TGF-beta 1 in Aplysia: Role in long-term changes in the excitability of sensory neurons and distribution of T beta R-II-like immunoreactivity

Exogenous recombinant human transforming growth factor beta-1 (TGF-beta 1) induced long-term facilitation of Aplysia sensory-motor synapses. In additi on, 5-HT-induced facilitation was blocked by application of a soluble fragm ent of the extracellular portion of the TGF-beta 1 type II receptor (T beta R-II), which presumably acted by scavenging an endogenous TGF-beta 1-like molecule. Because T beta R-II is essential for transmembrane signaling by T GF-beta, we sought to determine whether Aplysia tissues contained T beta R- II and specifically, whether neurons expressed the receptor. Western blot a nalysis of Aplysia tissue extracts demonstrated the presence of a T beta R- II-immunoreactive protein in several tissue types. The expression and distr ibution of T beta R-II-immunoreactive proteins in the central nervous syste m was examined by immunohistochemistry to elucidate sites that may be respo nsive to TGF-beta 1 and thus may play a role in synaptic plasticity. Sensor y neurons in the ventral-caudal cluster of the pleural ganglion were immuno reactive for T beta R-II, as well as many neurons in the pedal, abdominal, buccal, and cerebral ganglia. Sensory neurons cultured in isolation and coc ultured sensory and motor neurons were also immunoreactive. TGF-beta 1 affe cted the biophysical properties of cultured sensory neurons, inducing an in crease of excitability that persisted for at least 48 hr. Furthermore, exposure to TGF-beta 1 resulted. in a reduction in the firing threshold of sensory neurons. These results provide further support for the hypothesis that TGF-beta 1 plays a role in long-term synaptic plasticity i n Aplysia.