That Genius in the Brain (Einstein's Brain)

That%Genius%in%the%Brain% Maurizio(De(Pi,à( Department(of(Neurobiology( University(of(Chicago(

Chicago(Cultural(Center( Chicago,(June(16,(2016( To%be%or%not%to%be?% What%to%measure?% Is%it%a%ma4er%of%size?% Our%stonishing%rela:ve…%

EINSTEIN’S BRAIN

Einstein%

Corpus%callosum% Letter to the Editor Brain 2013: Page 5 of 8 | e5 What%age%was%Einstein’s%brain?%%Letter to the Editor Brain 2013: Page 5 of 8 | e5 Downloaded from Downloaded from http://brain.oxfordjournals.org/ http://brain.oxfordjournals.org/

Men(et(al.,(Brain,(2013( at TEL AVIV UNIVERSITY on June 21, 2014 at TEL AVIV UNIVERSITY on June 21, 2014

Figure 4 Distribution maps of corpus callosum thickness between Einstein and the elderly controls. The corpus callosum thickness map of Einstein (top row); maps for old age control group (second row), with the actual measured callosal thicknessFigure on 4 theDistributionleft and the maps registered of corpus callosum thickness between Einstein and the elderly controls. The corpus callosum thickness map of callosal thickness on the right. The corpus callosum thicknesses of Einstein are greater than respectiveEinstein thicknesses (top row in the); maps elderly for controls old age control group (second row), with the actual measured callosal thickness on the left and the registered (third row), as indicated by the actual (left) and registered (right) signiﬁcance maps between Einstein andcallosal the old thickness age control on the groupright (fourth. The corpus callosum thicknesses of Einstein are greater than respective thicknesses in the elderly controls row, P 5 0.05 corrected with FDR). (third row), as indicated by the actual (left) and registered (right) signiﬁcance maps between Einstein and the old age control group (fourth row, P 5 0.05 corrected with FDR).

Einstein’s corpus callosum in the genu is wider than that of both Several in vivo diffusion tensor imaging studies revealed the Einstein’s corpus callosum in the genu is wider than that of both Several in vivo diffusion tensor imaging studies revealed the the control groups (Fig. 3F). connectivity of cortical regions between hemispheres through the control groups (Fig. 3F). connectivity of cortical regions between hemispheres through The corpus callosum is the largest bundle of white matter neural the corpus callosum (Hofer and Frahm, 2006; Park et al., 2008; The corpus callosum is the largest bundle of white matter neural the corpus callosum (Hofer and Frahm, 2006; Park et al., 2008; fibres in the brain that connects the interhemispheric cortices, and Chao et al., 2009). The fibres that pass through the callosal ros- fibres in the brain that connects the interhemispheric cortices, and Chao et al., 2009). The fibres that pass through the callosal ros- it may be involved in any neuroanatomical substrate of hemi- trum and genu appear to connect the interhemispheric regions of it may be involved in any neuroanatomical substrate of hemi- trum and genu appear to connect the interhemispheric regions of sphere specialization (Witelson, 1989). Underlying assumptions orbital gyri and prefrontal cortices corresponding with the left and sphere specialization (Witelson, 1989). Underlying assumptions orbital gyri and prefrontal cortices corresponding with the left and of this research are that an increased callosal area indicates an right Brodmann areas 11/10, which are involved in planning, rea- of this research are that an increased callosal area indicates an right Brodmann areas 11/10, which are involved in planning, rea- increased total number of fibres crossing through the corpus cal- soning, decision-making, memory retrieval and executive function. increased total number of fibres crossing through the corpus cal- soning, decision-making, memory retrieval and executive function. losum and that post-mortem shrinkage of the corpus callosum is According to Aboitiz et al.(1992, 2003), thin fibres are denser in losum and that post-mortem shrinkage of the corpus callosum is According to Aboitiz et al.(1992, 2003), thin fibres are denser in uniform across its subregions (Aboitiz et al., 1992, 2003). We these rostral and genu regions of the corpus callosum compared to uniform across its subregions (Aboitiz et al., 1992, 2003). We these rostral and genu regions of the corpus callosum compared to therefore focused on the corpus callosum thickness which indi- its midbody and some of the caudal regions, and are involved in therefore focused on the corpus callosum thickness which indi- its midbody and some of the caudal regions, and are involved in cates the fibres crossing through the regional callosal cross-section transfer of cognitive information. Einstein’s callosum is thicker and cates the fibres crossing through the regional callosal cross-section transfer of cognitive information. Einstein’s callosum is thicker and area, rather than on the 3D volume of the corpus callosum, which greater than those of young controls in the rostrum and genu, area, rather than on the 3D volume of the corpus callosum, which greater than those of young controls in the rostrum and genu, would be impossible to measure in Einstein’s brain. which suggests that the orbital gyri and prefrontal cortices may would be impossible to measure in Einstein’s brain. which suggests that the orbital gyri and prefrontal cortices may The%Neuron(s)% It%is%a%ma4er%of…%colors%

