Table 1.
The Effect on Dopamine Release in Different TBI Animal Model.
| Nigrostriatal Pathway | Mesolimbic (VTA–NAC) Pathway | Dopamine Metabolism | Neuroinflammation | Reference(s) |
|---|---|---|---|---|
| Fluid percussion injury (FPI) | ||||
| Significant TH+ neuron loss in SN at 4 wk later | NA | Dopamine metabolism was altered at 28 days postinjury | Microglial activation (significant 40%) increase at 4 days | van Bregt et al.125 |
| ELISA method detect DA levels at the early post-TBI stages but not in later stage | NA | Muthuraju et al.126 | ||
| Significant suppression of dopamine-evoked signal in injured ipsilateral side striatum | The dopamine metabolism rate increased in chronic stage in injury ipsilateral side NAC | Dopamine metabolism in injured ipsilateral side striatum altered and increased at 8 wk postinjury; Reuptake prolonged in subacute stage after FPI | Microglia activation till chronic stage (post-FPI 8 wk) in severe FPI | Huang et al.71, Chen et al.75 |
| Control cortical injury (CCI) | ||||
| Significant TH+ neuron loss in SN at 4 wk later | NA | Dopamine transporter (DAT) expression was proportionally decreased but no injury-related changes in vesicular monoamine transporter or D2 receptor expression (DRD2) in the striatum | NA | Wagner et al.25 |
| No significant difference in synaptosomal uptake (Km, Vmax) was found at 2 wk and 4 wk after CCI injury | Wilson et al.127 | |||
| Hypodopaminergic environment and altered DRD2 autoreceptor DAT interactions that may influence DA transmission after TBI | Wagner et al.128 | |||
| In vivo TH activity showed no significant difference at 1 day, and there was a decreased activity in injured rats at 1 and 4 wk | Microdialysis and HPLC analysis revealed no significant differences in dopamine release at 1 day and 4 wk but significantly decrease at 1 wk post-CCI between sham and injured groups | Shin et al.73 | ||
| CCI increases TH protein levels, its activity, and tissue DA and NE content in the prelimbic (PL)/infralimbic (IL) | NA | NA | Kobori et al.129 | |
| Blast-wave injury (explosive) | ||||
| Increase DA turnover and/or release in the NAC, but no change in absolute DA level | Increase levels of HVA and HVA/DA at 24 h following blast, with no change in levels of DA, suggest increase CA turnover | Blast overpressure causes inflammation and neurochemical changes that trigger apoptosis in NAC | Sajja et al.130 |
Note: ELISA, enzyme-linked immunosorbent assa; HPLC, high performance liquid chromatography; HVA, homovanillic acid; NA, not applicable; SN, substantia nigra; TH, tyrosine hydroxylase; TBI, traumatic brain injury; VTA, ventral tegmental area.