The organizational hypothesis and final common pathways: Sexual differentiation of the spinal cord and peripheral nervous system

Forger, Nancy G.

doi:10.1016/j.yhbeh.2009.03.008

Cited by 27 publications

(25 citation statements)

References 75 publications

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“…These results are in accord with those of the spinal GRP system in terms of low-sensitivities for androgens in adult females (Sakamoto et al , 2009b. Consequently, these results could indicate that both testosterone and AR, as an androgen signaling system, are necessary to maintain both the GRP and SNB systems in the lumbar spinal cord (Sakamoto and Kawata 2009;Sengelaub and Forger 2008;Forger 2009). These two systems within the same lumbar spinal level could interact directly because the sexually dimorphic distribution of GRP-immunoreactive fibers in the lower lumbar spinal cord (L5-L6 level) is profoundly regulated by circulating androgen levels (Sakamoto et al 2009b) and mirrors changes in SNB motoneuron arborization and synapse number (Kurz et al 1986;Matsumoto 2001;Matsumoto et al 1988).…”

Section: The Afferent Inputs From the Spinal Grp System To Snb Systemsupporting

confidence: 83%

The gastrin-releasing peptide system in the spinal cord mediates masculine sexual function

Sakamoto

2010

Anat Sci Int

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The lumbar spinal segments are of particular interest because they are sexually dimorphic and contain several neuronal circuits that are important in eliciting male sexual responses such as erection and ejaculation. Gastrin-releasing peptide (GRP) is a member of the bombesin-like peptide family first isolated from the porcine stomach. A collection of neurons in the lumbar spinal cord (L3-L4 level) of male rats projects to the lower lumbar spinal cord (L5-L6 level), releasing GRP onto somatic and autonomic centers known to regulate male sexual reflexes. All these target neurons express and localize specific receptors for GRP. This system of GRP neurons is sexually dimorphic, being prominent in male rats but vestigial in females. The system is completely feminine in genetically XY rats with a dysfunctional androgen receptor gene, demonstrating the androgen-dependent nature of the dimorphism. Pharmacological stimulation of GRP receptors in this spinal region remarkably restores sexual reflexes in castrated male rats. Exposure of male rats to a severe traumatic stress decreases the local content and the axonal distribution of GRP in the lumbar spinal cord and results in an attenuation of penile reflexes in vivo. Administration of a specific agonist for GRP receptors restores penile reflexes in the traumatic stress-exposed male rats. This review summarizes findings on this recently identified spinal GRP system, which may be vulnerable to stress, that controls male reproductive function. The identification of a male-specific neuronal system regulating sexual functions offers new avenues for potential therapeutic approaches to masculine reproductive dysfunction.

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Section: The Afferent Inputs From the Spinal Grp System To Snb Systemsupporting

confidence: 83%

The gastrin-releasing peptide system in the spinal cord mediates masculine sexual function

Sakamoto

2010

Anat Sci Int

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“…In spinal levels, sexual dimorphic nuclei are comprised of Onuf's nucleus, the spinal nucleus of the bulbocavernosus (SNB), the spinal ejaculation center, the spinal gastrin-releasing peptide (GRP) system, and primary sensory afferents (97). (i) Onuf's nucleus is involved in the maintenance of micturition and defecatory continence as well as in muscular contraction during orgasm (267).…”

