It is well-known that prenatal chronic intermittent stress affects the reproductive system of both sexes. Investigating the effects of an acute maternal stress on the fetal neuroendocrine system, parameters such as hypothalamic catecholamines. CRF, GRF, LH-RH, beta-endorphin, hypophysial beta-endorphin and beta-LPH as well as plasma LH, corticosterone and androstenedione were measured. Pregnant rats of Wistar strain were exposed to restraint stress at day 22 of gestation or to forced immobilization at day 20 of gestation, respectively, and were sacrificed before stress and 10, 30, 60, and 120 min after starting stress. A decrease of fetal hypothalamic catecholamines and an increase of LH-RH content of the hypothalamus as well as of plasma catecholamines were observed under stress on day 22 of gestation. On day 20 of gestation hypothalamic beta-endorphin was depleted in male and unchanged in female fetuses under stress. A depletion of hypothalamic CRF was observed in male fetuses, whereas female fetuses showed an increase of hypothalamic CRF. An increase of GRF was found in fetuses of both sexes. Pituitary opioid content increased in fetuses of both sexes initially, but was depleted secondarily in male fetuses. The LH plasma level was markedly reduced in male, the corticosterone level was elevated in fetuses of both sexes as well as the androstenedione level in female fetuses. A simultaneous treatment of mother animals with tyrosine--a catecholamine precursor--prevented the depletion of hypothalamic and pituitary beta-endorphin as well as in part the reduction of plasma LH levels in male fetuses. Hypothalamic GRF content does not increase under tyrosine treatment in male fetuses, whereas in female fetuses the stress-induced increase of GRF content was rather pronounced under tyrosine than attenuated. These results indicate that fetal hypothalamic neurotransmitters and neurohormones (such as LH-RH, CRF, GRF and opioids) are involved in changing circulating hypophysial and adrenal hormones in fetuses exposed to maternal stress in late pregnancy, whereby sex-specific different pathways might be effective in fetal stress processing. The prenatal administration of tyrosine prevented at least in part--those neurohormonal changes which are affecting the sex-specific brain differentiation.

Rats deprived temporarily of maternal contact and nutrition from the 3rd to 14th day of life showed decreased emotionality and poor memory capacity when tested in adulthood. Simultaneous administration of choline chloride, an acetylcholine precursor, in neonatal life permanently increased the emotionality and restored memory capacity to levels of control animals. However, no effect was demonstrated when choline chloride administration occurred after the deprivation period. The results of this study reveal that the effects on later behaviour appear to be dependent on the timing of choline chloride exposure in early life. Profound and long-lasting abnormalities in brain function produced by early postnatal maternal deprivation can be attenuated by correcting abnormal acetylcholine levels during brain development. Hence, acetylcholine can be considered as an important, environment-dependent local organizer of the brain.

Maternal deprivation from the 3rd to 14th day of life, i.e., separation of the pups from their mother animals for 16 hours each day, gave rise to persistent significant changes of microstructures in the hippocampal stratum radiatum of the CA1-region, which were associated with significantly decreased emotionality, learning capability and memory capacity in adulthood. Such teratomorphogenic effects on the brain produced by psychosocial and/or nutritional deprivation during brain development could be partly prevented--as well as the teratophysiogenic and teratopsychogenic effects--by simultaneous administration of the acetylcholinesterase inhibitor pyridostigmine.

The effect of pargyline on 5 HT concentration in a combined forebrain and midbrain section ( FMB ) have been investigated in female rats which were temporarily deprived from their dams in postnatal life and daily injected with the monoamine oxidase inhibitor. Two hours after the last pargyline injection a marked increase in 5 HT concentration could be observed both in 12 and 30 days-old rats. The question is raised whether 5 HT may be involved in neuroendocrine mechanisms which are responsible for controlling the onset of puberty, since a significant advance of puberty could be achieved by this pargyline treatment in normal and deprived female rats.

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