Equal Numbers of Neuronal and Nonneuronal Cells Make the Human Brain an Isometrically Scaled-Up Primate Brain

Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Brazil.
The Journal of Comparative Neurology (Impact Factor: 3.23). 04/2009; 513(5):532-41. DOI: 10.1002/cne.21974
Source: PubMed


The human brain is often considered to be the most cognitively capable among mammalian brains and to be much larger than expected for a mammal of our body size. Although the number of neurons is generally assumed to be a determinant of computational power, and despite the widespread quotes that the human brain contains 100 billion neurons and ten times more glial cells, the absolute number of neurons and glial cells in the human brain remains unknown. Here we determine these numbers by using the isotropic fractionator and compare them with the expected values for a human-sized primate. We find that the adult male human brain contains on average 86.1 +/- 8.1 billion NeuN-positive cells ("neurons") and 84.6 +/- 9.8 billion NeuN-negative ("nonneuronal") cells. With only 19% of all neurons located in the cerebral cortex, greater cortical size (representing 82% of total brain mass) in humans compared with other primates does not reflect an increased relative number of cortical neurons. The ratios between glial cells and neurons in the human brain structures are similar to those found in other primates, and their numbers of cells match those expected for a primate of human proportions. These findings challenge the common view that humans stand out from other primates in their brain composition and indicate that, with regard to numbers of neuronal and nonneuronal cells, the human brain is an isometrically scaled-up primate brain.

