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Expression of the nerve growth factor receptors TrkA and p75NTR in the visual cortex of the rat: development and regulation by the cholinergic input.

Several lines of evidence have shown that nerve growth factor (NGF), the progenitor of the neurotrophin family of growth factors, plays a fundamental role in the developmental plasticity of the rat visual cortex. However, the expression of NGF receptors (NGFRs) TrkA and p75(NTR) and the possible sites of NGF action in the visual cortex remain to be elucidated so far. Using a highly sensitive ECL immunoblot analysis, we have been able to show, in the present study, that the TrkA protein is expressed in the rat visual cortex and that it is developmentally upregulated during the critical period for cortical plasticity. In contrast, the expression level of the low-affinity NGF receptor p75(NTR) seems to remain nearly constant throughout development. In the analysis of possible pathways involved in the regulation of NGFR expression, we found that neither blockade of the visual input nor NGF administration to the visual cortex resulted in a modulation of NGFR levels of expression. On the other hand, the selective destruction of cholinergic afferents to the visual cortex caused a dramatic, but not complete, reduction of the cortical NGFRs, which suggests that these receptors are located on cholinergic terminals predominantly. At the functional level, we found that, after the elimination of the cholinergic afferents to the visual cortex, the NGF-induced increase of both acetylcholine and glutamate release from cortical synaptosomes was strongly impaired. These results indicate that the cholinergic input is an important mediator of visual cortex responsiveness to NGF action.

Acetylcholine↗

Lesion and regeneration in the medial cerebral cortex of lizards.

The cerebral cortex of Squamate reptiles (lizards and snakes) may be regarded as an archicortex or "reptilian hippocampus". In lizards, one cortical area, the medial cortex, may be considered as a true "fascia dentata" on grounds of its anatomy, connectivity and cyto- chemo-architectonics of its main zinc-rich axonal projection. Moreover, its late ontogenesis and postnatal development support this view. In normal conditions, it shows delayed postnatal neurogenesis and growth during the lizard's life span. Remnant neuroblasts in the medial cortical ependyma of adult lizards seasonally proliferate. The late-produced immature neurocytes migrate to the medial cortex cell layer where they differentiate and give off zinc-containing axons directed to the rest of cortical areas. This results in a continuous growth of the medial cortex and its zinc-rich axonal projection. Perhaps the most important characteristic of the lizard medial cortex is that it can regenerate after having been almost completely destroyed. Recent experiments in our laboratory have shown that chemical lesion of its neurons (up to 95%) results in a cascade of events; first, those related with massive neuronal death and axonal-dendritic retraction and, secondly, those related with a triggered neuroblast proliferation and subsequent neo-histogenesis, and the regeneration of an almost new medial cortex that shows itself undistinguishable from a normal undamaged one. This is the only report to our knowledge that an amniote central nervous centre may regenerate by new neuron production and neo-histogenesis. Perhaps the medial cortex of lizards may be used as a model for neuronal regeneration and/or transplant experiments in mammals or even in primates.

Animals↗

Middle-latency auditory-evoked magnetic fields in patients with auditory cortex lesions.

OBJECTIVE: To demonstrate the influence of auditory cortex lesions on auditory middle-latency responses (AMLRs) and middle-latency auditory-evoked magnetic fields (MLAEFs) in humans. MATERIAL AND METHODS: A total of 15 normal subjects, 9 patients with left auditory cortex lesions and 1 patient with a right auditory cortex lesion were studied. MLAEFs were recorded from each hemisphere of the brain in a magnetically shielded room using a 37-channel SQUID gradiometer. Simultaneously, AMLRs were recorded from the scalp at the vertex, C3 and C4. Tone bursts were used as auditory stimuli. RESULTS: Pam responses of the MLAEF, which are typically evoked in the latency range of the Pa of the AMLR, and are localized at the auditory cortex as dipoles, were impaired or abolished over the left auditory cortex lesion in the patients with left-hemisphere lesions, but the Pa of the AMLR persisted. CONCLUSION: The main generator of the Pam in MLAEF was demonstrated to be the auditory cortex. The results also show that the Pa of the AMLR is evoked only partly from the auditory cortex.

Acoustic Stimulation↗

[The effect of posthypoxic hypothermia for lactate dehydrogenase activity in brain cortex and blood serum of 14-days-old rats].

