The evolution of brains from early mammals to humans

Kaas, Jon H.

doi:10.1002/wcs.1206

Cited by 211 publications

(173 citation statements)

References 85 publications

(184 reference statements)

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“…The Ac, MGN, and IC are closely related functionally, as the large central nucleus of the IC provides driving activation to the large principal (ventral) subnucleus of the MGN, which in turn activates the auditory core cortex [Kaas andHackett, 2000, 2008]. Such close functional correspondence may result in similar scaling relationships between these two subcortical structures and the Ac, a notion that our results support.…”

Section: Discussionsupporting

confidence: 68%

Faster Scaling of Auditory Neurons in Cortical Areas Relative to Subcortical Structures in Primate Brains

Wong

Peebles²,

Asplund³

et al. 2013

Brain Behav Evol

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Allometric studies in primates have shown that the cerebral cortex, cerebellum, and remaining brain structures increase in size as a linear function of their numbers of neurons and nonneuronal cells across primates. Whether such scaling rules also apply to functionally related structures such as those of the auditory system is unknown. Here, we investigate the scaling of brain structures in the auditory pathway of six primate species and the closely related tree shrew. Using the isotropic fractionator method to estimate the numbers of neurons and nonneuronal cells in the inferior colliculus, medial geniculate nucleus, and auditory cortex (Ac), we assessed how they scaled across species and examined the relative scaling relationships among them. As expected, each auditory structure scales in mass as a linear function of its number of neurons, with no significant changes in neuronal density across species. The Ac scales proportionately with the cerebral cortex as a whole, maintaining a relative mass of approximately 1% and a relative number of neurons of 0.7%. However, the Ac gains neurons faster than both subcortical structures examined. As a result, larger primate brains have increased ratios of cortical to subcortical neurons involved in processing auditory information.

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Section: Discussionsupporting

confidence: 68%

Faster Scaling of Auditory Neurons in Cortical Areas Relative to Subcortical Structures in Primate Brains

Wong

Peebles²,

Asplund³

et al. 2013

Brain Behav Evol

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“…Mounting evidence from experimental animals supports the idea that homeostasis is mediated by ascending and descending interconnections between brainstem nuclei and forebrain regions, which together regulate autonomic, respiratory, and arousal responses to stress (Azmitia and Gannon, 1986;Feldman et al, 2013;Harper, 1986;Vertes, 1984a,b). While the limbic lobe/system was historically regarded as the neuroanatomic substrate of emotion (Barger et al, 2014;Kaas, 2013), its role in the regulation of homeostasis has been increasingly recognized, and the originally defined sites have been encompassed in the central autonomic network (Beissner et al, 2013;Benarroch, 1993;Mraovitch and Calando, 1999;Saper, 2002), or ''flight or fight'' system (Nicolaides et al, 2015; Ulrich-Lai and Herman, 2009). In this study, we provide initial evidence for connectivity between forebrain and caudal brainstem regions that participate in the regulation of homeostasis in the human brain.…”

Section: Human Central Homeostatic Network 195 Discussionmentioning

confidence: 99%

“…Yet despite emerging evidence for brainstem-forebrain interactions in regulating homeostasis, little direct information about the neuroanatomic connections between homeostatic regions of the brainstem and forebrain is available in the human brain. Current knowledge is based almost solely upon extrapolations from animal studies (Barger et al, 2014;Kaas, 2013), which are inherently limited due to major species differences in limbic anatomy. Temporal lobes, for example, occur only in primates and are most fully developed in humans (Barger et al, 2014;Kaas, 2013).…”

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confidence: 99%

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The Structural Connectome of the Human Central Homeostatic Network

