The Effects Of 8-OH-DPAT On BDNF,GDNF In Prefrontal Cortex And Hippocampus In Puberty Rats

OBJECTIVETo explore the effects of 8-OH-DPAT,namely serotonin(5-HT)1A receptor agonist on pathological aggression and BDNF,GDNF in prefrontal cortex and hippocampus in puberty rats.METHODSFifty-six 21-day-old male Sprague-Dawley rats were randomized into 6 groups: experimental group(n=7),control group(n=7),experimental+8-OH-DPAT group(n=7),experimental+saline group(n=7),control+8-OH-DPAT group(n=7)and control+saline group(n=7),the remaining rats as intruders(n=14).Rats in experimental group,experimental+8-OH-DPAT group and experimental +saline group were given chronic stressors from early life for the modeling,rats in other three groups only grew up normally.After the modeling,8-OH-DPAT(0.5mg/kg)or saline(2ml/per)were respectively injected to the rats in experimental+8-OH-DPAT group,control+8-OH-DPAT group and experimental+saline group,control+saline group for two weeks.Resident-intruder test and Western Blot were used to test aggression and BDNF,GDNF,respectively.RESULTS1 Aggression and neurotrophic factors in adolescent rats after modeling1.1 Aggression: the latency to first attack in experimental group reduced significantly compared with the control group(P<0.01);Compared with the control group,the attack on vulnerable parts and the sustained attack after yield were increasing(P<0.01).1.2 Neurotrophic factors: both BDNF and GDNF in the prefrontal cortex and hippocampus of experimental group were relatively lower than control group(P<0.01).2 Aggression and neurotrophic factors in adolescent rats after treatment2.1 Aggression2.1.1 The latency to first attack: after the treatment of 8-OH-DPAT or saline,the latency to first attack in experimental+8-OH-DPAT group was significantly prolonged compared with the experimental+saline group(P<0.05);There was no significant difference among other groups(P>0.05).2.1.2 The attack on vulnerable parts: it decreased in experimental+8-OH-DPAT group,compared with the experimental+saline group(P<0.01);There was no significant difference among other groups(P>0.05).2.1.3 The sustained attack after yield: in experimental+saline group,it was still higher than control+saline group(P<0.01);In experimental+8-OH-DPAT group,the sustained attack after yield declined(P<0.01);No obvious difference was found after treatment among other groups(P>0.05).2.2Neurotrophic factors:2.2.1 Prefrontal cortex: in experimental+saline group,both BDNF and GDNF were significantly decreased compared with the control+saline group(P<0.01,P<0.05);In experimental+8-OH-DPAT group,there was a distinct rising of BDNF and GDNF,compared with experimental+saline group(P<0.01,P<0.05);No significant difference was discovered among other groups(P>0.05).2.2.2 Hippocampus: compared with the control+saline group,both of BDNF and GDNF in experimental+saline group descended(P<0.01,P<0.05);In experimental+8-OH-DPAT group,both BDNF and GDNF ascended,compared with experimental+saline group(P<0.01,P<0.05);No significant difference was discovered among other groups(P>0.05).CONCLUSIONS1 Early life chronic stress can produce pathologic aggression in puberty rats.2 The BDNF and GDNF in the prefrontal cortex and hippocampus are reduced after early life chronic stressors in puberty rats,which might result in pathological aggressive behaviors.3 5-HT1 A receptor agonist(8-OH-DPAT)can increase BDNF,GDNF in prefrontal cortex and hippocampus and reduce the pathological aggression induced by early life chronic stress of puberty rats.