OBJECTIVE: The effect of various degrees of hypobaric hypoxia and consequent hypothermia on lactate dehydrogenase (E.C.1.1.1.27) activity in blood serum and brain cortex in 14 day-old rats was investigated. DESIGN: Experimental study. SETTING: Institute of Physiology, 1st Med. Faculty, Charles University, Prague. METHODS: 14 day-old rats (Wistar of our own breed) were exposed to mild hypobaric hypoxia (corresponding to altitude of 7000 m, pO2 = 8.6 kPa, BP = 41.2 kPa, lasting 20 min) or strong hypobaric hypoxia (corresponding to altitude of 9000 m, pO2 = 6.4 kPa, BP = 30.7 kPa, lasting 30 min). Just after hypoxic stress the animals were killed by decapitation and on cooled block the grey cortical matter was removed. Blood serum samples as well as brain cortex homogenates were immediately incubated in three variously tempered media (38 degrees Celsius = control values, 30 degrees Celsius and 22 degrees Celsius = hypothermic conditions). The incubation was over (30 min.), and the lactate dehydrogenase (LDH) activity was followed using the Lachema test. RESULTS: The LDH activity was influenced by mild hypobaric hypoxia (7000 m) neither in blood serum nor in brain cortex. Also the values of LDH activities registered in normo or in hypothermic conditions were not different as compared with control values. The strong hypoxia (9000 m) evokes in brain cortex homogenates simultaneously with normothermia and posthypoxic hypothermia (30 degrees Celsius) significant increase of LDH activity. In blood serum the strong hypoxia increased the LDH activity; in subsequent hypothermic condition (22 degrees Celsius) the LDH activity was more lowered. CONCLUSION: The LDH activity in brain cortex as well as in blood serum of young rats (Wistar) seems to be resistent to mild hypoxia (7000 m) as well to hypothermic conditions. The strong hypoxia (9000 m) evokes quite different responses: in brain cortex the LDH activities in hypothermic conditions are higher, in blood serum lower as compared with control values (14 day-old rats stressed by hypoxia only). In control measurements the lowering temperature decreases the mentioned enzyme activity in brain cortex; in blood serum no significant differences could be found.

Air Pressure↗

[Effects of protein tyrosine kinase, protein tyrosine phosphatase and protein kinase C on the apoptosis of arsenic trioxide treated NB4 cells and human cortex neurons].

OBJECTIVE: To investigate the effects of protein tyrosine kinase (PTK), protein tyrosine phosphatase (PTP) and protein kinase C (PKC) on apoptosis and observe the changes of cytosolic calcium ([Ca(2+)]i) of arsenic trioxide (As2O3) treated human leukemia cells NB4 and cortex neurons. METHODS: [Ca(2+)]i of NB4 cells and cortex neurons was probed with Fluo-3/AM, its changes were assayed with laser confocal microscopy in real-time after As2O3 treatment at different concentrations, the effects of PTK and PTP and the activation of PKC on these changes with confocal microscopy and phosphorus radioisotope assay. DNA ladders of NB4 cells and cortex neurons after exposed to As2O3 were observed. RESULTS: As2O3 at 1 micromol/L could remarkably increase the [Ca(2+)]i of NB4 cells but had no effects on neurons. Vanadate, a kind of PTP inhibitor, could promote the increase of [Ca(2+)]i treated by 2, 5, 10 micromol/L As2O3 in a dose-dependent manner. The mean total increase rates at 240 seconds after exposed to As2O3 at different concentrations were (6.5 +/- 2.3)%, (21.7 +/- 2.1)%, (49.2 +/- 2.5)% for NB4 cells, and (6.7 +/- 2.1)%, (19.4 +/- 2.5)%, (52.3 +/- 2.7)% for cortex neurons, respectively. Genistein, a kind of PTK inhibitor, could decrease the increase of [Ca(2+)]i treated by 2, 5, 10 micromol/L As2O3 in a dose-dependent manner. The mean total inhibited rates at 240 seconds after As2O3 treatment at different concentrations were (6.7 +/- 2.9)%, (25.6 +/- 2.5)%, (52.2 +/- 3.5)% for NB4 cells, and (7.8 +/- 3.1)%, (18.1 +/- 2.8)%, (51.3 +/- 3.3)% for cortex neurons, respectively. The activation of PKC began to increase as exposed to As2O3 at 1 micromol/L for 3 h, and kept rising continuously in NB4 cells and at 24 h DNA ladders emerged. However, none of the above results was found in human cortex neurons, but when exposed to 2 micromol/L As2O3, the activation of PKC and DNA ladders did emerge in neurons. CONCLUSIONS: The phosphorylation and dephosphorylation of PTK and PTP participated in nonspecific apoptosis signal transduction pathway related to As2O3, and accompanied with PKC activation. The [Ca(2+)]i elevation was closely related to increased PKC activation. There existed difference in dose tolerances to As2O3 between NB4 cell and cortex neurons.