Download full-text


Available from: Lea Tenenholz Grinberg, Oct 05, 2015
546 Reads
  • Source
    • "Frontiers in Cellular Neuroscience | 1 July 2015 | that regulate the dynamics between stability and plasticity . With some 86 – 100 billion neurons and an approximately equalor larger number of glial cells , depending upon the brain region ( Azevedo et al., 2009), the study of the brain has been likened to the quest for understanding the universe , with multiple cellular and molecular interactions that account for brain plasticity . Yet many key mechanisms underlying synaptic plasticity are found not in these brain cells themselves but in their interactions with molecules in the extracellular space surrounding them ( reviewed by Ruoslahti , 1996a , b ; Nicholson and Sykova , 1998 ; Shi and Ethell , 2006 ; Šišková et al . "
    [Show abstract] [Hide abstract]
    ABSTRACT: The extracellular matrix (ECM) is a critical regulator of neural network development and plasticity. As neuronal circuits develop, the ECM stabilizes synaptic contacts, while its cleavage has both permissive and active roles in the regulation of plasticity. Matrix metalloproteinase 9 (MMP-9) is a member of a large family of zinc-dependent endopeptidases that can cleave ECM and several cell surface receptors allowing for synaptic and circuit level reorganization. It is becoming increasingly clear that the regulated activity of MMP-9 is critical for central nervous system (CNS) development. In particular, MMP-9 has a role in the development of sensory circuits during early postnatal periods, called 'critical periods.' MMP-9 can regulate sensory-mediated, local circuit reorganization through its ability to control synaptogenesis, axonal pathfinding and myelination. Although activity-dependent activation of MMP-9 at specific synapses plays an important role in multiple plasticity mechanisms throughout the CNS, misregulated activation of the enzyme is implicated in a number of neurodegenerative disorders, including traumatic brain injury, multiple sclerosis, and Alzheimer's disease. Growing evidence also suggests a role for MMP-9 in the pathophysiology of neurodevelopmental disorders including Fragile X Syndrome. This review outlines the various actions of MMP-9 during postnatal brain development, critical for future studies exploring novel therapeutic strategies for neurodevelopmental disorders.
    Frontiers in Cellular Neuroscience 07/2015; 9:280. DOI:10.3389/fncel.2015.00280 · 4.29 Impact Factor
    • "N CX , number of neurons in the cerebral cortex of both hemispheres; N M1 , number of neurons in area M1 of both hemispheres; N SC , total number of neurons in the spinal cord; N ROB , total number of neurons in the rest of brain (ensemble of diencephalon, striatum, mesencephalon, pons, and medulla); N M1 /N SC , ratio between numbers of neurons in M1 and spinal cord. (1) Values observed by Gabi et al. (2010); (2) values observed by Herculano-Houzel et al. (2007); (3) values predicted by Herculano- Houzel and Kaas (2011); (4) values observed by Azevedo et al. (2009); (5) values observed by Young et al. (2013); (6) values observed by Burish et al. (2010); (pred), values predicted as follows. pred 1 , value predicted from the equation for N CX 3 M CX in Table 1 using M CX of 252 g (Semendeferi and Damasio, 2000); pred 2 , values predicted from N CX in this table using the estimated 2.4% of cortical neurons in M1; pred 3 , value predicted from the equation for N SC 3 M SC in Table 1 using M SC of 13.231 g (MacLarnon, 1996); pred 4 , value predicted from the equation for N SC 3 M SC in Table 1 using M SC of 16.853 g (MacLarnon, 1996); pred 5 , value predicted from the equation for N SC 3 M SC in Table 1 using M SC of 29.700 g (MacLarnon, 1996). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Control over spinal and brainstem somatomotor neurons is exerted by two sets of descending fibers: corticospinal/pyramidal and extrapyramidal. While in nonhuman primates the effect of bilateral pyramidal lesions is mostly limited to an impairment of the independent use of digits in skilled manual actions, similar injuries in humans result in the locked-in syndrome, a state of mutism and quadriplegia in which communication can only be established by residual vertical eye movements. This behavioral contrast makes humans appear to be outliers compared to other primates because of our almost total dependence on the corticospinal/pyramidal system for the effectuation of movement. Here we propose, instead, that an increasing preponderance of the corticospinal/pyramidal system over motor control is an expected consequence of increasing brain size in primates due to the faster scaling of the number of neurons in the primary motor cortex over the brainstem and spinal cord motor neuron pools, thus explaining the apparent uniqueness of the corticalization of motor control in man. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    The Journal of Comparative Neurology 04/2015; DOI:10.1002/cne.23792 · 3.23 Impact Factor
  • Source
    • "The brain fits these properties well. In fact, it is constituted by about 86 billion neural cells and by a similar number of non-neural cells (Azevedo et al., 2009). All these constituents interact to form short-range and long-range mutual connections, resulting in an interplay between segregation and integration at different hierarchical spatial and temporal scales. "
    [Show abstract] [Hide abstract]
    ABSTRACT: To test the hypothesis that brain activity is modulated by trait social anxiety, we measured the Hurst Exponent (HE), an index of complexity in time series, in healthy individuals at rest in the absence of any social trigger. Functional magnetic resonance imaging (fMRI) time series were recorded in 36 subjects at rest. All volunteers were healthy without any psychiatric, medical or neurological disorder. Subjects completed the Liebowitz Social Anxiety Scale (LSAS) and the Brief Fear of Negative Evaluation (BFNE) to assess social anxiety and thoughts in social contexts. We also obtained the fractional Amplitude of Low Frequency Fluctuations (fALFF) of the BOLD signal as an independent control measure for HE data. BFNE scores correlated positively with HE in the posterior cingulate/precuneus, while LSAS scores correlated positively with HE in the precuneus, in the inferior parietal sulci and in the parahippocamus. Results from fALFF were highly consistent with those obtained using LSAS and BFNE to predict HE. Overall our data indicate that spontaneous brain activity is influenced by the degree of social anxiety, on a continuum and in the absence of social stimuli. These findings suggest that social anxiety is a trait characteristic that shapes brain activity and predisposes to different reactions in social contexts. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Psychiatry Research: Neuroimaging 03/2015; 232(2). DOI:10.1016/j.pscychresns.2015.03.005 · 2.42 Impact Factor
Show more