TY - JOUR
T1 - Contribution of glial-neuronal interactions to the neuroendocrine control of female puberty
AU - Ojeda, Sergio R.
AU - Lomniczi, Alejandro
AU - Sandau, Ursula
PY - 2010/12
Y1 - 2010/12
N2 - Mammalian puberty is initiated by an increased pulsatile release of the neuropeptide gonadotropin-releasing hormone (GnRH) from hypothalamic neuroendocrine neurons. Although this increase is primarily set in motion by neuronal networks synaptically connected to GnRH neurons, glial cells contribute to the process via at least two mechanisms. One involves production of growth factors acting via receptors endowed with either serine-threonine kinase or tyrosine kinase activity. The other involves plastic rearrangements of glia-GnRH neuron adhesiveness. Growth factors of the epidermal growth factor family acting via erbB receptors play a major role in glia-to-GnRH neuron communication. In turn, neurons facilitate astrocytic erbB signaling via glutamate-dependent cleavage of erbB ligand precursors. The genetic disruption of erbB receptors delays female sexual development due to impaired erbB ligand-induced glial prostaglandin E2 release. The adhesiveness of glial cells to GnRH neurons involves at least two different cell-cell communication systems endowed with both adhesive and intracellular signaling capabilities. One is provided by synaptic cell adhesion molecule (SynCAM1), which establishes astrocyte-GnRH neuron adhesiveness via homophilic interactions and the other involves the heterophilic interaction of neuronal contactin with glial receptor-like protein tyrosine phosphatase-β. These findings indicate that the interaction of glial cells with GnRH neurons involves not only secreted bioactive molecules, but also cell-surface adhesive proteins able to set in motion intracellular signaling cascades.
AB - Mammalian puberty is initiated by an increased pulsatile release of the neuropeptide gonadotropin-releasing hormone (GnRH) from hypothalamic neuroendocrine neurons. Although this increase is primarily set in motion by neuronal networks synaptically connected to GnRH neurons, glial cells contribute to the process via at least two mechanisms. One involves production of growth factors acting via receptors endowed with either serine-threonine kinase or tyrosine kinase activity. The other involves plastic rearrangements of glia-GnRH neuron adhesiveness. Growth factors of the epidermal growth factor family acting via erbB receptors play a major role in glia-to-GnRH neuron communication. In turn, neurons facilitate astrocytic erbB signaling via glutamate-dependent cleavage of erbB ligand precursors. The genetic disruption of erbB receptors delays female sexual development due to impaired erbB ligand-induced glial prostaglandin E2 release. The adhesiveness of glial cells to GnRH neurons involves at least two different cell-cell communication systems endowed with both adhesive and intracellular signaling capabilities. One is provided by synaptic cell adhesion molecule (SynCAM1), which establishes astrocyte-GnRH neuron adhesiveness via homophilic interactions and the other involves the heterophilic interaction of neuronal contactin with glial receptor-like protein tyrosine phosphatase-β. These findings indicate that the interaction of glial cells with GnRH neurons involves not only secreted bioactive molecules, but also cell-surface adhesive proteins able to set in motion intracellular signaling cascades.
KW - Female sexual development
KW - Glial cells
KW - Glial-neuronal interactions
KW - Hypothalamus
KW - Intercellular signaling
KW - Neuroendocrine neurons
UR - http://www.scopus.com/inward/record.url?scp=78649997074&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=78649997074&partnerID=8YFLogxK
U2 - 10.1111/j.1460-9568.2010.07515.x
DO - 10.1111/j.1460-9568.2010.07515.x
M3 - Article
C2 - 21143655
AN - SCOPUS:78649997074
SN - 0953-816X
VL - 32
SP - 2003
EP - 2010
JO - European Journal of Neuroscience
JF - European Journal of Neuroscience
IS - 12
ER -