Adult↗

Febrile seizure, but not hyperthermia alone, induces the expression of heme oxygenase-1 in rat cortex.

BACKGROUND: Febrile seizure (FS) is the most common seizure disorders. Approximately one third of children with a febrile seizure have recurrent events. The mechanism of FS remains unclear. Heme oxygenase-1 (HO-1) is a member of the heat shock proteins family and can be induced in the brain by various stresses, including hyperthemia and seizure. This study aimed at investigating the changes of HO-1 in the cortex of rats after recurrent FS. METHODS: FS in rats was induced ten times, once every 2 days. In a bath of warm water, developing rats were randomly divided into two groups: control group (n = 16) and warm water-treated group (n = 50). The latter group was subdivided into hyperthermia group (n = 19) and FS group (n = 23). The expression and content of HO-1 mRNA in cortex were observed using in situ hybridization and quantitative reverse transcription-polymerase chain reaction (RT-PCR). The content of HO-1 protein in cortex was measured using Western blotting. RESULTS: HO-1 mRNA expression of cortex neurons in FS group was markedly increased in comparison with those in hyperthermia and control groups (P = 0.00), however, there was no statistic difference between hyperthermia group and control group (P = 0.16). The relative amount of HO-1 mRNA in cortex in FS group was increased by 53.13% and 96% in comparison with those in hyperthermia group and control group respectively (P = 0.00), but there was no obvious difference between the later two groups (P = 0.051). Western blotting analysis showed that the HO-1 protein content in cortex in FS group was increased by 198% and 246% in comparison with those in hyperthermia group and control group respectively (P = 0.00). There was no obvious difference in HO-1 protein content between the later two groups (P = 0.09). CONCLUSIONS: Recurrent FS in rats can cause the increase of HO-1 mRNA and protein in cortex which may be involved in the mechanism of FS. The short-time recurrent hyperthermia can not induce the increase of HO-1 mRNA and protein.

Animals↗

Development and plasticity of the primate cerebral cortex.

The results of our studies of corticocortical connectivity in developing monkey association cortex contrast with those obtained in similar studies of sensory regions in other species. In association areas of the monkey, these connections emerge very early in development, and many of the details of their organization are well specified from their earliest appearance. The presence of an adultlike pattern of organization a full month before birth suggests that these events probably are determined in large part by forces independent of general environmental stimulation, unlike the pattern seen for sensory regions in the cat. Do these differences reflect variations between species or between the development of sensory and nonsensory regions of the cortex? The answer is probably both. Our results suggest that diverse areas of the brain may differ in the extent to which they respond to environmental influences. For example, many of the organizational features that apparently emerge from an initially diffuse organization in sensory areas appear to be more strictly specified in their initial formation in the prefrontal cortex. However, we should not rule out the possibility that many of the features of connectional organization that are responsive to the environment in the sensory areas (e.g., the distribution of corticocortical neurons) develop in the prefrontal cortex during the prenatal period and therefore may simply be buffered from the effects of environmental stimuli. In addition, many aspects of the circuitry of the prefrontal cortex clearly continue to develop well into the postnatal period and may be subject to modification by experience. Among these are the organization and density of synaptic contacts and the elaboration of dendritic surfaces. Although relatively little is known concerning the response of these features to stimulation in the prefrontal cortex, studies from sensory areas suggest that these may be good candidates for modification by external interventions. The text of this paper was taken from a presentation given at the 1986 Johnson and Johnson Pediatric Roundtable. In the period between the original talk and the publication of this article, several studies have emerged on the development of corticocortical connectivity in sensory cortical regions of nonhuman primates. In agreement with our data in the monkey prefrontal cortex, these studies have also found that the distribution of callosal neurons in the somatosensory and visual cortices is adultlike at least 1 month prior to birth.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Afferent basis of visual response properties in area MT of the macaque. I. Effects of striate cortex removal.

