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The Posterodorsal Medial Amygdala Regulates the Timing of Puberty Onset in Female Rats.

Li XF, Hu MH, Hanley BP, Lin YS, Poston L, Lightman SL, O'Byrne KT - Endocrinology (2015)

Bottom Line: In both dietary groups, MePD lesions resulted in an increase in socialization and a decrease in play fighting behavior.In conclusion, our results suggest the MePD regulates the timing of puberty via a novel mechanism independent of change in body weight and caloric intake.MePD glutamatergic systems advance the timing of puberty whereas local GABAergic activation results in a delay.

View Article: PubMed Central - PubMed

Affiliation: Division of Women's Health (X.F.L., M.H.L., B.P.H., Y.S.L., L.P., K.T.O.), Faculty of Life Sciences and Medicine, King's College London, Guy's Campus, London SE1 1UL, United Kingdom; and Henry Wellcome Laboratory for Integrative Neuroscience and Endocrinology (S.L.L.), University of Bristol, Bristol BS1 3NY, United Kingdom.

ABSTRACT
Obesity is the major risk factor for early puberty, but emerging evidence indicates other factors including psychosocial stress. One key brain region notable for its role in controlling calorie intake, stress, and behavior is the amygdala. Early studies involving amygdala lesions that included the medial nucleus advanced puberty in rats. More recently it was shown that a critical site for lesion-induced hyperphagia and obesity is the posterodorsal subnucleus of the medial amygdala (MePD), which may explain the advancement of puberty. Glutamatergic activity also increases in the MePD during puberty without a corresponding γ-aminobutyric acid (GABA)ergic change, suggesting an overall activation of this brain region. In the present study, we report that neurotoxic lesioning of the MePD advances puberty and increases weight gain in female rats fed a normal diet. However, MePD lesioned rats fed a 25% nonnutritive bulk diet also showed the dramatic advancement of puberty but without the increase in body weight. In both dietary groups, MePD lesions resulted in an increase in socialization and a decrease in play fighting behavior. Chronic GABAA receptor antagonism in the MePD from postnatal day 21 for 14 days also advanced puberty, increased socialization, and decreased play fighting without altering body weight, whereas glutamate receptor antagonism delayed puberty and decreased socialization without affecting play fighting. In conclusion, our results suggest the MePD regulates the timing of puberty via a novel mechanism independent of change in body weight and caloric intake. MePD glutamatergic systems advance the timing of puberty whereas local GABAergic activation results in a delay.

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The effect of MePD lesions on the behavioral activities monitored between pnd 27 and 33 in female rats fed with normal chow diet (ND) or 25% nonnutritive bulk diet (NND). A, In the 15-minute social interaction (SI) test, the MePD lesion significantly increased the time of behavioral interaction (sniffing, chasing, following, grooming, and mounting) in both the ND and NND groups. For the 20-minute play fighting behavioral test, the lesion significantly decreased the frequency of pinning events per 20-minute observation period (Pin frequency) (B) and the duration of play fighting behavior (pouncing, wrestling, boxing, and pinning) (C) in both ND and NND fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM, averaged for behavioral tests carried out on pnd 27, 29, 31, and 33 (n = 7–11 per group).
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Figure 4: The effect of MePD lesions on the behavioral activities monitored between pnd 27 and 33 in female rats fed with normal chow diet (ND) or 25% nonnutritive bulk diet (NND). A, In the 15-minute social interaction (SI) test, the MePD lesion significantly increased the time of behavioral interaction (sniffing, chasing, following, grooming, and mounting) in both the ND and NND groups. For the 20-minute play fighting behavioral test, the lesion significantly decreased the frequency of pinning events per 20-minute observation period (Pin frequency) (B) and the duration of play fighting behavior (pouncing, wrestling, boxing, and pinning) (C) in both ND and NND fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM, averaged for behavioral tests carried out on pnd 27, 29, 31, and 33 (n = 7–11 per group).

Mentions: The social interaction testing was performed on pnd 30. There was a marked impact of lesioning the MePD on social behavior, with a significant increase in the cumulative mean time spent engaged in social interaction behavior, including sniffing, chasing, following, grooming, and mounting in the MePD-lesioned compared with the sham-lesioned controls, irrespective of diet (normal diet: 73.2 ± 6.9 vs 116.5 ± 17.6 sec, control vs lesion, n = 10–11 per group, P < .05; nonnutritive bulk diet: 87.4 ± 8.3 vs 138.3 ± 1.7 sec, control vs lesion, n = 7–8 per group, mean ± SEM, P < .05; Figure 4A).


