[Vesicle population of synapses in the hippocampus of the rat following early postnatal deprivation and administration of pyridostigmine].

Newborn male Wistar rats were subjected to early postnatal social and nutritional deprivation by separation of the pups from their mother animals from Day 3 to Day 14 for 16 hours daily. One group of the deprived animals was treated by daily injections of pyridostigmine (1 microgram/0.05 ml saline from Day 1 to Day 4, 5 micrograms/0.05 ml saline from Day 5 to Day 14). At the age of 14 days or 6 months, 5 deprived, 5 deprived and pyridostigmine treated rats and 5 controls were investigated. In the stratum radiatum of the hippocampal CA 1-region the vesicle population of axospinodendritic synapses was examined for quantitative ultrastructural changes using electron microscopic and morphometric methods. The vesicle density (number of vesicles/micron 2 terminal area) was determined in the whole presynaptic terminal as well as in distinct zones in the presynaptic terminal. 14 days of deprivation did not change the vesicle density in the whole presynaptic terminal, but did change the distribution of the vesicles. In 14 days old deprived rats the vesicle density was found to be decreased by about 10% in the presynaptic area bordering the synaptic contact zone (area 1), and it was increased by about 7% in the more distant area of the presynaptic terminal (area 2). Deprivation and simultaneous pyridostigmine treatment resulted in an elevated vesicle density in the whole presynaptic terminal by about 25%, in area 1 by about 8%, and in area 2 by about 30%. At the age of 6 months, the early postnatally deprived rats showed an increase in the vesicle density by about 8% in all areas of the presynaptic terminal when compared with the controls. Simultaneous pyridostigmine treatment led to a reduced vesicle density in the whole presynaptic terminal by about 5%, in area 1 by about 9%, and in area 2 by about 4%. The findings obtained following deprivation are interpreted as being the expression of an insufficient requirement of synaptic mechanisms caused by a lack of sensoric inputs during the early postnatal period. The results obtained in the neonatally pyridostigmine treated rats suggest permanent changes in the neurotransmitter metabolism following treatment with the psychotrophic drug. This may reflect a mechanism to compensate the effect of deprivation by neonatal pyridostigmine administration.