Abstract □ 97

Among the causes that lead to sudden death during infancy two main classes implicate central neuro-transmitter as regulator of vegetative controls. Congenital abnormalities genetically or incidentally inherited (hypoplasia, late in development, heterotopia) facilitate the break-down of neuronal firing or detained loops of escape which are present to avoid apnea. The second class of critical factors is the maturation changes in brain. The behavioural necessities and the final neuron network organization (selective apoptosis) are the inducing factors of major change in the central nervous system. In all mammalian species the neuropeptides and their receptors increase dramatically during the perinatal period. Nevertheless in most cases there is no parallelism, neither succession in time, between the transient overexpression of a kind of neuropeptide and its -or their- specific receptor (s), respectively. Frequently there are clear discrepancies between the rostral and caudal timings in maturation profile. This has been established in rodents for opiate ligands and receptors (Tsang & Ng, 1980 ; Kornblum et al, 1987) and partly in human brainstem, (Kinney et al., 1990). Independently of opioid effect neurotensin (NT) is a second family of central peptides which is able to induce apnea (Morin-Surun et al, 1986). NT is a powerful inducer of hypothermia and analgesia, a dopamine modulator and an inducer of hypothalamo-pituitary hormone release. During the fetal life NT receptor (NTR) are highly expressed in medulla especially in nucleus tractus solitarius (cardio-respiratory controls) and the olive medullar complex. After birth this binding capacity decreases fastly while the NT content increases dramatically (Mailleux et al., 1988) in the inferior olive. Later, during the SIDS age period (1-6 months) the NT, like the potent opiate β-endorphin, is persisting at high levels in the brainstem (Coquerel et al., 1992). In most cases the receptor type is of high affinity. in case of stress the sedative peptides reach a critical level i.e. concentration reaching the KD value BE 100 pM. By contrast to brainstem, in basal ganglia and essentially in cortex, NTR overexpression occurs during the 1-6 month period with a dramatic peak at 6-8 weeks. The RNT levels reach about 100 time the adult values of NTR. This order of maturation linked changes implies to use radioimages (RI) in place of autoradiographic films. With a very sensitive real time RI we are now able to use 3H-tracers which available f for quite ligands. This is by accumulating the absolute values of binding sites and peptides contents with a blind analysis of the results that we could hope to find some specific discrepancies in true SIDS cases. Nevertheless the origin of the change will not be establish at this time : it could reflect a training in hypoxic experience during sleep as it could be due to a dysembryoplasia under genetic control. In any case we are attentive to find efficient drugs which could suppress the risk of fatal apnea without inducing definite brain changes by adverses effects. Opiate antagonists like naloxone and naltrexone are able to inhibit respiratory pauses in newborns (Myer et al., 1990). A special mention to NTR in infancy : it is associated with a Bcl-2 overexpression. These facts underline the specific trophic role of neuropeptide during infancy.