The middle temporal area (MT) of the macaque monkey is a region of extrastriate cortex involved in the analysis of visual motion. MT receives strong projections from striate cortex and from area V2, which is dependent on striate for visual responsiveness. Accordingly, the visual properties of MT neurons have been thought to reflect the further processing of its input from striate cortex. We examined the dependence of MT activity on pathways deriving from striate cortex by recording from MT neurons following removal of their striate input. Repeated recordings in area MT were made in 4 hemispheres of anesthetized macaques following either partial or total ablations of striate cortex. Cells in MT were tested for responsiveness, selectivity for direction of motion and direction tuning, and ocular dominance. Receptive fields were also plotted. In an additional animal, we recorded from MT neurons during reversible cooling of the central representation in striate cortex. We found that striate cortex removal or inactivation did not abolish the visual responsiveness of the majority of MT cells. Although the residual responses were generally much weaker than in the intact animal, direction selectivity and binocularity were still present. Moreover, receptive field size and overall topography appeared unaltered.

Afferent Pathways↗

Clonidine enhances the release of endogenous gamma-aminobutyric acid through alpha-2 and alpha-1 presynaptic adrenoceptors differentially located in rat cerebral cortex subregions.

UNLABELLED: Clonidine (0.001-1 microM) increased the basal release of endogenous gamma-aminobutyric acid (GABA) in superfused synaptosomes from whole rat cerebral cortex. The effects of 0.1 to 1 microM clonidine were only in part sensitive to the alpha-2 adrenoceptor antagonist yohimbine; a complete antagonism by yohimbine could be seen only with 0.001 microM clonidine. The release of GABA induced by 0.1 to 1 microM clonidine was increasingly sensitive to the alpha-1 adrenoceptor antagonist prazosin. At all the concentrations tested clonidine was antagonized fully by a mixture yohimbine-prazosin (1 microM). The release of GABA was increased by phenylephrine in a concentration-dependent (0.01-1 microM) manner. At 1 microM phenylephrine was antagonized fully by 1 microM prazosin. When synaptosomes prepared from frontal, parietal, temporal and occipital cortex were exposed to clonidine (0.005 microM) or to phenylephrine (0.1 microM), the release of GABA was found to be region specific. Clonidine-induced GABA release could not be seen in temporal and occipital cortex but it was pronounced in parietal and frontal cortex. The effect of phenylephrine did not parallel that of clonidine: for instance, GABA release was most sensitive to phenylephrine in the occipital cortex where clonidine was ineffective. The opposite occurred in parietal cortex synaptosomes, where phenylephrine was much less effective than clonidine. IN CONCLUSION: 1) clonidine stimulates the release of GABA in rat cerebral cortex synaptosomes; 2) the effect is likely to occur by activation of alpha-1 and alpha-2 adrenoceptors possibly situated on GABAergic nerve endings; and 3) a differential distribution of alpha-1 and alpha-2 adrenoceptors regulating GABA release exists within the cortical subregions.

Animals↗

Postnatal development of corticocortical efferents from area 17 in the cat's visual cortex.

