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PubMed1990

Modulation of 5-hydroxytryptamine release by presynaptic inhibitory alpha 2-adrenoceptors in the human cerebral cortex.

Slices and synaptosomes from human cerebral cortex (which had to be removed to reach deeply located tumours) and, for comparison, synaptosomes from guinea-pig and rat cerebral cortex were preincubated with [3H]5-hydroxytryptamine and superfused with physiological salt solution containing an inhibitor of 5-hydroxytryptamine uptake. The effects of alpha-adrenoceptor agonists and antagonists on the electrically (slices) or potassium-evoked (synaptosomes) tritium overflow were studied. In human cerebral cortical slices, the electrically-evoked [3H] overflow was inhibited by noradrenaline (pIC25 value: 6.35); the non-selective alpha-adrenoceptor antagonist phentolamine, at a concentration of 0.32 mumol/l, strongly antagonized the inhibitory effect of noradrenaline (apparent pA2 value: 8.19) but did not affect the evoked overflow by itself. In synaptosomes from humans, guinea-pigs and rats, noradrenaline also inhibited the K(+)-evoked [3H] overflow in a concentration dependent manner; the alpha 2-adrenoceptor clonidine (1 mumol/l), but not the alpha 1-adrenoceptor agonist methoxamine (1 mumol/l), mimicked the effects of noradrenaline; the effect of noradrenaline (0.3 mumol/l) was abolished by the alpha 2-adrenoceptor antagonist idazoxan (0.5 mumol/l), but not by the alpha 1-adrenoceptor antagonist prazosin (1 mumol/l). It is concluded that release-inhibiting adrenoceptors of the alpha 2-subtype exist on 5-hydroxytryptamine terminals innervating the cerebral cortex in human and guinea-pig brain.

Adrenergic alpha-Agonists↗

PubMed1986

A study on the microvasculature of the cerebral cortex. Fundamental architecture and its senile change in the frontal cortex.

The arterial architecture of the cerebral cortex and its changes along with aging were studied by microangiography, vascular staining, and scanning electron microscopy. The arteries distributed in the cerebral cortex and medulla were classified into cortical, subcortical, and medullary arteries. The cortical arteries were further classified into superficial, middle, and deep cortical branches according to the site of their termination. There were many fountain-like rami in the middle and deep cortical branches. These fountain-like rami were composed of several to many fine arteries, ramified from a small artery by repeated bifurcation within a short segment of its course. This structural pattern is probably responsible for the ease with which pronounced ischemic state may develop in their territories nourished by these branches, and they may play a significant role in the development of pseudolaminar necrosis of the cerebral cortex. Intertwining of small branches forming rope-like structures was observed with increasing frequency with age, suggesting that this phenomenon correlates with aging or is associated with brain atrophy. The intertwining was always clockwise when looking from the proximal side of the arteries towards their distal end. While the precise mechanism of the development of the intertwining remains unclear, torsion of the trunk of the blood vessels is thought to be the cause of the intertwining of the peripheral branches.

Adolescent↗

PubMed1985

Comparison of proteins involved with cyclic AMP metabolism between synaptic membrane and postsynaptic density preparations isolated from canine cerebral cortex and cerebellum.

