Table 1.

Post-traumatic inflammatory, neuronal and functional consequences in neonatal animals. Abbreviations: ↑: increase; ↓: decrease; CCI: controlled cortical impact; d: days post-injury; h: hours post-injury; NC: not compared; NMDA: N-methyl-D-aspartate; P: postnatal days; TBI: traumatic brain injury; WD: weight drop.

Animal and TBI Model	Age	Compa-rison Age	Main Highlights						Reference
			Microglia	Astrocytes	Cytokines and Other Immune Cells	Brain Lesion and Neuronal Death	Functional Deficits	Comparison to Other Ages
Mice WD, closed head, unilateral	P3/7	P10/14/30				- excitotoxic degeneration from 0.5 to 24 h; peak at 4 h (injury site) - apoptosis from 6 to 24 h (distant site)		- Brain injury P3/7 > P10/14/30	[140]
Mice WD closed head, unilateral	P7	NC				- neuronal death expansion from 0.5 to 6 h (edematous swelling of dendritic processes and acute edematous degeneration of neuronal cell bodies with pyknotic changes of the nuclei)			[141]
Mice WD, closed head, unilateral	P7	NC	- activation from 1 to 21 d	- activation from 5 to 21 d		- cellular death from 1 to 5 d - ventriculomegaly at 21 and 28 d			[142]
Mice WD, closed head, unilateral	P7	NC			- variation in pro- and anti-inflammatory cytokines/chemokines gene expression at 1 and 5 d - variation in pro- and anti-inflammatory immune cells gene expression at 1 and 5 d	- ventriculomegaly at 1 and 5 d			[143]
Mice WD, closed head, unilateral	P7	NC	- activation at 1 d - predominant reparatory/regenerative or immunomodulatory macrophage/microglia phenotype		- ↑ pro and anti-inflammatory cytokines expression from 1 to 5 d (< to adult) - microglia and macrophages depletion = transient ↓ pro-inflammatory cytokines	- thalamus, hippocampus and cortex tissue injury at 1 d - ventriculomegaly at 1 d- microglia and macrophages depletion = ↓ neuronal death and ventriculomegaly at 1 d			[144]
Mice WD, closed head, unilateral	P7	NC	- activation from 0.5 to 5 d			- excitotoxic degeneration at 1 d			[139]
Mice WD, closed head, unilateral	P7	NC				- ↑ neuronal mitochondrial activity and size at 1 d - ↓ 20% in sensorimotor cortical thickness at 30 d- Neuronal death still observed at 23 d			[145]
Rats WD, closed head, unilateral	P7	NC					- Neuronal death at 125 d (hippocampus) - Anxiety and spatial memory deficits at 125 d - NMDA antagonist improves morphological, histopathological, neurochemical and functional effects of brain injury at 125 d		[146]
Rats WD, closed head, unilateral	P3/7	P14/30				- cell death from 6 h to 5 d (peak at 24 h)		- apoptosis P3/P7 > P14/30	[147]
Rats CCI, closed head, unilateral	P11	NC				- ↑ intrinsic excitability and frequency of spontaneous excitatory post-synaptic currents at 28 d - ↓ frequency of spontaneous inhibitory post-synaptic currents at 28 d	- cognitive deficits at 28 d		[148]
Rats CCI, closed head, unilateral	P11	P17						- glial activation in P11, not in P17 at 3 d- brain atrophy and ventriculomegaly P11 > P17 at 14 and 28 d - acquisition and retention deficits P11 > P17 at 28 d	[149]
Rats CCI, closed head, unilateral	P11	NC	- activation at 3, 15 and 35 d (ipsilateral cortex)			- microglial depletion = ↑ neurodegeneration at 3 d	- microglial depletion = no spatial learning deficits at 28 d		[150]
Rats CCI, closed head, unilateral	P11	NC					- social recognition deficits, but intact sociability at 28 and 56 d - no memory deficit at 28 and 56 d		[151]