We are interested in the postnatal development of corticocortical connections in the cat's visual cortex. In this study, we injected the anterograde tracer 3H-proline into visual cortical area 17 of kittens, aged 4-70 d, and adult cats to visualize the distribution of terminals of the association projections to areas 18, 19, 21a, and the lateral suprasylvian visual cortex. The density of anterograde label was quantified using computerized image analysis. There was dense labeling at topographically appropriate locations in area 18 in animals of all ages. In 4- and 8-d-old kittens, other extrastriate areas (19, 21a and the lateral suprasylvian cortex) contained only sparse label, localized in a few solitary axons; these areas were densely labeled in animals aged 12 d or more. In kittens aged 4-20 d there was considerable, widespread label within fibers located in the white matter, and many of these axons lay underneath regions of extrastriate, and also striate, cortex that were almost certainly not destined to be persistently innervated by cells at the injection site. This pattern of extensive white matter label was not seen in animals older than 20 d. In each extrastriate region, from the earliest age at which we identified dense cortical innervation from area 17, the terminals were distributed in clusters. At first these patches were mainly in infragranular layers, but later, during the second and third postnatal weeks, they began to appear in more superficial laminae. By 70 d, an adult-like distribution of terminals was found in each extrastriate area: most fibers appeared to end in layers II and III in areas 18, 19, and 21a and centered on layer IV in the medial bank of the middle suprasylvian sulcus in adult cats. We suggest that the development of ipsilateral association projections from area 17 to extrastriate cortex is a 2-stage process. First, cells at a particular point in area 17 send immature fibers in a nonspecific fashion through white matter towards a very wide area of extrastriate cortex. Second, corticocortical axons penetrate extrastriate cortex mainly in patches at topographically appropriate regions and grow to their targets in a specific fashion.

Aging↗

3H-3-N-methylspiperone labels D2 dopamine receptors in basal ganglia and S2 serotonin receptors in cerebral cortex.

Detailed studies of the properties of 3H-3-N-methylspiperone (NMSP) binding in rat and human brain homogenates were performed at 37 degrees C. In homogenates of rat striatum and frontal cortex and human caudate and frontal cortex tissues, the specific binding was found to be saturable. Rat caudate contained 33.2 pmol/gm wet-weight tissue and displayed an equilibrium dissociation constant (Kd) of 8.7 X 10(-11) M; rat frontal cortex contained 18.5 pmol/gm wet-weight tissue and displayed a Kd of 1.5 X 10(-10) M. Human caudate contained 8.96 pmol/gm wet-weight tissue and displayed a Kd of 1.1 X 10(-10) M; human frontal cortex possessed 9.8 pmol/gm wet-weight tissue and a Kd of 4.4 X 10(-10) M. Kinetic studies revealed a very rapid rate of association in all the tissues studied. The rate of dissociation was relatively slow in all 4 tissue preparations; the dissociation rate was somewhat slower in rat striatum and human caudate relative to rat and human frontal cortex. This was consistent with the somewhat higher affinity, relative to frontal cortex, displayed by 3H-NMSP in rat striatal and human caudate tissue. The pharmacological properties of the specific binding in rat striatal and human caudate tissues were very similar and indicated the presence of brain D2 dopamine receptors. In rat and human frontal cortex tissue homogenates, the pharmacological characteristics of the specific binding indicated the presence of 5-HT2 receptors.

Animals↗

The co-occurrence of a substance P-like peptide and cholecystokinin-8 in a fiber system of turtle cortex.

Single-label and double-label immunohistochemical techniques were used to demonstrate the coexistence of substance P-like immunoreactivity (SPLI) and cholecystokinin-8-like immunoreactivity (CCK-8-LI) in an extensive fiber system within the telencephalic cortex of turtle. All SPLI-containing fibers and terminals of this system contain CCK-8-LI and vice versa. The fibers of this system course from more medial cortical regions to more lateral ones, originating either from neurons in the more medial cortices or from extracortical neurons, the axons of which ascend the medial wall of the cortex. The precise location of the neurons that give rise to this cortical projection system is uncertain, but a hypothalamic location seems most likely at present. The fibers and terminals of this system are found throughout the entire mediolateral and rostrocaudal extent of the telencephalic cortex of turtle and are largely confined to the cell body layer of the cortex. Fewer SPLI/CCK-8-LI-containing fibers are found in pyriform (olfactory) cortex than in the other cortices. Ultrastructural studies indicate that SPLI/CCK-8-LI-containing terminals make asymmetric synapses on cell bodies or their proximal dendrites. Both SPLI and CCK-8-LI are found in large dense core vesicles in these labeled terminals. Labeled terminals also contained numerous small, round, unlabeled vesicles clustered near synaptic release sites and a number of unlabeled large dense core vesicles. Quantification of the percentage of the large dense core vesicles that were labeled in SP-labeled terminals, in CCK-8-labeled terminals, and in terminals labeled for both SP and CCK-8 provided suggestive evidence that SPLI and CCK-8-LI must be contained within the same large dense core vesicles. Radioimmunoassay indicated that the SP/CCK-8-containing system of turtle cortex contains 0.93 +/- 0.090 pg of SP/microgram of cortical tissue protein and 0.31 +/- 0.11 pg of CCK-8/micrograms of cortical tissue protein. The CCK-8-like material in turtle cortex coelutes with CCK-8-sulfate, using gradient elution high pressure liquid chromatography (HPLC). The SP-like material, although immunologically highly similar to undecapeptide SP (Reiner, A., J. E. Krause, K. T. Keyser, W. D. Eldred, and J. F. McKelvy (1984) J. Comp. Neurol. 226: 50-75), does not coelute with undecapeptide SP using gradient elution HPLC.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Organization of individual afferent axons in layer IV of striate cortex in a primate.

