Elongation of the CA1 field of the septal hippocampus in ungulates

Abstract

It is widely assumed that the hippocampal formation seen in laboratory rodents and in primates is typical of that seen in other mammals. We have tested this assumption by examining sections of brains of 56 mammals from 20 mammalian orders from images on the http://brainmuseum.org website. We found wide variation in the form of the hippocampal formation, the most extreme examples of which are seen in ungulates, which possess an unusual elongation of the distal CA1 of the septal hippocampus. This phenomenon has not previously been reported. In individual coronal sections of the brains of seven artiodactyl ungulates, the pyramidal layer of CA1 is four times as long as CA2 + CA3. In a perissodactyl ungulate (Burchell's zebra) the distal end of CA1 is so large that it forms a number of folds. A similar but less pronounced CA1 elongation was seen in the brains of 14 carnivores. A modest elongation of CA1 is also present in some other placental mammals, notably the elephant shrew, hyrax, capybara, beaver, and rabbit. The elongation was not present in brains of primates, marsupials, or monotremes. The distal part of CA1 has been shown to play a role in object integration into the spatial map. We hypothesize that the distal CA1 enlargement could serve to enhance the ability to integrate objects into spatial navigation, which would be an advantage for migrating herds of ungulates. We suggest that the remarkable elongation of Q5 CA1 represents a major evolutionary specialization in the ungulates.

Further refining the boundaries of the hippocampus CA2 with gene expression and connectivity: Potential subregions and heterogeneous cell types

“…The lack of distinguishable characteristics in Nissl cytoarchitecture led some authors to be unable to determine if the CA2 exists within that species (Buhl & Dann, 1991). Possibly, the ‘bump’ in CA2 may be more related to the thicknesses of the adjacent CA3 and CA1 pyramidal layer which can vary significantly across species (Slomianka et al, 2011; Watson & Binks, 2019).…”

“…In rodent coronal sections, the classic CA2 region is most notable due to a ‘bump’ in the pyramidal layer, although the exact CA2 boundaries around this landmark are not easily distinguishable based on cytoarchitecture. Furthermore, while this ‘bump’ is present in other mammals (Keuker et al, 2003), there are many other species which do not contain this landmark (Buhl & Dann, 1991; Mustapha et al, 2019; Wang & Barbas, 2018; Watson & Binks, 2019) (for comparison, Nissl stained tissue series from numerous animal species can be found online at http://www.brainmuseum.org and http://www.brainmaps.org, see Figure 2). The lack of distinguishable characteristics in Nissl cytoarchitecture led some authors to be unable to determine if the CA2 exists within that species (Buhl & Dann, 1991).…”

“…The lack of distinguishable characteristics in Nissl cytoarchitecture led some authors to be unable to determine if the CA2 exists within that species (Buhl & Dann, 1991). Possibly, the 'bump' in CA2 may be more related to the thicknesses of the adjacent CA3 and CA1 pyramidal layer which can vary significantly across species (Slomianka et al, 2011;Watson & Binks, 2019). CA2-specific gene expression provides a way to more easily distinguish anatomical CA2 boundaries compared to cytoarchitecture alone and experiments targeting CA2 using viral vector-based strategies and differential gene expression in CA2 has been reported in multiple species (Dudek et al, 2016).…”

Clade-specific forebrain cytoarchitectures of the extinct Tasmanian tiger

“…5 D , arrow). The length of the CA1 has been proposed as an evolutionary adaptation linked to navigation and migration and is on average 3.1 times longer than the CA2 + CA3 in ungulates, and 2.6 times in carnivores ( 45 ). The thylacine displays a CA1/(CA2 + 3) ratio of 1 ( Fig.…”

Behavior of KCNQ Channels in Neural Plasticity and Motor Disorders

“…The discovery of this behavior has led to a growing body of literature on potential therapeutic applications in Alzheimer’s Disease due to its nature as a cholinergic deficiency-related cognitive impairment [ 66 , 67 ]. In addition, the inhibition of KCNQ channels via linopirdine is also well-established in enhancing cognition via increased ACh release [ 63 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 ].…”