Brain-derived neurotrophic factor (BDNF) and polysialylated-neural cell adhesion molecule (PSA-NCAM) in the human brainstem precerebellar nuclei from prenatal to adult age.
Occurrence and distribution of the neurotrophin brain-derived neurotrophic factor (BDNF)
and polysialylated-neural cell adhesion molecule (PSA-NCAM), a neuroplasticity marker
known to modulate BDNF signalling, were examined by immunohistochemistry in the
human brainstem precerebellar nuclei at prenatal, perinatal and adult age. Western blot
analysis performed in human brainstem showed for both molecules a single protein band
compatible with the molecular weight of the dimeric form of mature BDNF and with that of
PSA-NCAM. Detectability of both molecules up to 72 h post-mortem was also assessed in rat
brain. In neuronal perikarya, BDNF-like immunoreactivity (LI) appeared as intracytoplasmic
granules, whereas PSA-NCAM-LI appeared mostly as peripheral staining, indicative of
membrane labelling; immunoreactivity to both substances also labelled nerve fibres and
terminals. BDNF- and PSA-NCAM-LI occurred in the external cuneate nucleus,
perihypoglossal nuclei, inferior olive complex, arcuate nucleus, lateral reticular formation,
vestibular nuclei, pontine reticulotegmental and paramedian reticular nuclei, and pontine
basilar nuclei. With few exceptions, for both substances the distribution pattern detected at
prenatal age persisted later on, though the immunoreactivity appeared often higher in preand
full-term newborns than in adult specimens. The results obtained suggest that BDNF
operates in the development, maturation, maintenance and plasticity of human brainstem
precerebellar neuronal systems. They also imply a multiple origin for the BDNF-LI of the
human cerebellum. The codistribution of BDNF- and PSA-NCAM-LI in analyzed regions
suggests that PSA-NCAM may modulate the functional interaction between BDNF and its
high and low affinity receptors, an issue worth further analysis, particularly in view of the
possible clinical significance of neuronal trophism in cerebellar neurodegenerative
disorders.