Synaptic membrane and postsynaptic density (PSD) fractions isolated from canine cerebral cortex and cerebellum were assayed for the following proteins: adenylate cyclase and phosphodiesterase (PDE) activities against cyclic AMP and cyclic GMP, the regulatory subunit of the cyclic AMP-dependent protein kinase, and the substrate proteins for this kinase. The results were expressed on the basis of both the protein content of the fractions and the number of synapses in the synaptic membrane fractions. The number of synapses on a constant protein content basis was about three times higher in the cerebral cortex synaptic membrane fraction than in the comparable cerebellar fraction. Adenylate cyclase activity was from 3.4 to 5.6 times higher in the cerebral cortex membrane fraction than in the cerebellar membrane fraction based on protein content but only slightly higher based on synapse counts. PSD fractions had no adenylate cyclase activity. The cyclic AMP-PDE activity was from 17 to 27 times higher in the cerebral cortex membrane fraction than in the cerebellar membrane fraction based on protein content, and about five times higher based on synapse counts. By doing PDE histochemistry at the electron microscopy level it was found that all the cerebral cortex PSDs in the isolated fraction contained PDE activity, none being found associated with the broken-up material in the fraction. The amount of the regulatory subunit of the cyclic AMP-dependent protein kinase was about equal in the two fractions based on protein, but about one-third lower in cerebral cortex fraction than in cerebellar fractions. In the cerebral cortex membrane fraction the primary substrate for the cyclic AMP-dependent protein kinase is synapsin I, with much lower amounts in the cerebellar membrane fraction. The PSD fraction from the two sources also showed these differences in synapsin I content. In the cerebellar membrane fraction, the primary substrate for the enzyme is a approximately 245,000 Mr protein not found in the cerebral cortex membrane fraction. The findings that the turnover of cyclic AMP is much higher in cerebral cortex synapses than in cerebellar synapses, and that differences are found between the cerebral cortex and cerebellum with regard to the substrate proteins for the cyclic AMP-dependent protein kinase indicate a divergence in the effect of cyclic AMP between cerebral cortex and cerebellar synapses.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMedDate not supplied

[Ontogenic differences of glutamate decarboxylase, GABA-aminotransferase, monoamine oxidase activities of cerebral cortex mitochondria and hypothalamic cerebral area].

It is shown that the glutamate decarboxylase activity in the initial mitochondrial fraction of "light" and "heavy" synaptosomes of cerebral hemispheres changes on the 14th, 21st day, 1st, 3d, 12th and 24th months of rat development: in the hypothalamus area it lowers in the initial mitochondria in the 21-day animals, and in the fraction of "heavy" synaptosomes--in the 24 day animals as compared to the adult ones. The GABA-aminotransferase activity in the cortex synaptosome fraction rises in the period between the 14th and 21st day after birthday and in the initial mitochondrial fraction of the hypothalamus area--between the 14th day and the first month of life. In adult rats the glutamate decarboxylase and GABA-aminotransferase activities in the "heavy" synaptosome fraction are higher than in the "light" synaptosome one. The amine oxidase activity of the subcellular fractions which is determined with serotonin as a substrate (form A) is stable during the whole developmental period of studies. The intensity of benzylamine (amine oxidase B) desamination in the cortex fraction and hypothalamus area rises sharply in the second half of ontogenesis.

4-Aminobutyrate Transaminase↗

PubMed1998

Spatial stability of extracellular potassium ion and blood flow distribution in rat cerebral cortex after permanent middle cerebral artery occlusion.

Extracellular potassium ion activity ([K+]o) increases precipitously during brain ischemia when blood flow falls below threshold values less than approximately 15 mL/100 g/min. This flow threshold for increase of [K+]o occurs also in focal ischemia producing gradient from ischemic core to adjacent normally perfused brain. In this study we investigated the spatial and temporal stability of extracellular potassium ion and blood flow gradients after permanent middle cerebral artery occlusion (MCAO) in rats. [K+]o and regional CBF were measured, respectively, with K+-sensitive and polarographic hydrogen-sensitive microelectrodes at different cortical locations in the middle cerebral artery distribution region. Spatial assessment of [K+]o and regional CBF was conducted at 30, 90, and 180 minutes after MCAO. [K+]o in the more lateral cortex (core) increased from near 3 mmol/L before MCAO to greater than 50 mmol/L and was associated with flow values less than 25% of pre-ischemic levels. Measurements medial to the core (penumbra) indicated progressively decreasing levels of [K+]o and improvement of CBF. There was a tendency for [K+]o in penumbral zones to decrease toward normal levels with time, but there was little dissipation of [K+]o in core regions. In contrast, the spatial CBF profile remained remarkably constant for the entire recording period. Thus, unlike infarction which has been reported to expand with time after focal ischemia, the spatial [K+]o disturbance tends to contract primarily due to decreasing [K+]o with time in the penumbra. Thus, steady state levels of [K+]o after focal ischemia may not be a valuable predictor of cell viability.

Animals↗

PubMed2006

Brain-derived neurotrophic factor participates in determination of neuronal laminar fate in the developing mouse cerebral cortex.

