# Mixed Signals and Interspecies Variation in the Plasticity of Adult Mammal Brains

**Authors:** Alessia Pattaro, Marco Ghibaudi, Alessandro Zanone, Valentina Cerrato, Chet C. Sherwood, Luca Bonfanti

PMC · DOI: 10.3390/cells15060520 · Cells · 2026-03-13

## TL;DR

This paper explores how brain plasticity varies across mammalian species, highlighting evolutionary trade-offs and the complexity of interpreting findings due to interspecies differences.

## Contribution

The paper introduces the concept of evolutionary trade-offs in brain plasticity and highlights the role of immature neurons in explaining conflicting results.

## Key findings

- Adult neurogenesis decreases in large-brained mammals compared to small-brained species.
- Immature neurons are more prevalent in the neocortex and amygdala of larger-brained mammals.
- Evolutionary pressures have shaped distinct plastic processes across species.

## Abstract

Increased understanding of brain structural plasticity in mammals has led to increasing conceptual complexity and conflicting results in the field.The growing recognition of interspecies variation in neuroplasticity, from mice to humans, and the overlapping of cell markers in different cell populations are the main elements of confusion.Some cell types, cell markers, and biological processes markedly differ among species due to the non-linear sculpting that took place during evolution, including trade-offs in plasticity.The discovery of non-dividing, immature (late-maturing) neurons has increased the heterogeneity in brain plasticity and can explain some controversial findings.Understanding how brain structural plasticity has adapted to diverse mammalian neuroanatomies is essential for meaningful translational research.

Increased understanding of brain structural plasticity in mammals has led to increasing conceptual complexity and conflicting results in the field.

The growing recognition of interspecies variation in neuroplasticity, from mice to humans, and the overlapping of cell markers in different cell populations are the main elements of confusion.

Some cell types, cell markers, and biological processes markedly differ among species due to the non-linear sculpting that took place during evolution, including trade-offs in plasticity.

The discovery of non-dividing, immature (late-maturing) neurons has increased the heterogeneity in brain plasticity and can explain some controversial findings.

Understanding how brain structural plasticity has adapted to diverse mammalian neuroanatomies is essential for meaningful translational research.

Despite the growing interest in brain structural plasticity and the substantial body of knowledge that has accumulated over recent decades, some issues remain poorly defined, leading to confusion in the interpretation of results. In addition to stem cell-driven neurogenesis in adult neurogenic niches (adult neurogenesis), neuronal precursors in a state of arrested maturation have also been described, representing a form of neurogenesis without division based on so-called “immature” or late-maturing neurons. These processes occur in different brain regions yet share certain molecular markers and temporal windows. Recent advances in comparative neuroplasticity have further complicated our understanding. Studies reveal a reduction in adult neurogenesis in the olfactory bulb and hippocampus of large-brained, gyrencephalic mammals compared with small-brained species such as rodents. Conversely, a higher prevalence of immature neurons has been reported in the neocortex and amygdala of larger-brained mammals. It is becoming evident that evolutionary trade-offs took place in distinct plastic processes, resulting in the predominance of certain forms in particular species, while others coexist and share overlapping markers. Regardless of the approach employed (neuroanatomical, immunocytochemical, phylogenetic, or transcriptional), current evidence indicates substantial heterogeneity in cell types with different origins and fates across diverse mammalian species. These patterns appear to be sculpted by evolutionary pressures yet unified by shared transient maturational states.

