EFFECTS OF NERVE GROWTH-FACTOR ON SPLENIC NOREPINEPHRINE AND PINEAL N-ACETYL-TRANSFERASE IN NEONATE RATS EXPOSED TO ALCOHOL IN-UTERO - NEUROIMMUNE CORRELATES
Z. Gottesfeld et al., EFFECTS OF NERVE GROWTH-FACTOR ON SPLENIC NOREPINEPHRINE AND PINEAL N-ACETYL-TRANSFERASE IN NEONATE RATS EXPOSED TO ALCOHOL IN-UTERO - NEUROIMMUNE CORRELATES, International journal of developmental neuroscience, 14(5), 1996, pp. 655-662
Prenatal alcohol exposure (FAE) has been associated with multiple anom
alies, including a selective developmental delay of sympathetic innerv
ation in lymphoid organs. Sympathetic neurons require nerve growth fac
tor (NGF) for their development and maintenance, and recent evidence h
as suggested that alcohol impairs the synthesis and/or biological acti
vity of NGF in selected central and peripheral neurons. Thus, the pres
ent study examined the hypothesis that NGF administration to FAE rats
during early postnatal development would reverse some of the periphera
l sympathetic deficits. Neonate rats, FAE and the corresponding contro
l cohorts, received daily treatments of NGF or cytochrome C (0.3 mg/kg
; s.c.) for various time intervals, and were killed 24hr or 10 days af
ter the last treatment. The measured parameters included norepinephrin
e (NE) concentrations in the spleen and heart, which receive noradrene
rgic innervation from the coeliac ganglion and the superior cervical g
anglion (SCG), respectively. In addition, we measured the activity of
pineal N-acetyltransferase (NAT), the rate-limiting enzyme of melatoni
n biosynthesis, which depends on sympathetic innervation from the SCG.
The data show that chronic, but not acute, NGF treatments reversed th
e FAE-related deficits in splenic NE concentrations as well as in pine
al NAT activity in a time- and age-dependent manner. Sympathetic neuro
ns play an important role in immune modulation. Thus, the altered sple
nic NE levels and pineal NAT activity may play a role in immune defici
ts associated with exposure to alcohol in utero. Copyright (C) 1996 IS
DN.