Table 1.

Effect of development and experience on spine dynamics in different regions of rodent cortex in vivo.

Species/cells labeled	Age	Main findings	Refs.
Visual cortex
Mouse (H-line), L5 neurons	1–10m	Spines in the adult visual cortex were found to be very stable, with a half-life of >13 months. Over 95% of spines persisted over 1 month.	[39]
Mouse (H/M-line), L2/3/5 neurons	P28-61	Spine motility varied in different cortices at 1 month of age, with the visual cortex being the most stable. Rewiring visual inputs into the auditory cortex did not change intrinsic spine motility in the auditory cortex.	[40]
Mouse (M-line), L5 neurons	>3m	Focal retinal lesions dramatically increased spine turnover in the lesion projection zone, leading to an almost complete replacement of original spines within 2 months.	[46]
Mouse (M-line), L2/3/5 neurons	>1.5m	MD increased spine formation in L5, but not L2/3 neurons, in the binocular cortex. Spines formed during MD persisted during binocular vision restoration, and were strengthened during the second MD.	[30]
Mouse (M-line), L5 neurons	~P28	Dark-rearing resulted in high motility and immature morphology of spines. While brief light exposure increased spine motility, prolonged light exposure stabilized spines over time.	[32]
Barrel cortex
Rat, virus-labeled L2/3 neurons	P8-16	Spines and filopodia were highly motile during early postnatal development. Trimming all the whiskers unilaterally reduced spine and filopodium motility in the contralateral barrel cortex during a critical period between P11 and P13.	[17]
Mouse (M-line), L5 neurons	P34-74	Spines displayed a spectrum of stability. Chessboard deprivation increased the pool of transient spines and decreased the pool of stable spines.	[19]
Mouse (M/H-line), L2/3/5 neurons	P14-511	The fraction of persistent spines increased with an animal’s age. The visual cortex was observed to be more stable than the barrel cortex in 6m old mice.	[28]
Mouse (H-line), L5 neurons	P14-23m	Spines and filopodia displayed distinct dynamics. Spine dynamics decreased with age. In adults, a majority of spines were stable throughout the animal’s life.	[36]
Mouse (H-line), L5 neurons	1–6m	Trimming all the whiskers unilaterally prevented spine elimination in the contralateral barrel cortex in both adolescent and adult mice. This activity-dependent spine elimination was NMDA receptor dependent.	[27]
Mouse (M-line), L5 neurons	2–5m	Chessboard whisker trimming stabilized new spines and destabilized previously persistent spines, preferentially on L5 neurons with complex apical tufts.	[29]
Mouse (H-line), L5 neurons	1–18.5m	Sensory enrichment increased spine formation and elimination. Most spines formed early during development and a small fraction of new spines induced by novel experience survived experience-dependent elimination and were preserved into adulthood.	[38]
Mouse (M-line), L5 neurons	2–3m	Chessboard whisker trimming increased new spine stabilization at the border between spared and deprived barrel columns. CaMKII autophosphorylation-defective mutant mice lacked such experience-dependent spine stabilization.	[31]
Motor cortex
Mouse (H-line) L5 neurons	1m, >4m	Forelimb-specific motor skill training induced rapid spine formation, followed by prolonged spine reorganization selectively in the forelimb region. Different motor skills affected different populations of spines.	[37]
Mouse (H-line) L5 neurons	1m, >4m	Rotarod training increased spine turnover.	[38]

Abbreviations: months (m), Ca²⁺/calmodulin-dependent protein kinase II (CAMKII).