The Posterodorsal Medial Amygdala Regulates the Timing of Puberty Onset in Female Rats.

Li XF, Hu MH, Hanley BP, Lin YS, Poston L, Lightman SL, O'Byrne KT - Endocrinology (2015)

The effect of MePD lesions on the behavioral activities monitored between pnd 27 and 33 in female rats fed with normal chow diet (ND) or 25% nonnutritive bulk diet (NND). A, In the 15-minute social interaction (SI) test, the MePD lesion significantly increased the time of behavioral interaction (sniffing, chasing, following, grooming, and mounting) in both the ND and NND groups. For the 20-minute play fighting behavioral test, the lesion significantly decreased the frequency of pinning events per 20-minute observation period (Pin frequency) (B) and the duration of play fighting behavior (pouncing, wrestling, boxing, and pinning) (C) in both ND and NND fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM, averaged for behavioral tests carried out on pnd 27, 29, 31, and 33 (n = 7–11 per group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4588820&req=5

Figure 4: The effect of MePD lesions on the behavioral activities monitored between pnd 27 and 33 in female rats fed with normal chow diet (ND) or 25% nonnutritive bulk diet (NND). A, In the 15-minute social interaction (SI) test, the MePD lesion significantly increased the time of behavioral interaction (sniffing, chasing, following, grooming, and mounting) in both the ND and NND groups. For the 20-minute play fighting behavioral test, the lesion significantly decreased the frequency of pinning events per 20-minute observation period (Pin frequency) (B) and the duration of play fighting behavior (pouncing, wrestling, boxing, and pinning) (C) in both ND and NND fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM, averaged for behavioral tests carried out on pnd 27, 29, 31, and 33 (n = 7–11 per group).
Mentions: The social interaction testing was performed on pnd 30. There was a marked impact of lesioning the MePD on social behavior, with a significant increase in the cumulative mean time spent engaged in social interaction behavior, including sniffing, chasing, following, grooming, and mounting in the MePD-lesioned compared with the sham-lesioned controls, irrespective of diet (normal diet: 73.2 ± 6.9 vs 116.5 ± 17.6 sec, control vs lesion, n = 10–11 per group, P < .05; nonnutritive bulk diet: 87.4 ± 8.3 vs 138.3 ± 1.7 sec, control vs lesion, n = 7–8 per group, mean ± SEM, P < .05; Figure 4A).

Bottom Line: In both dietary groups, MePD lesions resulted in an increase in socialization and a decrease in play fighting behavior.In conclusion, our results suggest the MePD regulates the timing of puberty via a novel mechanism independent of change in body weight and caloric intake.MePD glutamatergic systems advance the timing of puberty whereas local GABAergic activation results in a delay.

View Article: PubMed Central - PubMed

Affiliation: Division of Women's Health (X.F.L., M.H.L., B.P.H., Y.S.L., L.P., K.T.O.), Faculty of Life Sciences and Medicine, King's College London, Guy's Campus, London SE1 1UL, United Kingdom; and Henry Wellcome Laboratory for Integrative Neuroscience and Endocrinology (S.L.L.), University of Bristol, Bristol BS1 3NY, United Kingdom.

ABSTRACT
Obesity is the major risk factor for early puberty, but emerging evidence indicates other factors including psychosocial stress. One key brain region notable for its role in controlling calorie intake, stress, and behavior is the amygdala. Early studies involving amygdala lesions that included the medial nucleus advanced puberty in rats. More recently it was shown that a critical site for lesion-induced hyperphagia and obesity is the posterodorsal subnucleus of the medial amygdala (MePD), which may explain the advancement of puberty. Glutamatergic activity also increases in the MePD during puberty without a corresponding γ-aminobutyric acid (GABA)ergic change, suggesting an overall activation of this brain region. In the present study, we report that neurotoxic lesioning of the MePD advances puberty and increases weight gain in female rats fed a normal diet. However, MePD lesioned rats fed a 25% nonnutritive bulk diet also showed the dramatic advancement of puberty but without the increase in body weight. In both dietary groups, MePD lesions resulted in an increase in socialization and a decrease in play fighting behavior. Chronic GABAA receptor antagonism in the MePD from postnatal day 21 for 14 days also advanced puberty, increased socialization, and decreased play fighting without altering body weight, whereas glutamate receptor antagonism delayed puberty and decreased socialization without affecting play fighting. In conclusion, our results suggest the MePD regulates the timing of puberty via a novel mechanism independent of change in body weight and caloric intake. MePD glutamatergic systems advance the timing of puberty whereas local GABAergic activation results in a delay.

Show MeSH
Related in: MedlinePlus