Dual-Component Structural Plasticity Mediated by αCaMKII Autophosphorylation on Basal Dendrites of Cortical Layer 2/3 Neurones

Abstract

Sensory cortex exhibits receptive field plasticity throughout life in response to changes in sensory experience and offers the experimental possibility of aligning functional changes in receptive field properties with underpinning structural changes in synapses. We looked at the effects on structural plasticity of two different patterns of whisker deprivation in male and female mice: chessboard deprivation, which causes functional plasticity; and all deprived, which does not. Using 2-photon microscopy and chronic imaging through a cranial window over the barrel cortex, we found that layer 2/3 neurones exhibit robust structural plasticity, but only in response to whisker deprivation patterns that cause functional plasticity. Chessboard pattern deprivation caused dual-component plasticity in layer 2/3 by (1) increasing production of new spines that subsequently persisted for weeks and (2) enlarging spine head sizes in the preexisting stable spine population. Structural plasticity occurred on basal dendrites, but not apical dendrites. Both components of plasticity were absent in ␣CaMKII-T286A mutants that lack LTP and experience-dependent potentiation in barrel cortex, implying that ␣CaMKII autophosphorylation is not only important for stabilization and enlargement of spines, but also for new spine production. These studies therefore reveal the relationship between spared whisker potentiation in layer 2/3 neurones and the form and mechanisms of structural plasticity processes that underlie them.

Hebbian and homeostatic plasticity mechanisms are segregated in sub-types of layer 5 neuron in the visual cortex

“…Similarly, blocking NMDA receptor function by acute knock-out prevents the increase in mEPSC levels seen in visual cortex L2/3 cells (36). This type of L2/3 NMDA dependent mechanism seems to be similar to the one we describe for L5 IB cells, since NMDA receptors induce plasticity via calcium and CaMKII-autophosphorylation (to produce LTP), promote new spine survival and enlargement of pre-exiting spines (28,29,31). However, the same mechanism is not triggered in layers 5 RS cells during dark exposure; they do not show potentiation and their homeostatic recovery is not CaMKII dependent.…”

Reduced exploratory behavior in neuronal nucleoredoxin knockout mice

“…To screen for further functional partners of NXN we used a yeast-2-hybrid screen and identified calcium calmodulin kinase 2a as one strong interaction partner in a brain library. Neuronal Camk2a is mostly localized at postsynaptic sites and in dendritic spines and is involved in functional and structural forms of neuronal plasticity [ [9] , [10] , [11] , [12] , [13] ]. Camk2a is activated upon calcium influx via NMDA-receptors.…”

Experience-dependent structural plasticity in the adult brain: How the learning brain grows

“…We analyzed basal dendrites, since they allowed a definite attribution to pyramidal cells. Furthermore, basal dendrites receive input from layer 4 and also directly from the thalamus (Petreanu et al, 2009; Hooks et al, 2011) and have been reported to show a more pronounced use-dependent plasticity than apical dendrites (Seaton et al, 2020). Compared with controls, the lengths of 1 st order basal pyramidal dendrites remained unchanged in all brain areas examined (for detailed data and statistics see supplementary table S4), except for an small increase over time in AU ipsi-OE (F (2,53) : 3.835, p: 0.028, 1way ANOVA, Tukey HSD, Fig.…”