Kinesin superfamily-associated protein 3 is preferentially expressed in glutamatergic neurons and contributes to the excitatory control of female puberty

Jungil Choi, Man Ha Chang, Jung Choi Eun, Soo Jeong Choon, Woo Park Jeong, Ja Hyun Baik, Jae Yong Park, Maria E. Costa, Sergio Ojeda, Ju Lee Byung

    Research output: Contribution to journalArticle

    11 Citations (Scopus)

    Abstract

    It was earlier shown that expression of kinesin superfamily-associated protein 3 (KAP3), involved in the neuronal anterograde, microtubule-dependent transport of membrane organelles, increases in the hypothalamus of female rats during the juvenile phase of sexual development. KAP3 mRNA is abundant in the hypothalamus, suggesting that it might be expressed in broadly disseminated neuronal systems controlling neuroendocrine function. The present study identifies one of these systems and provides evidence for an involvement of KAP3 in the excitatory control of female puberty. In situ hybridization and immunohistofluorescence studies revealed that the KAP3 gene is expressed in glutamatergic neurons but not in GABAergic or GnRH neurons. Hypothalamic KAP3 mRNA levels increase during the juvenile period of female prepubertal development, remaining elevated throughout puberty. These changes appear to be, at least in part, estradiol dependent because ovariectomy decreases and estradiol increases KAP3 mRNA abundance. Lowering hypothalamic KAP3 protein levels via intraventricular administration of an antisense oligodeoxynucleotide resulted in reduced release of both glutamate and GnRH from the median eminence and delayed the onset of puberty. The median eminence content of vesicular glutamate transporter 2, a glutamate neuronselective synaptic protein, and synaptophysin, a synaptic vesicle marker, were also reduced, suggesting that the loss of KAP3 diminishes the anterograde transport of these proteins. Altogether, these results support the view that decreased KAP3 synthesis diminishes GnRH output and delays female sexual development by compromising hypothalamic release of glutamate.

    Original languageEnglish (US)
    Pages (from-to)6146-6156
    Number of pages11
    JournalEndocrinology
    Volume149
    Issue number12
    DOIs
    StatePublished - Dec 2008

    Fingerprint

    Kinesin
    Puberty
    Neurons
    Proteins
    Gonadotropin-Releasing Hormone
    Glutamic Acid
    Median Eminence
    Sexual Development
    Messenger RNA
    Hypothalamus
    Estradiol
    Vesicular Glutamate Transport Protein 2
    Delayed Puberty
    Synaptophysin
    Neurosecretory Systems
    Synaptic Vesicles
    Oligodeoxyribonucleotides
    Ovariectomy
    Microtubules
    Organelles

    ASJC Scopus subject areas

    • Endocrinology

    Cite this

    Kinesin superfamily-associated protein 3 is preferentially expressed in glutamatergic neurons and contributes to the excitatory control of female puberty. / Choi, Jungil; Chang, Man Ha; Eun, Jung Choi; Choon, Soo Jeong; Jeong, Woo Park; Baik, Ja Hyun; Park, Jae Yong; Costa, Maria E.; Ojeda, Sergio; Byung, Ju Lee.

    In: Endocrinology, Vol. 149, No. 12, 12.2008, p. 6146-6156.

    Research output: Contribution to journalArticle

    Choi, Jungil ; Chang, Man Ha ; Eun, Jung Choi ; Choon, Soo Jeong ; Jeong, Woo Park ; Baik, Ja Hyun ; Park, Jae Yong ; Costa, Maria E. ; Ojeda, Sergio ; Byung, Ju Lee. / Kinesin superfamily-associated protein 3 is preferentially expressed in glutamatergic neurons and contributes to the excitatory control of female puberty. In: Endocrinology. 2008 ; Vol. 149, No. 12. pp. 6146-6156.
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    abstract = "It was earlier shown that expression of kinesin superfamily-associated protein 3 (KAP3), involved in the neuronal anterograde, microtubule-dependent transport of membrane organelles, increases in the hypothalamus of female rats during the juvenile phase of sexual development. KAP3 mRNA is abundant in the hypothalamus, suggesting that it might be expressed in broadly disseminated neuronal systems controlling neuroendocrine function. The present study identifies one of these systems and provides evidence for an involvement of KAP3 in the excitatory control of female puberty. In situ hybridization and immunohistofluorescence studies revealed that the KAP3 gene is expressed in glutamatergic neurons but not in GABAergic or GnRH neurons. Hypothalamic KAP3 mRNA levels increase during the juvenile period of female prepubertal development, remaining elevated throughout puberty. These changes appear to be, at least in part, estradiol dependent because ovariectomy decreases and estradiol increases KAP3 mRNA abundance. Lowering hypothalamic KAP3 protein levels via intraventricular administration of an antisense oligodeoxynucleotide resulted in reduced release of both glutamate and GnRH from the median eminence and delayed the onset of puberty. The median eminence content of vesicular glutamate transporter 2, a glutamate neuronselective synaptic protein, and synaptophysin, a synaptic vesicle marker, were also reduced, suggesting that the loss of KAP3 diminishes the anterograde transport of these proteins. Altogether, these results support the view that decreased KAP3 synthesis diminishes GnRH output and delays female sexual development by compromising hypothalamic release of glutamate.",
    author = "Jungil Choi and Chang, {Man Ha} and Eun, {Jung Choi} and Choon, {Soo Jeong} and Jeong, {Woo Park} and Baik, {Ja Hyun} and Park, {Jae Yong} and Costa, {Maria E.} and Sergio Ojeda and Byung, {Ju Lee}",
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    AU - Choi, Jungil

    AU - Chang, Man Ha

    AU - Eun, Jung Choi

    AU - Choon, Soo Jeong

    AU - Jeong, Woo Park

    AU - Baik, Ja Hyun

    AU - Park, Jae Yong

    AU - Costa, Maria E.

    AU - Ojeda, Sergio

    AU - Byung, Ju Lee

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    AB - It was earlier shown that expression of kinesin superfamily-associated protein 3 (KAP3), involved in the neuronal anterograde, microtubule-dependent transport of membrane organelles, increases in the hypothalamus of female rats during the juvenile phase of sexual development. KAP3 mRNA is abundant in the hypothalamus, suggesting that it might be expressed in broadly disseminated neuronal systems controlling neuroendocrine function. The present study identifies one of these systems and provides evidence for an involvement of KAP3 in the excitatory control of female puberty. In situ hybridization and immunohistofluorescence studies revealed that the KAP3 gene is expressed in glutamatergic neurons but not in GABAergic or GnRH neurons. Hypothalamic KAP3 mRNA levels increase during the juvenile period of female prepubertal development, remaining elevated throughout puberty. These changes appear to be, at least in part, estradiol dependent because ovariectomy decreases and estradiol increases KAP3 mRNA abundance. Lowering hypothalamic KAP3 protein levels via intraventricular administration of an antisense oligodeoxynucleotide resulted in reduced release of both glutamate and GnRH from the median eminence and delayed the onset of puberty. The median eminence content of vesicular glutamate transporter 2, a glutamate neuronselective synaptic protein, and synaptophysin, a synaptic vesicle marker, were also reduced, suggesting that the loss of KAP3 diminishes the anterograde transport of these proteins. Altogether, these results support the view that decreased KAP3 synthesis diminishes GnRH output and delays female sexual development by compromising hypothalamic release of glutamate.

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