scholarly journals Cellular Scaling Rules for the Brains of Marsupials: Not as “Primitive” as Expected

2017 ◽  
Vol 89 (1) ◽  
pp. 48-63 ◽  
Author(s):  
Sandra E. Dos Santos ◽  
Jairo Porfirio ◽  
Felipe B. da Cunha ◽  
Paul R. Manger ◽  
William Tavares ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Brain Structure ◽  
Cortical Neurons ◽  
Neuronal Cell ◽  
Sister Group ◽  
Mammalian Evolution ◽  
Cerebellar Neurons ◽  
Scaling Relationships ◽  
Cerebral Cortical Neurons ◽  
The Brain

In the effort to understand the evolution of mammalian brains, we have found that common relationships between brain structure mass and numbers of nonneuronal (glial and vascular) cells apply across eutherian mammals, but brain structure mass scales differently with numbers of neurons across structures and across primate and nonprimate clades. This suggests that the ancestral scaling rules for mammalian brains are those shared by extant nonprimate eutherians - but do these scaling relationships apply to marsupials, a sister group to eutherians that diverged early in mammalian evolution? Here we examine the cellular composition of the brains of 10 species of marsupials. We show that brain structure mass scales with numbers of nonneuronal cells, and numbers of cerebellar neurons scale with numbers of cerebral cortical neurons, comparable to what we have found in eutherians. These shared scaling relationships are therefore indicative of mechanisms that have been conserved since the first therians. In contrast, while marsupials share with nonprimate eutherians the scaling of cerebral cortex mass with number of neurons, their cerebella have more neurons than nonprimate eutherian cerebella of a similar mass, and their rest of brain has fewer neurons than eutherian structures of a similar mass. Moreover, Australasian marsupials exhibit ratios of neurons in the cerebral cortex and cerebellum over the rest of the brain, comparable to artiodactyls and primates. Our results suggest that Australasian marsupials have diverged from the ancestral Theria neuronal scaling rules, and support the suggestion that the scaling of average neuronal cell size with increasing numbers of neurons varies in evolution independently of the allocation of neurons across structures.

scholarly journals 6B4 proteoglycan/phosphacan is a repulsive substratum but promotes morphological differentiation of cortical neurons

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 647-658
Author(s):  
N. Maeda ◽  
M. Noda
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Tyrosine Phosphatase ◽  
Neuronal Cell ◽  
Morphological Differentiation ◽  
Cell Types ◽  
Thalamic Neurons ◽  
Neurite Extension ◽  
The Brain

6B4 proteoglycan/phosphacan is one of the major phosphate-buffered saline-soluble chondroitin sulfate proteoglycans of the brain. Recently, this molecule has been demonstrated to be an extracellular variant of the proteoglycan-type protein tyrosine phosphatase, PTPzeta (RPTPbeta). The influence of the 6B4 proteoglycan, adsorbed onto the substratum, on cell adhesion and neurite outgrowth was studied using dissociated neurons from the cerebral cortex and thalamus. 6B4 proteoglycan adsorbed onto plastic tissue culture dishes did not support neuronal cell adhesion, but rather exerted repulsive effects on cortical and thalamic neurons. When neurons were densely seeded on patterned substrata consisting of a grid-like structure of alternating poly-L-lysine and 6B4 proteoglycan-coated poly-L-lysine domains, they were concentrated on the poly-L-lysine domains. However, 6B4 proteoglycan did not retard the differentiation of neurons but rather promoted neurite outgrowth and development of the dendrites of cortical neurons, when neurons were sparsely seeded on poly-L-lysine-conditioned coverslips continuously coated with 6B4 proteoglycan. This effect of 6B4 proteoglycan on the neurite extension of cortical neurons was apparent even on coverslips co-coated with fibronectin or tenascin. By contrast, the neurite extension of thalamic neurons was not modified by 6B4 proteoglycan. Chondroitinase ABC or keratanase digestion of 6B4 proteoglycan did not affect its neurite outgrowth promoting activity, but a polyclonal antibody against 6B4 proteoglycan completely suppressed this activity, suggesting that a protein moiety is responsible for the activity. 6B4 proteoglycan transiently promoted tyrosine phosphorylation of an 85x10(3) Mr protein in the cortical neurons, which correlated with the induction of neurite outgrowth. These results suggest that 6B4 proteoglycan/phosphacan modulates morphogenesis and differentiation of neurons dependent on its spatiotemporal distribution and the cell types in the brain.

scholarly journals Heme–Hemopexin Complex Attenuates Neuronal Cell Death and Stroke Damage

