The effect of prenatal exposure to music on fetal movements and fetal heart rate: a pilot study.

OBJECTIVE: To assess and compare fetal cardiac parameters of fetuses listening to music before and during nonstress test, only during the test or never. STUDY DESIGN: Thirty healthy mother-fetus dyads were randomized in a 1:1:1 ratio to one of three groups: group A in which fetuses were submitted to prelistening phase (33rd + 0 to 36th + 3 week) and listening sessions during 4 nonstress tests, group B in which fetuses were submitted to listening sessions during 4 nonstress tests, and group C receiving 4 nonstress tests without any listening. We assessed mean fetal heart rate, fetal heart rate accelerations, fetal heart rate decelerations, fetal movements and uterine contractility. RESULTS: Fetuses of the group A, who had already listened to a particular piece of music during previous sessions, had significantly increased their heart rate accelerations and movements during the music listening session of the last nonstress test. No significant changes were observed in the number of uterine contractions. CONCLUSIONS: Our findings show that fetuses slightly respond to that music they know, but they do not significantly respond to unknown music.

The selective A2A receptor antagonist SCH 58261 reduces striatal transmitter outflow, turning behavior and ischemic brain damage induced by permanent focal ischemia in the rat.

Adenosine A(2A) receptor antagonists have been proved protective in different ischemia models. In this study we verified if the protective effect of the selective A(2A) antagonist, SCH 58261, could be attributed to the reduction of the excitatory amino acid outflow induced by cerebral focal ischemia. A vertical microdialysis probe was inserted into the striatum of male Wistar rats and, after 24 h, permanent right intraluminal middle cerebral artery occlusion (MCAo) was induced. Soon after waking, rats showed a definite contralateral turning behavior, which persisted up to 7 h after MCAo. During 4 h after MCAo, glutamate, aspartate, GABA, adenosine and taurine outflow increased. SCH 58261 (0.01 mg/kg, i.p.), administered 5 min after MCAo, suppressed turning behavior and significantly reduced the outflow of glutamate, aspartate, GABA and adenosine. At 24 h after MCAo, the rats showed severe sensorimotor deficit and damage in both the striatum and cortex. SCH 58261 significantly reduced cortical damage but did not protect against the sensorimotor deficit. The protective effect of SCH 58261 against turning behavior and increased outflow of excitatory amino acids in the first hours after MCAo suggests the potential utility of selective adenosine A(2A) antagonists when administered in the first hours after ischemia. Furthermore, this study, for the first time, proposes that turning behavior after permanent intraluminal MCAo, be used as a precocious index of neurological deficit and neuronal damage.