Evidence from a number of anatomical and physiological studies shows that information is transmitted from the retina to visual cortex via physiologically and anatomically distinct populations of neurons in the lateral geniculate nucleus (LGN). In order to gain a better understanding of the functional roles of these parallel channels from the LGN to cortex in primates, individual afferent axons to layer IV of striate cortex of galagos were filled with HRP by bulk injection into the white matter underlying striate cortex. A total of 55 axons and their terminal arbors, from zones representing both the central and peripheral visual fields, were completely reconstructed through serial sections. Based upon the sublaminar distribution and the morphology of these axons, they have been categorized into 2 groups, designated type I and II axons. Evidence from both past work and the present study suggests that type I axons represent the projections from physiologically defined Y-like cells in the magnocellular layers of the LGN, while type II axons represent the projections from X-like cells in the parvocellular LGN layers. Our results show that type I (presumed Y-like) arbors occupy relatively more cortical space within their main terminal sublayer (IV alpha) than is the case for the type II (presumed X-like) arbors which ramify primarily in layer IV beta. In addition, type I arbors have larger parent axons, fewer boutons along a restricted length of axon, and a greater tendency to branch in layer VI than type II arbors. Finally, both axon types are larger in the area of cortex representing central vision than in the area representing peripheral vision. These morphological characteristics suggest that the physiological differences between magnocellular and parvocellular geniculate cells may be amplified in cortex by differences in the organization of their terminal arbors. Further, within each afferent population, the terminal organization of axons reflects their visuotopic relationships in striate cortex. Comparison of these findings with data from cats and monkeys supports the idea that the relationship between the size of the terminal arbors of LGN X-like or parvocellular cells and the size of the cortical spatial subunit varies with differences in visual acuity across species; for LGN Y-like (or magnocellular) cells this relationship remains constant.

Afferent Pathways↗

Study of descending inhibitory and facilitory effect of the orbital cortex on the electrical discharges of medial geniculate body (MGB) neurons in rabbits.

Experiments were performed on 16 rabbits immobilized with flaxedil. The recording of spontaneous discharges and the discharges of single MGB neurons caused by clicks showed that when the cerebral-orbital cortex was stimulated, of 92 MGB neurons responding to clicks, 25 units (27.2%) were inhibited, 14 units (15.2%) were facilitated, and 15 units with spontaneous discharges were completely inhibited. The topographical distribution of stimulated points with such inhibitory and facilitory effect is quite concentrated on the orbital cortex. Stimulation of two adjacent points of the orbital cortex could respectively result in different kinds of inhibitory and facilitory effect on discharges of a same MGB neuron. Due to the existence of this descending effect with a short latent period (2-3 ms), the authors have reason to believe that there might be an "orbital cortex-MGB" direct pathway. Moreover, application of 2% procaine to block the auditory cortex behind the rhinal sulcus (ACBRS) could abolish the facilitory effect, with a long latency, of the orbital cortex. Therefore, the influence of the orbital cortex on MGB might be also transmitted via the "orbital-ACBRS-MGB" circuit.

Animals↗

The development of synapses in striate cortex of man.

