Research reportAmantadine preserves dopamine level and attenuates depression-like behavior induced by traumatic brain injury in rats

- Amantadine ameliorated the depression-like behavior caused by traumatic brain injury (TBI).
- Amantadine reduced the neuronal degeneration in the impaired substantia nigra (SN) instead of the striatum.
- Amantadine alleviated the dopaminergic neuronal apoptosis following TBI in the SN.
- Amantadine reversed the decrease of dopamine in the striatum induced by TBI.

Traumatic brain injury (TBI) often results in multiple neuropsychiatric sequelae, including cognitive, emotional, and behavioral problems. Among them, depression is a common psychiatric symptom, and links to poorer recovery. Amantadine, as an antiparkinsonian, increases dopamine release, and blocks dopamine reuptake, but has recently received attention for its effectiveness as an antidepressant. In the present study, we first induced a post-TBI depression rat model to probe the efficacy of amantadine therapy in reducing post-TBI depression. The DA concentration in the striatum of the injured rats, as well as the degeneration and apoptosis of dopaminergic neurons in the substantia nigra (SN), were checked along with the depression-like behavior. The results showed that amantadine therapy could significantly ameliorate the depression-like behavior, improving the DA level in the striatum and decreasing the degeneration and apoptosis of dopaminergic neurons in the SN. The results indicated that the anti-depression effect may result from the increase of extracellular DA concentration in the striatum and/or the indirect neuroprotection on the dopaminergic neurons in the SN. We conclude that DA plays a critical role in post-TBI depression, and that amantadine shows its potential value in anti-depression treatment for TBI.

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