## Linked entities

- **Species:** Mus musculus (taxon 10090), Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** NCAM1 (neural cell adhesion molecule 1) [NCBI Gene 4684] {aka CD56, MSK39, NCAM}, FGFR1 (fibroblast growth factor receptor 1) [NCBI Gene 2260] {aka BFGFR, CD331, CEK, ECCL, FGFBR, FGFR-1}, Pax2 [NCBI Gene 100347596], CALB2 (calbindin 2) [NCBI Gene 794] {aka CAB29, CAL2, CR}, ETNPPL (ethanolamine-phosphate phospho-lyase) [NCBI Gene 64850] {aka AGXT2L1}, SNAP25 (synaptosome associated protein 25) [NCBI Gene 6616] {aka CMS18, DEE117, RIC-4, RIC4, SEC9, SNAP}, Dcx (doublecortin) [NCBI Gene 13193] {aka Dbct}, NEUROD4 (neuronal differentiation 4) [NCBI Gene 58158] {aka ATH-3, ATH3, Atoh3, MATH-3, MATH3, bHLHa4}, DSCAML1 (DS cell adhesion molecule like 1) [NCBI Gene 57453] {aka DSCAM2}, STMN2 (stathmin 2) [NCBI Gene 11075] {aka SCG10, SCGN10}, DCX (doublecortin) [NCBI Gene 1641] {aka DBCN, DC, LISX, SCLH, XLIS}, DCX [NCBI Gene 100349534], ARC (activity regulated cytoskeleton associated protein) [NCBI Gene 23237] {aka Arg3.1, hArc}, NFIA (nuclear factor I A) [NCBI Gene 4774] {aka BRMUTD, C1DELp32p31, CTF, DEL1P32P31, NF-I/A, NF1-A}, RBFOX3 (RNA binding fox-1 homolog 3) [NCBI Gene 146713] {aka FOX-3, FOX3, HRNBP3, NEUN}, STMN1 (stathmin 1) [NCBI Gene 3925] {aka C1orf215, LAP18, Lag, OP18, PP17, PP19}, COL25A1 (collagen type XXV alpha 1 chain) [NCBI Gene 84570] {aka AMY, CFEOM5, CLAC, CLAC-P, CLACP}, Mapk3 (mitogen-activated protein kinase 3) [NCBI Gene 26417] {aka Erk-1, Erk1, Ert2, Esrk1, Mnk1, Mtap2k}, FNBP1L (formin binding protein 1 like) [NCBI Gene 54874] {aka C1orf39, TOCA1}, MAPK3 (mitogen-activated protein kinase 3) [NCBI Gene 5595] {aka ERK-1, ERK1, ERT2, HS44KDAP, HUMKER1A, P44ERK1}, SEMA3A (semaphorin 3A) [NCBI Gene 10371] {aka COLL1, HH16, Hsema-I, Hsema-III, SEMA1, SEMAD}, LPAR1 (lysophosphatidic acid receptor 1) [NCBI Gene 1902] {aka EDG2, Gpcr26, LPA1, Mrec1.3, VZG1, edg-2}, DPYSL5 (dihydropyrimidinase like 5) [NCBI Gene 56896] {aka CRAM, CRMP-5, CRMP5, CV2, RTSC4, Ulip6}, PROX1 (prospero homeobox 1) [NCBI Gene 5629], PLAG1 (PLAG1 zinc finger) [NCBI Gene 5324] {aka PSA, SGPA, SRS4, ZNF912}, NRP2 (neuropilin 2) [NCBI Gene 8828] {aka NP2, NPN2, PRO2714, VEGF165R2}
- **Diseases:** inflammation (MESH:D007249), neurological disorders (MESH:D009461), Alzheimer's disease (MESH:D000544), nerve tissue lesion (MESH:D009380), confusion (MESH:D003221), dementia (MESH:D003704), ischemia (MESH:D007511), pain (MESH:D010146), excitotoxic lesion (MESH:D009059), stroke (MESH:D020521), injury to (MESH:D014947)
- **Chemicals:** 5'-bromo-2'-deoxyuridine (MESH:D001973)
- **Species:** Sus scrofa (pig, species) [taxon 9823], Elephantidae (elephants, family) [taxon 9780], Equus caballus (domestic horse, species) [taxon 9796], Oryctolagus cuniculus (domestic rabbit, species) [taxon 9986], Delphinidae (marine dolphins, family) [taxon 9726], Rattus norvegicus (brown rat, species) [taxon 10116], Callitrichinae sp. (species) [taxon 38020], Cetacea (cetaceans, infraorder) [taxon 9721], Canis lupus familiaris (dog, subspecies) [taxon 9615], Delphinus delphis (Black Sea dolphin, species) [taxon 9728], Ovis aries (domestic sheep, species) [taxon 9940], Pan troglodytes (chimpanzee, species) [taxon 9598], Cavia porcellus (domestic guinea pig, species) [taxon 10141], Homo sapiens (human, species) [taxon 9606], Macaca (macaque, genus) [taxon 9539], Mus musculus (house mouse, species) [taxon 10090]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13024822/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13024822/full.md

## References

186 references — full list in the complete paper: https://tomesphere.com/paper/PMC13024822/full.md

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Source: https://tomesphere.com/paper/PMC13024822