Receptors to Steroid Hormones and Aromatase Are Expressed by Cultured Motoneurons but Not by Glial Cells Derived from Rat Embryo Spinal Cord

Rakotoarivelo, Clovis; Petite, Didier; Lambard, Sophie; Fabre, Christine; Rouleau, Caroline; Lumbroso, Serge; Weille, Jan de; Privat, Alain; Carreau, Serge; Mersel, Marcel

doi:10.1159/000083611

Cited by 20 publications

(23 citation statements)

References 132 publications

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“…This neuroprotective activity of 17b-estradiol was not modified by the estrogen receptor antagonist ICI 182,780 added directly to the astrocyte-motor neuron co-culture during the 24 h of damage development, thus ruling out an interaction of the hormone with neuronal estrogen receptor. In addition, despite the recently reported expression of estrogen receptors on cultured spinal cord motor neurons [Rakotoarivelo et al, 2004], we have not been able to detect any protective activity when 17b-estradiol was added directly to motor neurons exposed to AMPA [Platania et al, 2005].…”

Section: Amyotrophic Lateral Sclerosis (Als)contrasting

confidence: 93%

A major role for astrocytes in the neuroprotective effect of estrogen

Sortino

Platania

Chisari

et al. 2005

Drug Development Research

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Estrogen exerts neurotrophic and neuroprotective activity as suggested by both in vitro and in vivo evidence. Expression of estrogen receptors has been demonstrated in neurons and also in glial cells. Glia, and in particular astrocytes, represent a target for estrogen and contribute to the neuroprotective effect of the steroid hormone. Particular emphasis is given here to the role of astrocytes in mediating some of the protective effects of estrogen in models of neuronal damage. Estrogen receptors are up-regulated in different brain areas during neurodegeneration, a phenomenon that may potentiate neuroprotective mechanisms, and estrogen appears effective in modulating the uptake of the excitotoxin glutamate. In addition, following neuronal insults, astrocytes may represent a source of estrogen through overexpression of the estrogen-synthesizing enzyme, aromatase. The contribution of astrocytes as a source of growth factors is also discussed in terms of the neuroprotection obtained in different in vitro models of neurodegenerative conditions. Drug Dev. Res. 66:126-135, 2006.

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Section: Amyotrophic Lateral Sclerosis (Als)contrasting

confidence: 93%

A major role for astrocytes in the neuroprotective effect of estrogen

Sortino

Platania

Chisari

et al. 2005

Drug Development Research

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“…Sex steroids can be synthesized in a number of tissues, including the central nervous system [56]. In the spinal cord, enzymes in the biosynthetic pathway for androgens are found both in motoneurons [57], [58] and glial cells [59], [60], [61], [62], indicating that these cells could be a source of localized production of androgens. Of particular interest is the enzyme cytochrome C P450 aromatase, which catalyzes the conversion of testosterone and its precursors into estradiol, a potent neurosteroid.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Exercise on Synaptic Stripping Require Androgen Receptor Signaling

2014

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Following peripheral nerve injury, synapses are withdrawn from axotomized motoneurons. Moderate daily treadmill exercise, which promotes axon regeneration of cut peripheral nerves, also influences this synaptic stripping. Different exercise protocols are required to promote axon regeneration in male and female animals, but the sex requirements for an effect of exercise on synaptic stripping are unknown. In male and female C57BL/6 mice, the sciatic nerve was transected in the mid-thigh. Mice were then exercised five days per week for two weeks, beginning on the third post-transection day. Half of the exercised mice were trained by walking slowly (10 M/min) on a level treadmill for one hour per day (continuous training). Other mice were interval trained; four short (two min) sprints at 20 M/min separated by five minute rest periods. A third group was untrained. The extent of synaptic contacts made by structures immunoreactive to vesicular glutamate transporter 1 and glutamic acid decarboxylase 67 onto axotomized motoneurons was studied in confocal images of retrogradely labeled cells. Both types of presumed synaptic contacts were reduced markedly in unexercised mice following nerve transection, relative to intact mice. No significant reduction was found in continuous trained males or interval trained females. Reductions in these contacts in interval trained males and continuous trained females were identical to that observed in untrained mice. Treatments with the anti-androgen, flutamide, blocked the effect of sex-appropriate exercise on synaptic contacts in both males and females. Moderate daily exercise has a potent effect on synaptic inputs to axotomized motoneurons. Successful effects of exercise have different requirements in males and females, but require androgen receptor signaling in both sexes.

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“…This gestational period is thought to be when masculinization of the GFN occurs [3], as it is when flutamide inhibits inguinoscrotal TD [8]. Some studies have found AR in the motor neurons of E rats [10,11]. In addition, AR messenger RNA has been isolated in the spinal cord and DRG of E male mice [12]; however, this did not include protein expression.…”

Section: Discussionmentioning

confidence: 99%