Lamina formation in the developing cerebral cortex requires precisely regulated generation and migration of the cortical progenitor cells. To test the possible involvement of brain-derived neurotrophic factor (BDNF) in the formation of the cortical lamina, we investigated the effects of BDNF protein and anti-BDNF antibody separately administered into the telencephalic ventricular space of 13.5-d-old mouse embryos. BDNF altered the position, gene-expression properties, and projections of neurons otherwise destined for layer IV to those of neurons for the deeper layers, V and VI, of the cerebral cortex, whereas anti-BDNF antibody changed some of those of neurons of upper layers II/III. Additional analysis revealed that BDNF altered the laminar fate of neurons only if their parent progenitor cells were exposed to it at approximately S-phase and that it hastened the timing of the withdrawal of their daughter neurons from the ventricular proliferating pool by accelerating the completion of S-phase, downregulation of the Pax6 (paired box gene 6) expression, an essential transcription factor for generation of the upper layer neurons, and interkinetic nuclear migration of cortical progenitors in the ventricular zone. These observations suggest that BDNF participates in the processes forming the neuronal laminas in the developing cerebral cortex. BDNF can therefore be counted as one of the key extrinsic factors that regulate the laminar fate of cortical neurons.

Animals↗

PubMed1988

Neurons in the medial cortex give rise to Timm-positive boutons in the cerebral cortex of lizards.

The origin of Timm-positive presynaptic boutons in the cerebral cortex of the lizard, Podarcis hispanica, was investigated by injections of horseradish peroxidase (HRP)-saponine in Timm-positive areas, i.e. the dorsal and dorsomedial cortices. A broad retrograde labelling of cell somata in the medial cortex was found. Injections of HRP-saponine in the medial cortex resulted in broad anterograde labelling of boutons located in the Timm-positive zones. A double-labelling of the HRP labelled boutons was obtained by using the Neo-Timm or the sulphide-osmium methods. The present results suggest that neurons of the medial cortex send axons that terminate in Timm-positive boutons in the cerebral cortex of lizards.

Animals↗

PubMed1966

Hypercapnia and acetylcholine release from the cerebral cortex and medulla.

1. The cerebral cortex and medulla of fifty-eight anaesthetized dogs released ACh spontaneously through push-pull cannulae after perfusion with the anticholinesterase, sarin. Hypercapnia (12% CO(2)) evoked a significant release of ACh above the basic spontaneous level, from the medullary and cortical areas. Hypercapnia + hypoxia (12% CO(2) + 8% O(2)), in combination, produced an ACh release comparable to hypercapnia; hypoxia (8% O(2)) had no effect in any region.2. Areas in the medullary reticular formation responsive to injections of CO(2)-bicarbonate solutions (;respiratory responsive areas') produced a significant increase of ACh after exposure to hypercapnia or hypercapnia + hypoxia, over that obtained from either the ;non-respiratory responsive areas' of the medulla or the cerebral cortex.3. The evidence supports the concept that ACh may participate as a neurotransmitter within the cerebral cortex and medulla. Also the results would suggest but do not prove, that a cholinergic factor may be a component in respiratory control under certain circumstances, such as exposure to hypercapnia.

Acetylcholine↗

PubMedDate not supplied

Regional differences in the stratified transitional field and the honeycomb matrix of the developing human cerebral cortex.

The neurons of the cerebral cortex originate in the proliferative neuroepithelium and settle in the cortical plate during embryonic development. Interposed between these two sites is a large transitional field. We have earlier demonstrated experimentally in rats with 3H-thymidine autoradiography that this transitional field is a stratified structure composed of discrete layers of migrating and sojourning cells, and fiber bands. Here we show that the different layers of the stratified transitional field are identifiable without experimental procedures in the developing human cerebral cortex and that there are conspicuous regional differences in its stratification. At the peak of its development, the stratified transitional field contains three fibrous bands in an inside-out order: the commissural fibers of the corpus callosum, the thalamocortical and corticofugal projection fibers, and the expanding white matter. There are regional differences in the thickness of these fibrous layers as well as in the number and configuration of the perikaryal layers. This preview focuses on laminar differences of the transitional fields of the agranular frontal lobe and the granular parietal and occipital lobes. At the latter sites, but not in the frontal lobe, there is a distinctive multi-layered band, the honeycomb matrix, where radially oriented fiber columns are sandwiched between two perikaryal sublayers and are separated from one another by radially oriented cells. We postulate that the radial fiber columns of the honeycomb matrix are composed of topographically organized thalamocortical fibers and that the unspecified young neurons acquire their enduring topographic identity by making selective contacts with tagged fibers here before they resume their radial or tangential migration to the cortical plate.