2009 ◽  
Vol 29 (5) ◽  
pp. 953-964 ◽  
Author(s):  
Rung-chi Li ◽  
Sofiyan Saleem ◽  
Gehua Zhen ◽  
Wangsen Cao ◽  
Hean Zhuang ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Neuronal Cultures ◽  
Tert Butyl Hydroperoxide ◽  
Primary Mouse ◽  
Free Heme ◽  
Cerebral Artery Occlusion ◽  
The Brain

Hemoproteins undergo degradation during hypoxic/ischemic conditions, but the prooxidant free heme that is released cannot be recycled and must be degraded. The extracellular heme associates with its high-affinity binding protein, hemopexin (HPX). Hemopexin is shown here to be expressed by cortical neurons and it is present in mouse cerebellum, cortex, hippocampus, and striatum. Using the transient ischemia model (90-min middle cerebral artery occlusion followed by 96-h survival), we provide evidence that HPX is protective in the brain, as neurologic deficits and infarct volumes were significantly greater in HPX−/− than in wild-type mice. Addressing the potential protective HPX cellular pathway, we observed that exogenous free heme decreased cell survival in primary mouse cortical neuron cultures, whereas the heme bound to HPX was not toxic. Heme-HPX complexes induce HO1 and, consequently, protect primary neurons against the toxicity of both heme and prooxidant tert-butyl hydroperoxide; such protection was decreased in HO1−/− neuronal cultures. Taken together, these data show that HPX protects against heme-induced toxicity and oxidative stress and that HO1 is required. We propose that the heme-HPX system protects against stroke-related damage by maintaining a tight balance between free and bound heme. Thus, regulating extracellular free heme levels, such as with HPX, could be neuroprotective.

scholarly journals A prokaryotic viral sequence is expressed and conserved in mammalian brain

2017 ◽  
Vol 114 (27) ◽  
pp. 7118-7123 ◽  
Author(s):  
Yang-Hui Yeh ◽  
Vignesh Gunasekharan ◽  
Laura Manuelidis
Keyword(s):  
Maternal Inheritance ◽  
Neuronal Cell ◽  
Proteinase K ◽  
Mammalian Brain ◽  
Neural Cells ◽  
Mammalian Evolution ◽  
Western Blots ◽  
Neuronal Cell Lines ◽  
Viral Sequences ◽  
The Brain

A natural and permanent transfer of prokaryotic viral sequences to mammals has not been reported by others. Circular “SPHINX” DNAs <5 kb were previously isolated from nuclease-protected cytoplasmic particles in rodent neuronal cell lines and brain. Two of these DNAs were sequenced after Φ29 polymerase amplification, and they revealed significant but imperfect homology to segments of commensalAcinetobacterphage viruses. These findings were surprising because the brain is isolated from environmental microorganisms. The 1.76-kb DNA sequence (SPHINX 1.8), with an iteron before its ORF, was evaluated here for its expression in neural cells and brain. A rabbit affinity purified antibody generated against a peptide without homology to mammalian sequences labeled a nonglycosylated ∼41-kDa protein (spx1) on Western blots, and the signal was efficiently blocked by the competing peptide. Spx1 was resistant to limited proteinase K digestion, but was unrelated to the expression of host prion protein or its pathologic amyloid form. Remarkably, spx1 concentrated in selected brain synapses, such as those on anterior motor horn neurons that integrate many complex neural inputs. SPHINX 1.8 appears to be involved in tissue-specific differentiation, including essential functions that preserve its propagation during mammalian evolution, possibly via maternal inheritance. The data here indicate that mammals can share and exchange a larger world of prokaryotic viruses than previously envisioned.

scholarly journals Lactate is an energy substrate for rodent cortical neurons and enhances their firing activity

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Anastassios Karagiannis ◽  
Thierry Gallopin ◽  
Alexandre Lacroix ◽  
Fabrice Plaisier ◽  
Juliette Piquet ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Cortical Neurons ◽  
Brain Function ◽  
Lactate Metabolism ◽  
Firing Activity ◽  
Energy Substrate ◽  
Relative Contribution ◽  
Neuronal Types ◽  
Neuronal Energy Metabolism ◽  
The Brain

Glucose is the mandatory fuel for the brain, yet the relative contribution of glucose and lactate for neuronal energy metabolism is unclear. We found that increased lactate, but not glucose concentration, enhances the spiking activity of neurons of the cerebral cortex. Enhanced spiking was dependent on ATP-sensitive potassium (KATP) channels formed with KCNJ11 and ABCC8 subunits, which we show are functionally expressed in most neocortical neuronal types. We also demonstrate the ability of cortical neurons to take-up and metabolize lactate. We further reveal that ATP is produced by cortical neurons largely via oxidative phosphorylation and only modestly by glycolysis. Our data demonstrate that in active neurons, lactate is preferred to glucose as an energy substrate, and that lactate metabolism shapes neuronal activity in the neocortex through KATP channels. Our results highlight the importance of metabolic crosstalk between neurons and astrocytes for brain function.

