The influence of James and Darwin on Cajal and his research into the neuron theory and evolution of the nervous system

Abstract

In this article we discuss the influence of William James and Charles Darwin on the thoughts of Santiago Ramón y Cajal concerning the structure, plasticity, and evolution of the nervous system at the cellular level. Here we develop Cajal’s notion that neuronal theory is a necessary condition to explain the plasticity of neural connections. Although the roots of the term “plasticity” in reference to neuroscience are not completely clear, Cajal was an important figure in the propagation and popularization of its use. It is true that he carried out a large number of studies throughout his career in favor of the neuronal theory, but perhaps one of the most interesting aspects of his studies was his innovative capacity to interpret structure as being the result of evolutionary mechanisms, i.e., natural selection. This capacity would ultimately lead Cajal to the conclusion that, in relation to the histology of the nervous system, such selection occurs in the establishment of connections between cells. The present article is divided into five sections: (1) Learning and general notions of organic plasticity in the 19th century; (2) The idea of “mental” plasticity proposed by James; (3) Neuronal theory and “structural” plasticity: general considerations; (4) Evolutionary factors of the nervous system in Cajal’s work; and (5) Final considerations.

Assessing segmental versus non-segmental features in the ventral nervous system of onychophorans (velvet worms)

“…For neuronal staining, adult specimens were anaesthetised in chloroform vapour for 10–20 s and cut open longitudinally along the dorsal side using fine scissors as described previously [18]. The ventral nerve cords were dissected in physiological saline [84] and pinned down with tungsten needles in small Petri dishes coated with Sylgard® (184 Silicone Elastomer Kit, DowCorning GmbH, Wiesbaden, Germany).…”

Dendritic spine dysgenesis in autism related disorders

“…Mouse models of RTT are widely used and recapitulate many of the behavioral and anatomical abnormalities associated with the human disorder [111, 112] and additionally show impairments in both LTP and LTD [113, 114]. Commonly used strains of Mecp2 KO mice have impaired dendritic complexity [115, 116] and lower dendritic spine density [117–120] as well as a lack of mushroom spines in cortical and hippocampal neurons [121, 122].…”

“…Potential mechanisms include enhanced hippocampal network activity promoting dendritic spine formation [123], deranged homeostatic plasticity stimulating spinogenesis while affecting pyramidal neuron function [124, 125], or lack of developmental synaptic pruning. Among the many genes regulated by MeCP2, brain derived neurotrophic factor (BDNF) may be the most prominent in RTT spine dysgenesis due to its role in neuronal growth, synapse formation and activity-dependent plasticity through the activation of tropomyosin-related kinase B(TrkB) receptors [100, 126–129] and has been shown to be lowered in RTT [112, 130–132]. Additionally, mutations in MeCP2 lead to lower expression of mGluR [133].…”

Persistent cognitive and morphological alterations induced by repeated exposure of adolescent rats to the abused inhalant toluene

“…The present findings add to these data by showing that protracted abstinence from toluene exposure (7 weeks) is associated with increases in long-thin spines in the NAc. The effect of drugs of abuse on spine morphology is variable, presumably due to different mechanisms of action, differences in drug treatment (chronic vs acute), and time of measurement (no abstinence vs hours or weeks; for review see: Mulholland, Chandler, & Kalivas, 2016; Spiga et al, 2014). Similar to toluene, chronic treatment with cocaine (Rasakham et al, 2014), alcohol (Peterson, McCool, & Hamilton, 2015), and nicotine (Gipson et al, 2013) causes selective and persistent enhancements in the NAc dendritic spine morphology.…”

“…The postsynaptic dendritic spine is a key component of this neuroplasticity, with long-thin immature spines giving way to mushroom-headed spines over the course of excitatory synaptic growth (Holtmaat et al, 2006). While nearly every drug of abuse examined to date alters dendritic spine morphology in the mPFC and NAc (Mulholland, Chandler, & Kalivas, 2016; Spiga et al, 2014), it is not known whether similar changes occur following toluene exposure.…”