The effect of tetanus toxin on neuropeptide hormone release from isolated nerve endings of the neural lobe of rat pituitaries (neurosecretosomes) was measured in a perfusion system. Tetanus toxin inhibited depolarization-evoked release of oxytocin and vasopressin in a time- and dose-dependent manner. At 1 microgram/ml, tetanus toxin blocked stimulated release by 85%. Tetanus toxin that was preincubated with a neutralizing monoclonal antibody or heated to 100 degrees C had no effect on hormone release. The ionophores A23187 and ionomycin were potent stimulators of hormone release in control nerve endings, but were not able to overcome the effect of tetanus toxin in intoxicated nerve endings. 8-Bromo-cyclic GMP, which has been reported to reverse the action of tetanus toxin in PC12 cells, had no effect on the action of tetanus toxin in neurosecretosomes. Neurosecretosomes are the first system in which tetanus toxin has been shown to block release from peptidergic nerve terminals. They appear to be a valuable in vitro system for studying the biochemical mechanism of tetanus toxin action.
The effect of neonatal deafferentation of the rat superior cervical ganglion (SCG) on the expression of two synaptic vesicle proteins was studied to assess the role of transsynaptic influences in the regulation of these neural antigens in the SCG. The two proteins studied were a 65 kilodalton integral membrane protein of synaptic vesicles (SV), and synapsin-1 (S-1), a synaptic vesicle phosphoprotein. Antigen levels were quantified by radioimmunoassay using antibodies directed against the proteins. Distribution of SV in control, deafferented and reinnervated ganglia from 30-day-old rats was visualized by immunohistochemical labeling. Levels of both antigens were reduced following deafferentation of the SCG on postnatal days 1-3. The reduction in S-1 levels at 30 days was less than that observed for SV. The amount of S-1 remaining in deafferented ganglia was consistent with estimates of the postsynaptic pool in the SCG reported previously. SV levels, in contrast, were reduced to 24% of control levels, suggesting that SV synthesis in principal ganglionic neurons might be affected. The time course of postnatal development of S-1 in the SCG differed from previous studies of SV expression, with significant increases occurring after the second week after birth. The differences in response to deafferentation may reflect functional differences of the two vesicle-associated proteins. These studies demonstrate that transsynaptic regulation of antigens other than those directly associated with neurotransmitters occurs in the SCG.
The effect of neonatal deafferentation on the expression of a neuronal cell surface heparan sulfate proteoglycan (HeS-PG) was investigated in the developing rat superior cervical ganglion. Two monoclonal antibodies, one directed against the core protein of HeS-PG, and one to a determinant associated with a heparan sulfate side-chain, were used to monitor postnatal increases of HeS-PG by radioimmunoassay. Following neonatal deafferentation by section of the cervical sympathetic trunk, total protein per ganglion was slightly reduced at survival times of 7, 14, and 30 days. Expression of the core protein determinant on HeS-PG was not altered in deafferented ganglia. In contrast, levels of side-chain determinant were significantly reduced at 14 and 30 days. These results suggest that processing of HeS-PG side-chains by principal ganglionic neurons is partially regulated by transsynaptic influences during development. Transsynaptic regulation of neuronal development may be a more general process than was believed previously, with effects not limited to molecules associated with synaptic development.
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