The actions of motilin, luteinizing hormone releasing hormone, cholecystokinin, somatostatin, vasoactive intestinal peptide, and other peptides on rat cerebral cortical neurons

1980 ◽  
Vol 58 (6) ◽  
pp. 612-623 ◽  
Author(s):  
J. W. Phillis ◽  
J. R. Kirkpatrick
Keyword(s):  
Cerebral Cortex ◽  
Luteinizing Hormone ◽  
Vasoactive Intestinal Peptide ◽  
Cortical Neurons ◽  
Spontaneous Firing ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Depressant Action ◽  
Cerebral Cortical Neurons ◽  
Excitatory Action

The effects of a number of neuronally localized peptides have been ascertained on corticospinal and other unidentified neurons in the rat cerebral cortex. Motilin, somatostatin, and luteinizing hormone releasing hormone excited most of the corticospinal neurons on which they were tested. Cholecystokinin, Met-enkephalin, vasoactive intestinal peptide, and neurotensin also excited some corticospinal neurons. Many nonidentified neurons were excited by all of these peptides. Met-enkephalin had a depressant action on some (14%) corticospinal neurons. Leu-enkephalin depressed many identified and nonidentified neurons and had an excitatory action on a few neurons. Both excitatory and inhibitory actions of the enkephalins were antagonized by naloxone. Thyrotropin-releasing hormone had predominantly depressant actions on the spontaneous firing of corticospinal and nonidentified neurons but did excite some unidentified cortical neurons. Secretin had no effect on the firing of most of the neurons tested.

Pentobarbital Enhances Cyclic Adenosine Monophosphate Production in the Brain by Effects on Neurons but Not Glia

1996 ◽  
Vol 84 (5) ◽  
pp. 1148-1155 ◽  
Author(s):  
Jerry M. Gonzales ◽  
Iris Mendez-Bobe
Keyword(s):  
Cerebral Cortex ◽  
Cyclic Amp ◽  
Cortical Neurons ◽  
Neuronal Excitability ◽  
Primary Cultures ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Camp Accumulation ◽  
Camp Production ◽  
The Brain

Background Cyclic adenosine monophosphate (cAMP) is an important regulator of neuronal excitability. The effects of barbiturates on cAMP production in intact neurons are not known. This study used cultures of cortical neurons, cultures of glia, and slices of cerebral cortex from the rat to study the effects of barbiturates on cAMP regulation in the brain. Methods Primary cultures of cortical neurons or glia were prepared from 17-day gestational Sprague-Dawley rat fetuses and were used after 12-16 days in culture. Cross-cut slices (300 microns) were prepared from cerebral cortex of adult rats. Cyclic AMP accumulation was determined by measuring the conversion of [3H]adenosine triphosphate (ATP) to [3H]cAMP in cells preloaded with [3H]adenine. Results Pentobarbital enhanced isoproterenol- and forskolin-stimulated, but not basal, cAMP accumulation in cultures of cerebral neurons. Cyclic AMP production was enhanced by pentobarbital in a dose-dependent fashion up to a concentration of 250 microM; This concentration of pentobarbital increased cAMP production by 40-50% relative to that in controls without pentobarbital. At 500 microM pentobarbital, the magnitude of the enhancement was less. Pentobarbital had no effect on isoproterenol-stimulated cAMP production in cultures containing only glia. Pentobarbital also enhanced isoproterenol-stimulated, but not basal, cAMP production in slices of cerebral cortex by approximately 30% at concentrations of 62.5-250 microM and by almost 100% at 500 microM. Conclusions Pentobarbital enhances stimulated cAMP accumulation in cultured preparations from brain and fresh cortical slices. Neurons are required for this effect. Because cAMP modulates neuronal excitability, this effect of pentobarbital may be an important mechanism by which this anesthetic influences brain function.