NEURONS+GLIA%

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210 1906 C.GOLGI

NEURON DOCTRINE: THEORY AND FACTS 211

i.e. of supposed paths of conduction, and state that the fibrils may pass directly from one protoplasmic process to another without forming any sort of con- nection with the interior of nerve cells, while Donaggio tries to prove that fibrilsCamillo penetrate to the(Golgi( inside of the cells and that the cell body has an ex- tremely complicated and fine reticular arrangement around the nucleus. San`ago(Ramon(y(Cajal( (1843[1926)( (1852[1934)( Fig.13

Fig.14 Fig.15 After the work which I have just briefly quoted comes that of Bethe and of Donaggio, who have demonstrated the exquisite fibrillar structure of nerve cells. Using similar methods, based on the use of a mordant before applying the stain, these two last authors have achieved results which are essentially in agreement with each other. However, Bethe’s studies aim at emphasizing the independence of fibrils,

Fig.16 Neuronal%Electrical%Pulses%%

40 Electrophysiology of Neurons

Alan(Lloyd(Hodgkin( Andrew(Huxley( (1914[1988)( (1917[2012)(

Figure 2.14: Studies of spike-generation mechanism in “giant squid axons” won Alan I( Hodgkin and Andrew Huxley the 1963 Nobel prize in physiology or medicine (shared V( with Sir John Eccles); see also Fig. 4.1 in Keener and Sneyd (1998).

The rest state is stable: A small pulse of current applied via I(t) produces a small positive perturbation of the membrane potential (depolarization), which results in a small net current that drives V back to rest (repolarization). However, an intermediate size pulse of current produces a perturbation that is amplified significantly because membrane conductances depend on V . Such a non-linear amplification causes V to deviate considerably from Vrest – a phenomenon referred to as an action potential or spike. In Fig. 2.15 we show a typical time course of an action potential in the Hodgkin- Huxley system. Strong depolarization increases activation variables m and n and de- creases inactivation variable h. Since m(V ) is relatively small, variable m is relatively + fast. Fast activation of Na conductance drives V toward ENa resulting in further depolarization and further activation of gNa. This positive feedback loop, depicted in Fig. 2.16 results in the upstroke of V . While V moves toward ENa, the slower gating variables catch up. Variable h 0 causing inactivation of Na+ current, and variable n 1 causing slow activation of outward K+ current. The latter and the leak current repolarize the membrane potential toward Vrest.

When V is near Vrest, the voltage-sensitive time constants n(V ) and h(V )are relatively large, as one can see in Fig. 2.13. Therefore, recovery of variables n and h is slow. In particular, outward K+ current continues to be activated (n is large) even after the action potential downstroke, thereby causing V to go below Vrest toward EK – a phenomenon known as afterhyperpolarization. In addition, Na+ current continues to be inactivated (h is small) and not available for any regenerative function. The Hodgkin-Huxley system cannot generate another action potential during this absolute refractory period. While the current deinactivates, Glia:%the%brain’s%“glue”% Astrocytes:%Glia%Rediscovered%%

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