Imaging of striatal injury in a songbird brain.

Neurological insults affect both, brain structure and behavior. The injury-induced brain plasticity and associated changes in behavior are difficult to study using classical histological methods. The magnetic resonance imaging (MRI), however, enables repeated inspection of the brain in the same individual. Here we took advantage of the songbird model with discrete brain circuitry controlling song learning and production and assessed if a conventional MRI is suitable to detect even relatively small brain changes. Our aim was to monitor injury and the following regeneration in the striatal vocal nucleus Area X that controls vocal learning in juveniles and affects song in adult songbird zebra finch (Taeniopygia guttata). The regeneration process was detected using T2-weighted images and validated by immunohistochemical (IHC) staining up to 6 months after the injury. Despite the small volume of the zebra finch brain, a satisfactory signal-to-noise ratio was achieved with reasonably short measurement times. No significant difference was found between the measurements of the lesion size obtained by MRI and IHC staining. Our data show that the non-invasive MRI technique can reliably measure and quantify the regeneration process even in a relatively small part of the brain and that the avian striatum progressively regenerates after its neurotoxic injury.

Dopamine D3 receptors modulate the rate of neuronal recovery, cell recruitment in Area X, and song tempo after neurotoxic damage in songbirds.

Songbirds, like humans, learn vocalizations and their striatum recruits new neurons in adulthood. Injury in striatal vocal nucleus Area X, involved in song learning and production in songbirds, is followed by massive regeneration. The newborn neurons arise from the subventricular zone (SVZ) rich in dopamine D3 receptors (D3Rs). The aim of this study was to investigate whether the D3Rs affect the rate of neuronal recovery in Area X. Male zebra finches (Taeniopygia guttata) received bilateral neurotoxic lesion of Area X and were implanted with osmotic minipumps containing D3R agonist 7-OH-DPAT, antagonist U99194, or saline. Treatment with 7-OH-DPAT but not U99194 led to significant reduction of lesion size and increased numbers of migrating neuroblasts and newborn cells in the Area X. These cells were detected in the lesion border as well as the lesion center. Lesion also led to increased mRNA expression of the D3Rs in the neurogenic SVZ and in the nucleus robustus arcopallialis (RA) involved in song production. Moreover, lesion alone prolonged the song duration and this may be facilitated by D3Rs in RA. Parallel lesion and stimulation of D3Rs prolonged it even more, while blocking of D3Rs abolished the lesion-induced effect. These data suggest that D3R stimulation after striatal injury accelerates the striatal recovery and can cause behavioral alterations.