Body Patterning↗

PubMed2001

Cytoarchitectonic study of the cerebral cortex in the horse brain--classification of the cortex area.

A cytoarchitectural classification of the horse cerebral cortex was done to determine whether functional locations exist or not such as found in the human cerebral cortex. Two adult horse brains were examined by Nissl and myelin stained methods. Six cell layers of the cerebral cortex were identified and classified into five types areas based on the cytoarchitectural organization: agranular, frontal, parietal, polar and granulous types. The agranular type was seen around the gyrus sylvius. In layer V of the agranular type, there were the many large cells that seemed like Betz cells. This type was recognized as motor area. The frontal type was seen in the lower and parietal parts of the cortex. The parietal type was seen in the rostral and occipital lobes. The polar type was seen in the frontal and dorsal-occipital sides. The granulous type was seen in the anterior-lower and posterior-lateral part of the cortex. The occupational ratios of the five types, that is, agranular, frontal, parietal, polar and granulous, to the whole cerebral cortex, were calculated by three-dimensional analysis using computer system as 19.6, 27.0, 28.9, 13.6 and 10.9%, respectively. As a result of myelin stain, horizontal fibers were seen in layer IV of parietal and polar types which looked liked the line of Gennari, therefore this area was recognized as the primary visual area.

Animals↗

PubMed1972

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

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

Animals↗

PubMed1999

Abnormalities of retinal metabolism in diabetes or experimental galactosemia. VI. Comparison of retinal and cerebral cortex metabolism, and effects of antioxidant therapy.

Metabolic abnormalities observed in retina and in cerebral cortex were compared in diabetic rats and experimentally galactosemic rats. Diabetes or experimental galactosemia of 2 months duration significantly increased oxidative stress in retina, as shown by elevation of retinal thiobarbituric acid reactive substances (TBARS) and subnormal activities of antioxidant defense enzymes, but had no such effect in the cerebral cortex. Activities of sodium potassium adenosine triphosphatase [(Na,K)-ATPase] and calcium ATPase became subnormal in retina as well as in cerebral cortex. In contrast, protein kinase C (PKC) activity was elevated in retina but not in cerebral cortex in the same hyperglycemic rats. Dietary supplementation with an antioxidant mixture (containing ascorbic acid, Trolox, alpha-tocopherol acetate, N-acetyl cysteine, beta-carotene, and selenium) prevented the diabetes-induced and galactosemia-induced elevation of retinal oxidative stress, the elevation of retinal PKC activity and the decrease of retinal ATPases. In cerebral cortex, administration of the antioxidant diet also prevented the diabetes-induced decreases in (Na,K)-ATPase and calcium ATPases, but had no effect on TBARS and activities of PKC and antioxidant-defense enzymes. The results indicate that retina and cerebral cortex differ distinctly in their response to elevation of tissue hexose, and that cerebral cortex is more resistant than retina to diabetes-induced oxidative stress. The greater resistance to oxidative stress in cerebral cortex, as compared to retina, is consistent with the resistance of cerebral cortex to microvascular disease in diabetes, and with a hypothesis that oxidative stress contributes to microvascular disease in diabetes. Dietary supplementation with these antioxidants offers a means to inhibit multiple hyperglycemia-induced retinal metabolic abnormalities.

Animals↗

PubMedDate not supplied

Free radical scavengers suppress the accumulation of platinum in the cerebral cortex.