et al. 2016

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Homeostatic adaptations to stress are regulated by interactions between the brainstem and regions of the forebrain, including limbic sites related to respiratory, autonomic, affective, and cognitive processing. Neuroanatomic connections between these homeostatic regions, however, have not been thoroughly identified in the human brain. In this study, we perform diffusion spectrum imaging tractography using the MGH-USC Connectome MRI scanner to visualize structural connections in the human brain linking autonomic and cardiorespiratory nuclei in the midbrain, pons, and medulla oblongata with forebrain sites critical to homeostatic control. Probabilistic tractography analyses in six healthy adults revealed connections between six brainstem nuclei and seven forebrain regions, several over long distances between the caudal medulla and cerebral cortex. The strongest evidence for brainstem-homeostatic forebrain connectivity in this study was between the brainstem midline raphe and the medial temporal lobe. The subiculum and amygdala were the sampled forebrain nodes with the most extensive brainstem connections. Within the human brainstem-homeostatic forebrain connectome, we observed that a lateral forebrain bundle, whose connectivity is distinct from that of rodents and nonhuman primates, is the primary conduit for connections between the brainstem and medial temporal lobe. This study supports the concept that interconnected brainstem and forebrain nodes form an integrated central homeostatic network (CHN) in the human brain. Our findings provide an initial foundation for elucidating the neuroanatomic basis of homeostasis in the normal human brain, as well as for mapping CHN disconnections in patients with disorders of homeostasis, including sudden and unexpected death, and epilepsy.

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“…Cortical size expansion and the increase in cortical neuronal number suggest that regulation of neurogenesis has changed over evolution (48,49). The mathematical model of cortical neurogenesis we developed provided insights on how the timing of different phases in neurogenesis affect the size and composition of the cortex.…”

Section: Discussionmentioning

confidence: 99%

Lhx2 regulates the timing of β-catenin-dependent cortical neurogenesis

Hsu

Nam

Cui

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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The timing of cortical neurogenesis has a major effect on the size and organization of the mature cortex. The deletion of the LIMhomeodomain transcription factor Lhx2 in cortical progenitors by Nestin-cre leads to a dramatically smaller cortex. Here we report that Lhx2 regulates the cortex size by maintaining the cortical progenitor proliferation and delaying the initiation of neurogenesis. The loss of Lhx2 in cortical progenitors results in precocious radial glia differentiation and a temporal shift of cortical neurogenesis. We further investigated the underlying mechanisms at play and demonstrated that in the absence of Lhx2, the Wnt/β-catenin pathway failed to maintain progenitor proliferation. We developed and applied a mathematical model that reveals how precocious neurogenesis affected cortical surface and thickness. Thus, we concluded that Lhx2 is required for β-catenin function in maintaining cortical progenitor proliferation and controls the timing of cortical neurogenesis.cortical neurogenesis | Lhx2 | β-catenin U nderstanding how genetic mechanisms interact to set up a precise developmental timing is a fundamental issue in biology. In the cerebral cortex, excitatory neurons are generated by progenitor cells in the dorsal telencephalon (dTel) lining the lateral ventricle. During the early developmental stages, cortical progenitors undergo symmetric divisions, resulting in the proliferation of progenitors and thereby allowing expansion of the developing cortex. Soon after, cortical progenitors start generating distinct types of neurons through asymmetric differentiative divisions (1-5). The precise timing of the switch from proliferative division to differentiative division is crucial to determining the number of cortical neurons, and thus the cortical size.The switch from proliferation to differentiation is reportedly regulated by the canonical Wnt signaling pathway, in which β-catenin (β-Cat) is the major downstream effector. In the absence of Wnt signaling, β-Cat is phosphorylated by glycogen synthase kinase 3 and targeted for proteosome degradation. Once Wnt ligands bind to the Frizzled-Lrp5/6 receptors, the activity of glycogen synthase kinase 3-Axin-APC (adenomatous polyposis coli) destruction complex is inhibited. As a consequence, β-Cat accumulates in the cytoplasm, translocates to the nucleus, and activates downstream gene transcription together with the lymphoid enhancer-binding factor (LEF)/ T-cell factor (TCF) transcription factors (6). Overexpression of the stabilized, N-terminally truncated form of β-Cat in cortical progenitors during early neurogenesis promotes their overproliferation (7,8), whereas inactivation of β-Cat in the cortex promotes neurogenesis (9, 10). However, stabilized β-Cat was also shown to promote cortical progenitor differentiation (11). Thus, it has been proposed that Wnt/β-Cat signaling promotes proliferation and differentiation of cortical progenitors at early and late developmental stages, respectively (12). This raises the essential and largely open question of ho...

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The evolution of brains from early mammals to humans

Cited by 211 publications

References 85 publications

Faster Scaling of Auditory Neurons in Cortical Areas Relative to Subcortical Structures in Primate Brains

Faster Scaling of Auditory Neurons in Cortical Areas Relative to Subcortical Structures in Primate Brains

The Structural Connectome of the Human Central Homeostatic Network

Lhx2 regulates the timing of β-catenin-dependent cortical neurogenesis

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