlations). Factors that approached significance (0.05 < or = P < or = 0.10) were a history of hypertension, hyperbilirubinemia (positive), the serum calcium level, and phenytoin use (negative). In the multiple regression analysis, after controlling for the cisplatin dose per course and the time from the last treatment to death, only concurrent metoclopramide and phenytoin use entered the model. The hydration volume did not affect corrected kidney-cortex or kidney-medulla platinum concentrations. The following conclusions were reached: (1) it may be feasible to use lower hydration volumes than those used routinely, (2) any effect of hydration volume on cisplatin nephrotoxicity may not be mediated via a reduction in kidney-cortex platinum concentrations, (3) higher cisplatin doses might be tolerated with new 5-hydroxytryptamine-3 (5HT-3) antiemetics than were tolerated with metoclopramide, and (4) phenytoin should be tested for its ability to reduce cisplatin nephrotoxicity.

Autopsy↗

PubMed1985

The temporal evolution of hypoglycemic brain damage. I. Light- and electron-microscopic findings in the rat cerebral cortex.

In the course of a study on the pathogenesis of neuronal necrosis in severe hypoglycemia, the morphological characteristics reflecting reversible and irreversible neuronal lesions were examined as a function of time following normalization of blood glucose. To that end, closely spaced time intervals were studied in the rat cerebral cortex before, during, and up to 1 year after standardized pure hypoglycemic insults of 30 and 60 min of cerebral isoelectricity. Both the superficial and deep layers of the cerebral cortex showed dark and light neurons during and several hours after the insult. By electron microscopy (EM) the dark neurons were characterized by marked condensation of both karyoplasm and cytoplasm, with discernible, tightly packed cytoplasmic organelles. The light neurons displayed clustering of normal organelles around the nucleus with clearing of the peripheral cytoplasm. Some cells, both dark neurons and neurons of normal electron density, contained swollen mitochondria with fractured cristae. Light neurons disappeared from the cerebral cortex by 4 h of recovery. Some dark neurons in the superficial cortex and almost all in the deep cortex evolved through transitional forms into normal neurons by 6 h recovery. Another portion of the dark neurons in the superficial cortex became acidophilic between 4 and 12 h, and by EM they demonstrated karyorrhexis with stippled electron-dense chromatin. The plasma membrane was disrupted, the cytoplasm was composed of amorphous granular debris, and the mitochondria contained flocculent densities. These definitive indices of irreversible neuronal damage were seen as early as 4-8 h recovery. Subsequently, the acidophilic neurons were removed from the tissue, and gliosis ensued. Thus, even markedly hyperchromatic "dark" neurons are compatible with survival of the cell, as are neurons with conspicuous mitochondrial swelling. Definite nerve cell death is verified as the appearance of acidophilic neurons at which stage extensive damage to mitochondria is already seen in the form of flocculent densities, and cell membranes are ruptured. Our previous results have shown that hypoglycemic neocortical damage affects the superficial laminae, chiefly layer 2. The present results demonstrate that, following the primary insult, this damage evolves relatively rapidly within the first 4-12 h. We have obtained no evidence that additional necrotic neurons are recruited after longer recovery periods.

Animals↗

PubMedDate not supplied

Activity of neurons in limbic cortex during stimulation of somatosensory zones.

The effect of high-frequency and burst stimulation of the first and second somatosensory zones on the activity of identical neurons in the anterior limbic cortex was studied comparatively in acute experiments with cats. A histogramic analysis of neuronal responses in the limbic cortex showed that most background-active cells responded to stimulation of both the first and the second somatosensory zones. Both zones variously adjusted the activity of neurons in the limbic cortex. It was found that the responses in the limbic cortex with the maximum density of the potentials of long-latent reactions are recorded during stimulation of the first somatosensory zone. It was established that the first and second somatosensory zones exert a preferentially activating influence on neurons in the anterior limbic cortex (51.5 and 66.6%, respectively), inhibitory responses comprised 33.3 and 20.0%, while mixed responses were recorded in 15.5 and 13.3% of the neurons, respectively. It was shown that the somatosensory zones exert a modulating influence on the activity of neurons, thus participating in the regulation and processing of information entering the limbic cortex.

Animals↗

PubMed1995

Localization of glial fibrillary acidic protein and glutamine synthetase in the human cerebral cortex and subcortical white matter--a double immunolabelling and electron microscopic study.

Astrocytes in the human cerebral cortex and subcortical white matter were labelled using antibodies to glial fibrillary acidic protein, or double labelled for glial fibrillary acidic protein and glutamine synthetase, and studied by light and electron microscopy. We described two types of astrocytic processes in an earlier study of human cortex: glial-filament-rich but mitochondria-poor, and filament-poor but mitochondria-rich. The question arose as to whether these were different segments of the same process, or whether the filament-rich processes belonged to a subpopulation of 'fibrous' astrocytes. In the present study no such fibrous astrocytes were found in histologically normal cortex, and all glial fibrillary acidic protein positive cell bodies in the cortex were also glutamine synthetase-positive, and had features of protoplasmic astrocytes. Since the processes of fibrous astrocytes in the white matter seldom extended more than 40-50 microns beyond the cell bodies, they were unlikely to account for the filament-rich astrocytic processes that were observed in the cortex by electron microscopy. The filament-rich but mitochondria-poor, and the filament-poor but mitochondria-rich processes are seen in continuity in the cortex and must therefore both stem from cell bodies with features of protoplasmic astrocytes.

Adolescent↗