Effect of testosterone on pathological aggression behavior and expression of postsynaptics density-95 and growth associated protein-43 in prefrontal cortex in puberty rats / 第二军医大学学报

Objective To explore the effect of serum testosterone level on the pathologically aggressive behavior and the synaptic plasticity in the prefrontal cortex of puberty rats after gonadectomy. Methods Thirty male rats, 21 days old, were randomly divided into 3 groups: gonadectomized group, model group and control group. The gonadectomized and model groups were given a series of standard stress from 21 days old to puberty to induce animal model of pathological aggressive behavior. Resident-intruder experiment was performed to observe the variation of aggressive behaviors of animals. Enzyme-linked immunosorbent assay was used to examine the serum testosterone level. Western blotting analysis was used to determine the expression of postsynaptics density-95 (PSD-95) and growth associated protein-43 (GAP-43) in the prefrontal cortex. Results Resident-intruder experiment showed that the latency to the first attack in the gonadectomized group decreased significantly (P<0.01,P<0.01) and the attack times after yield increased significantly compared with those in the other two groups (P<0.01,P<0.01). The serum testosterone in the gonadectomized group was significantly decreased compared with the other two groups as shown by ELISA results (P<0.01, P<0.01). In addition, the aggressive-related behavior indices had a moderate to high negative correlation with the testosterone level (P<0.01). Western blotting analysis showed that prefrontal cortex expression of PSD-95 and GAP-43 in the gonadectomized group was significantly lower than those in the other two groups(P<0.01, P<0.01). Conclusion Low serum testosterone level can cause damage to the neuroplasticity of prefrontal cortex in puberty rats, which might be related to the pathologically aggressive behavior.

Estudio de la instigación social en un modelo de agresión inducida por aislamiento: efectos de la administración de JNJ16259685, un antagonista de receptores mGlu1 / Study of the Social Instigation in a Model of Isolation-Induced Aggression: Effects of JNJ16259685 Administration, an mGlu1 Receptor Antagonist

La instigación social intensifica la conducta agresiva permitiendo observar niveles más extremos de agresión. Estudios recientes indican que el receptor metabotrópico del glutamato mGlu1 está implicado en la regulación de la conducta agresiva en un modelo de agresión inducida por aislamiento. El objetivo de este trabajo fue evaluar los efectos de la administración de un antagonista del receptor mGlu1 (JNJ16259685) sobre la conducta agresiva normal e intensificada, utilizando instigación social en un modelo animal de agresión inducida por aislamiento. Varios grupos de animales aislados fueron expuestos a 5 minutos de instigación social, recibiendo la mitad de ellos JNJ16259685 (0.5 mg/kg, ip) o vehículo. Las interacciones agonísticas de 10 min de duración se realizaron en un área neutral 30 min después de la inyección. Dichos encuentros fueron grabados en vídeo para el posterior análisis etológico de diez categorías conductuales. La instigación redujo la latencia de ataque y aumentó la frecuencia y duración de los ataques frente a los animales no instigados. La administración de JNJ16259685 redujo de forma significativa la conducta agresiva en ambos casos, sugiriendo la implicación del receptor mGlu1 en la modulación de la agresión normal e intensificada.

Social instigation intensifies aggressive behavior in rodents allowing observe more extreme levels of aggression. Recent studies indicate that glutamate metabotropic receptor 1 (mGlu1) are involved in the regulation of aggressive behavior in isolation-induced aggression model. The object of this work was to examine social instigation in an animal model of isolation-induced aggression and assess the anti-aggressive effects of an mGlu1 receptor antagonist (JNJ16259685) on normal and heightened aggressive behavior. Several groups of individually housed mice were exposed to 5 minutes of social instigation, and half of them received an acute administration ofJNJ16259685 (0.5 mg/kg, ip) or vehicle. Ten minute of dyadic interactions were staged between a singly housed and an anosmic mouse in a neutral area 30 min after drug or vehicle administration. The encounters were videotaped for subsequent analysis of ten ethological behavioural categories. Social instigation reduced latency of attack and increased the frequency and duration of attacks against not instigated animals. JNJ16259685 administration significantly reduced aggressive behavior in both cases, suggesting the involvement of mGlu1 receptor in the modulation of normal and heightened aggression.

Preliminary establish of the puberty pathological aggression animal model / 中华行为医学与脑科学杂志

Objective To establish the preferable puberty pathological aggression animal model.Methods The experimental models were established towards puberty rats by frustration test of non-reward and instigation test.Rat models were tested for specificity using open-field test,saccharine test,elevated plus-maze(EPM)and olfactory sensibility.Results ①Compared with normal aggression(52.5±5.36)and control group(8.83±1.34)in total aggressive times,the pathological aggression group(101.17±2.85)increased significantly(P0.05).However,the normal aggression group displayed obvious depressive mood.Conclusion Each behavioral index matches the criteria of pathological aggression model.Meanwhile,it also excludes other factors of disturbing the specificity of the model.It suggests this model may be preferable puberty pathological aggression animal model.