On the Specificity of Histamine H2-Receptor Antagonists in the Rat Cerebral Cortex

1975 ◽  
Vol 53 (6) ◽  
pp. 1205-1209 ◽  
Author(s):  
J. W. Phillis ◽  
G. K. Kostopoulos ◽  
A. Odutola
Keyword(s):  
Cerebral Cortex ◽  
Cortical Neurons ◽  
Rat Cerebral Cortex ◽  
Receptor Antagonists ◽  
H2 Receptor Antagonists ◽  
Histamine H2 Receptor ◽  
H2 Receptor ◽  
Cerebral Cortical Neurons

The effects of iontophoretically applied histamine H2-receptor antagonists and their antagonism of various amines, acetylcholine (ACh), and adenosine 5′-monophosphate (5′-AMP) were studied on spontaneously active rat cerebral cortical neurons. Metiamide selectively blocked the depressant actions of histamine. Burimamide, in amounts necessary for histamine antagonism, also antagonized the depressant effects of noradrenaline, dopamine, and 5-hydroxytryptamine. Neither antagonist affected 5′-AMP-induced depressions, but both reduced or blocked the excitatory actions of ACh. It is concluded that metiamide may be useful as a reliable antagonist of H2 receptors on cerebral cortical neurons.

scholarly journals Mammalian Brains Are Made of These: A Dataset of the Numbers and Densities of Neuronal and Nonneuronal Cells in the Brain of Glires, Primates, Scandentia, Eulipotyphlans, Afrotherians and Artiodactyls, and Their Relationship with Body Mass

2015 ◽  
Vol 86 (3-4) ◽  
pp. 145-163 ◽  
Author(s):  
Suzana Herculano-Houzel ◽  
Kenneth Catania ◽  
Paul R. Manger ◽  
Jon H. Kaas
Keyword(s):  
Cerebral Cortex ◽  
Body Mass ◽  
Comparative Studies ◽  
Mammalian Species ◽  
Neuronal Cell ◽  
The Body ◽  
Area Of Interest ◽  
Extant Species ◽  
The Brain ◽  
Scaling Rule

Comparative studies amongst extant species are one of the pillars of evolutionary neurobiology. In the 20th century, most comparative studies remained restricted to analyses of brain structure volume and surface areas, besides estimates of neuronal density largely limited to the cerebral cortex. Over the last 10 years, we have amassed data on the numbers of neurons and other cells that compose the entirety of the brain (subdivided into cerebral cortex, cerebellum, and rest of brain) of 39 mammalian species spread over 6 clades, as well as their densities. Here we provide that entire dataset in a format that is readily useful to researchers of any area of interest in the hope that it will foster the advancement of evolutionary and comparative studies well beyond the scope of neuroscience itself. We also reexamine the relationship between numbers of neurons, neuronal densities and body mass, and find that in the rest of brain, but not in the cerebral cortex or cerebellum, there is a single scaling rule that applies to average neuronal cell size, which increases with the linear dimension of the body, even though there is no single scaling rule that relates the number of neurons in the rest of brain to body mass. Thus, larger bodies do not uniformly come with more neurons - but they do fairly uniformly come with larger neurons in the rest of brain, which contains a number of structures directly connected to sources or targets in the body.

scholarly journals Response of the brain to enrichment

2001 ◽  
Vol 73 (2) ◽  
pp. 211-220 ◽  
Author(s):  
MARIAN C. DIAMOND
Keyword(s):  
Cerebral Cortex ◽  
Rat Brain ◽  
Genetic Control ◽  
Cognitive Processing ◽  
Brain Structure ◽  
Environmental Enrichment ◽  
Structural Components ◽  
Policy Makers ◽  
Environmental Input ◽  
The Brain

Before 1960, the brain was considered by scientists to be immutable, subject only to genetic control. In the early sixties, however, investigators were seriously speculating that environmental influences might be capable of altering brain structure. By 1964, two research laboratories proved that the morphology and chemistry or physiology of the brain could be experientially altered (Bennett et al. 1964, Hubel and Wiesel 1965). Since then, the capacity of the brain to respond to environmental input, specifically "enrichment,'' has become an accepted fact among neuroscientists, educators and others. In fact, the demonstration that environmental enrichment can modify structural components of the rat brain at any age altered prevailing presumptions about the brain's plasticity (Diamond et al. 1964, Diamond 1988). The cerebral cortex, the area associated with higher cognitive processing, is more receptive than other parts of the brain to environmental enrichment. The message is clear: Although the brain possesses a relatively constant macrostructural organization, the ever-changing cerebral cortex, with its complex microarchitecture of unknown potential, is powerfully shaped by experiences before birth, during youth and, in fact, throughout life. It is essential to note that enrichment effects on the brain have consequences on behavior. Parents, educators, policy makers, and individuals can all benefit from such knowledge.

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