We investigated whether free radical scavengers and antioxidants inhibit the accumulation of platinum (Pt) in the cerebral cortex. Pt was detected in the cerebral cortex of mice after administration of cisplatin and exposure to short-term hypoxia. When mice were treated with either allopurinol (20 mg/kg) or catalase (100 mg/kg) before cisplatin administration and low oxygen exposure, Pt was not detected in the cerebral cortex. However, Pt was detected in the cerebral cortex of mice pretreated with either a low dosage of allopurinol or heat-denatured catalase. Furthermore, Pt was detected in the cerebral cortex of mice preadministered vitamin C, vitamin E, or deferoxamine. Lipid peroxide levels in the cerebral cortex increased 10 min after the treatment of hypoxia, and peaked 30 min after the treatment. These results suggested that short-term hypoxia produces free radicals, which allows Pt to pass through the blood-brain barrier and accumulate in the cerebral cortex, and that the production of free radicals is reduced by the administration of either allopurinol or catalase, which prevents Pt from passing through the barrier.

Allopurinol↗

PubMed1989

Age-dependence of the solubility fractions of acetylcholinesterase in the cerebral cortex and cerebellum of the rat.

Choline acetyltransferase (ChAT) activity in the cerebral cortex and the different solubility fractions of acetylcholinesterase (AChE) in the cerebral cortex and cerebellum were investigated in rats of different ages. ChAT activity was not decreased markedly in the cerebral cortex of 24- to 25-month-old rats compared to 3- to 4-month-old rats. The activity of detergent-soluble (DS) AChE in the cerebral cortex and cerebellum was lower in the older rats (24-25 months) rats than in younger (3-4 months) ones. The activity of DS-AChE in the cerebral cortex and cerebellum did not differ between 10- to 11-month-old and 24- to 25-month-old rats. The activity of low salt soluble (LSS) AChE in the cerebral cortex and cerebellum did not differ between older and younger rats.

Acetylcholinesterase↗

PubMed1990

Expression of neurotrophic activity in Xenopus oocytes injected with mRNA from wounded rat cerebral cortex.

Injury to the cerebral cortex of the rat brain has been shown to induce the expression of neurotrophic factors for dissociated peripheral and central neurons in culture. We confirm this phenomenon and report that Xenopus laevis oocytes injected with mRNA extracted from wounded rat cortex expressed similar neurotrophic activity. To detect the low amounts of neurotrophic factors that could be expected from the oocyte translation system, a miniaturization of the assay for neurotrophic and cell-surviving activity was developed using Terasaki microtiter plates for culture of chicken embryo sympathetic ganglion cells. Messenger RNA (mRNA) was size-fractionated on a sucrose gradient and RNAs from each fraction were injected into oocytes. Neurotrophic activity was recovered from the homogenates and from the incubation media of oocytes injected with mRNA from 7 day post-lesion cortex. Messenger RNAs in the active fractions ranged in size from 0.8 to 1.8 kb. As much as 20% of the activity was secreted by the oocytes. No significant neurotrophic activity was detected from oocytes injected with mRNA fractions extracted from the cortex of control rats or from other gradient fractions from post-lesion cortex.

Animals↗

PubMed1992

Neuronal mechanisms of interaction of Deiters nucleus with the cerebral cortex.

The effects of stimulation of the vestibular nerve and five different cerebral cortex areas on the neuronal activity of the lateral vestibular nucleus of Deiters were studied. Stimulation of the cerebral cortex is shown to lead to antidromic and synaptic activation of Deiters neurons. The synaptic potentials of Deiters neurons evoked from the cerebral cortex were of mono- and polysynaptic origin. In particular, stimulation of the cerebral cortex evoked in Deiters neurons mono- and polysynaptic excitatory postsynaptic potentials. Collaterals of vestibulospinal neurons reaching different cortex fields as well as convergence of influences from these cortex fields on Deiters neurons were revealed. Inhibitory effects of the cerebral cortex on Deiters neurons were of polysynaptic origin and occurred rarely. The topical correlation between Deiters nucleus and different areas of the cerebral cortex was found. The peculiarities and functional significance of the effects obtained are discussed.

Action Potentials↗

PubMed1992

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↗

PubMed2003

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

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

Animals↗