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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 body weight gain and day of vaginal opening in rats. A, Cumulative body weight gain was significantly greater from pnd 27 onward in the lesioned group compared with the sham-lesioned female rats fed with normal chow diet. B, In contrast, there is no significant difference in body weight gain between the lesioned and sham-lesioned animals fed the 25% nonnutritive bulk diet. The MePD lesion resulted in a significant advancement of pubertal onset (vaginal opening) in both normal (C) and nonnutritive bulk diet (D) fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM (n = 7–11 per group).
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Figure 2: The effect of MePD lesions on body weight gain and day of vaginal opening in rats. A, Cumulative body weight gain was significantly greater from pnd 27 onward in the lesioned group compared with the sham-lesioned female rats fed with normal chow diet. B, In contrast, there is no significant difference in body weight gain between the lesioned and sham-lesioned animals fed the 25% nonnutritive bulk diet. The MePD lesion resulted in a significant advancement of pubertal onset (vaginal opening) in both normal (C) and nonnutritive bulk diet (D) fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM (n = 7–11 per group).

Mentions: Although there was no significant difference in body weight (Figure 2, A and B) at weaning among the experimental groups, MePD lesioning on pnd 21 increased body weight gain in animals fed normal standard diet, and this was evident from pnd 27 onward (Figure 2A; P < .05). Unsurprisingly, this was associated with a significant advancement of puberty onset compared with sham-lesioned controls (vaginal opening: 34.4 ± 0.5 vs 37.8 ± 0.7 d, respectively; Figure 2C; n = 10–11 per group; P < .05; first estrus: 34.6 ± 0.7 vs 37.9 ± 0.7 d, respectively, mean ± SEM; P < .0.05).


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 body weight gain and day of vaginal opening in rats. A, Cumulative body weight gain was significantly greater from pnd 27 onward in the lesioned group compared with the sham-lesioned female rats fed with normal chow diet. B, In contrast, there is no significant difference in body weight gain between the lesioned and sham-lesioned animals fed the 25% nonnutritive bulk diet. The MePD lesion resulted in a significant advancement of pubertal onset (vaginal opening) in both normal (C) and nonnutritive bulk diet (D) fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM (n = 7–11 per group).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: The effect of MePD lesions on body weight gain and day of vaginal opening in rats. A, Cumulative body weight gain was significantly greater from pnd 27 onward in the lesioned group compared with the sham-lesioned female rats fed with normal chow diet. B, In contrast, there is no significant difference in body weight gain between the lesioned and sham-lesioned animals fed the 25% nonnutritive bulk diet. The MePD lesion resulted in a significant advancement of pubertal onset (vaginal opening) in both normal (C) and nonnutritive bulk diet (D) fed rats. *, P < .05 vs sham lesion control. Results represent mean ± SEM (n = 7–11 per group).
Mentions: Although there was no significant difference in body weight (Figure 2, A and B) at weaning among the experimental groups, MePD lesioning on pnd 21 increased body weight gain in animals fed normal standard diet, and this was evident from pnd 27 onward (Figure 2A; P < .05). Unsurprisingly, this was associated with a significant advancement of puberty onset compared with sham-lesioned controls (vaginal opening: 34.4 ± 0.5 vs 37.8 ± 0.7 d, respectively; Figure 2C; n = 10–11 per group; P < .05; first estrus: 34.6 ± 0.7 vs 37.9 ± 0.7 d, respectively, mean ± SEM; P < .0.05).

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