Early polyamine treatment enhances survival of sympathetic neurons after postnatal axonal injury or immunosympathectomy.

We have recently demonstrated that following injury of their axon, sympathetic neurons of the rat superior cervical ganglion become dependent on polyamine synthesis for their survival. In addition we have observed that the treatment of newborn rats with biogenic polyamines can prevent the naturally occurring reduction in the number of neurons in the ganglion. In the present study groups of newborn rats were subjected to either postganglionic nerve crush (axotomy) or to treatment with antiserum to nerve growth factor (immunosympathectomy), two treatments which result in a massive loss of neurons in the ganglion. Daily injections of the polyamines putrescine, spermidine and spermine (10 mg/kg each), for 7 days after the operation to the axotomized group, and for 9 days starting with the first antiserum injection to the immunosympathectomized group, attenuated the nerve cell loss. The polyamine treatment also attenuated the reduction in the activity of the neurotransmitter-synthesizing enzyme tyrosine hydroxylase observed after both axotomy and immunosympathectomy in the ganglion. These results further indicate that polyamines are important for the survival of sympathetic neurons and, while their mechanism of action is unknown, an interaction with nerve growth factor regulation cannot be excluded. In the iris, the reduction observed in [3H]norepinephrine uptake after the two noxious treatments was unproportionately small when compared to the large drop in the number of parent neurons in the ganglion. This suggests that compensatory mechanisms exist which act to adjust the number of functional axon terminals per neuron so that the number of terminals innervating the target remains relatively constant.