Synaptic density in human striate cortex was determined at various ages, utilizing a computer assisted method. Simultaneous measurement of total volume of striate cortex made it possible to estimate total number of synapses. Synaptogenesis in human striate cortex was found to be most rapid between ages 2-4 months, a time which also is critical for the development of function in visual cortex of the infant. Synapse elimination occurred subsequently with loss of about 40% of synapses between ages 8 months and 11 years. Synapse numbers were stable in adults, except for a slightly lower value in a single brain at age 71 years. Analysis by individual cortical layers showed similar age related changes in all strata of striate cortex, except for somewhat later synaptogenesis in cortical layers V and VI. Total volume of striate cortex reached adult size remarkably early, at about age 4 months. The findings support the hypothesis that exuberant synaptic connections are an anatomical substrate for plasticity in developing cerebral cortex.

Adolescent↗

Neuronal types of the cerebral cortex of the adult chicken (Gallus gallus). A Golgi study.

The telencephalic cortex of adult chicken (Gallus gallus) consists of two anatomical regions: the medial cortex (or hippocampal cortex) and the dorsal cortex (or parahippocampal cortex) which we have denominated "dorsomedial cortex" (DMC) as a whole. The dorsomedial cortex shows, with Nissl's technique, two main layers of lamination, besides the ependymal layer: plexiform layer and granular layer. In the plexiform layer, there is a sub-layer called periventricular. In Golgi impregnations, the plexiform layer of the DMC is filled with neurons of horizontal type and fibers. The granular layer of the medial region is mainly occupied with pyramidal and bipyramidal neurons, as well as some short-axon and long-axon multipolar neurons. In the granular layer of the dorsal region basically long-axon multipolar neurons are found and, to a lesser extend, short-axon multipolar ones are also seen. In the periventricular sub-layer of all the DMC are located the periventricular neurons. In general, we can say that the chicken DMC is a poorly developed cortical structure.

Animals↗

An application of numerical taxonomy to the study of the cerebral cortex of Natrix maura (L).

The separate cellular regions of the reptilian cerebral cortex were studied using Numerical Taxonomy. Three parameters were employed: a) The area occupied by each region at the several levels studied. b) The total area of the cell nuclei present in each level. c) The average are of these nuclei. Numerical Taxonomy resolves the problem by means of a dendrogram which represents the normalised distances, which indicate levels of similarity on absciassas. The elements studies are on the ordinate axis. The dendrogram shows the different levels of similarity existing between each one of the chosen populations. Depending upon the degree of similarity one may deduce the similarities or differences existing between these populations, and also the characteristics of each cellular population throughout the length of its presence in the cerebral cortex and the variations between the regions. These results, in the first place, relate to the four cortical regions: medialis cortex, dorsomedialis cortex, dorsalis cortex, and lateralis cortex, and in the second place, to each one of the regions within the entire telencephalic cortex.

Animals↗

Effects of duloxetine, a new serotonin and norepinephrine uptake inhibitor, on extracellular monoamine levels in rat frontal cortex.

The effects of duloxetine (LY248686), a new inhibitor of serotonin (5-hydroxytryptamine; 5-HT) and norepinephrine (NE) uptake on extracellular levels of NE, 5-HT and dopamine (DA), were studied in the rat frontal cortex and nucleus accumbens, using in vivo microdialysis. The oral administration of duloxetine (3.125-12.5 mg/kg) produced a dose-dependent increase in the output of both NE and 5-HT from the frontal cortex, this increase being maintained throughout the 4-hr observation period. Chronic administration of duloxetine (6.25 mg/kg, p.o.) for 14 days failed to alter basal NE and 5-HT levels in the frontal cortex, but augmented the duloxetine-induced increase in output of NE and 5-HT. Amitriptyline and maprotiline, administered p.o. at doses of 6.25 to 25 mg/kg, increased NE output, but the effect was weaker than that of duloxetine, and neither amitriptyline nor maprotiline changed 5-HT output from the frontal cortex. Duloxetine, amitriptyline, and maprotiline brought about increases in DA levels in the rat frontal cortex, the increase in DA levels induced by duloxetine being approximately two or three times more potent than that induced by amitriptyline and maprotiline. In the nucleus accumbens, duloxetine also produced a dose-dependent increase in DA output more potent than that produced by amitriptyline and maprotiline. These results show that duloxetine causes a potent and sustained increase in the output of both NE and 5-HT in the rat frontal cortex, related to its inhibition of NE and 5-HT uptake; these results also show that duloxetine increases DA output in the frontal cortex.

Amitriptyline↗