Section: Sexual Dysfunctionmentioning

confidence: 99%

Autonomic Consequences of Spinal Cord Injury

Hou

Rabchevsky

2014

Comprehensive Physiology

179

112

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Spinal cord injury (SCI) results not only in motor and sensory deficits but also in autonomic dysfunctions. The disruption of connections between higher brain centers and the spinal cord, or the impaired autonomic nervous system itself, manifests a broad range of autonomic abnormalities. This includes compromised cardiovascular, respiratory, urinary, gastrointestinal, thermoregulatory, and sexual activities. These disabilities evoke potentially life-threatening symptoms that severely interfere with the daily living of those with SCI. In particular, high thoracic or cervical SCI often causes disordered hemodynamics due to deregulated sympathetic outflow. Episodic hypertension associated with autonomic dysreflexia develops as a result of massive sympathetic discharge often triggered by unpleasant visceral or sensory stimuli below the injury level. In the pelvic floor, bladder and urethral dysfunctions are classified according to upper motor neuron versus lower motor neuron injuries; this is dependent on the level of lesion. Most impairments of the lower urinary tract manifest in two interrelated complications: bladder storage and emptying. Inadequate or excessive detrusor and sphincter functions as well as detrusor-sphincter dyssynergia are examples of micturition abnormalities stemming from SCI. Gastrointestinal motility disorders in spinal cord injured-individuals are comprised of gastric dilation, delayed gastric emptying, and diminished propulsive transit along the entire gastrointestinal tract. As a critical consequence of SCI, neurogenic bowel dysfunction exhibits constipation and/or incontinence. Thus, it is essential to recognize neural mechanisms and pathophysiology underlying various complications of autonomic dysfunctions after SCI. This overview provides both vital information for better understanding these disorders and guides to pursue novel therapeutic approaches to alleviate secondary complications.

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“…For example, the amygdala, the intermediate nucleus of the hypothalamus, the bed nucleus of the stria terminalis (BnST), and the human homologue of the medial preoptic area, INAH1, are larger in men than in women, while prefrontal cortices are larger in women than in men (Goldstein et al, 2001; Hamann 2005; Bao and Swaab, 2011). In rodents, it has been well demonstrated that early organizational actions of sex steroids result in sex-specific differences in cell number and critical chemical signaling pathways in these same regions, suggesting that by adolescence, the neural templates that give rise to anxiety are explicitly different in the male versus the female brain (Toufexis, 2007; Forger, 2009; Harada et al, 2009; Hisasue et al, 2010; Bangasser and Valentino, 2012; Gilmore et al, 2012; Valentino et al, 2012, 2013). …”

Section: Introductionmentioning

confidence: 99%

Sex and exercise interact to alter the expression of anabolic androgenic steroid-induced anxiety-like behaviors in the mouse

Onakomaiya

Porter

Oberlander

et al. 2014

Hormones and Behavior

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Anabolic androgenic steroids (AAS) are taken by both sexes to enhance athletic performance and body image, nearly always in conjunction with an exercise regime. Although taken to improve physical attributes, chronic AAS use can promote negative behavior, including anxiety. Few studies have directly compared the impact of AAS use in males versus females or assessed the interaction of exercise and AAS. We show that AAS increase anxiety-like behaviors in female but not male mice and that voluntary exercise accentuates these sex-specific differences. We also show that levels of the anxiogenic peptide corticotrophin releasing factor (CRF) are significantly greater in males, but that AAS selectively increase CRF levels in females, thus abrogating this sex-specific difference. Exercise did not ameliorate AAS-induced anxiety or alter CRF levels in females. Exercise was anxiolytic in males, but this behavioral outcome did not correlate with CRF levels. Brain-derived neurotrophic factor (BDNF) has also been implicated in the expression of anxiety. As with CRF, levels of hippocampal BDNF mRNA were significantly greater in males than females. AAS and exercise were without effect on BDNF mRNA in females. In males, anxiolytic effects of exercise correlated with increased BDNF mRNA, however AAS-induced changes in BDNF mRNA and anxiety did not. In sum, we find that AAS elicit sex-specific differences in anxiety and that voluntary exercise accentuates these differences. In addition, our data suggest that these behavioral outcomes may reflect convergent actions of AAS and exercise on a sexually differentiated CRF signaling system within the extended amygdala.

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The organizational hypothesis and final common pathways: Sexual differentiation of the spinal cord and peripheral nervous system

Cited by 27 publications

References 75 publications

The gastrin-releasing peptide system in the spinal cord mediates masculine sexual function

The gastrin-releasing peptide system in the spinal cord mediates masculine sexual function

Autonomic Consequences of Spinal Cord Injury

Sex and exercise interact to alter the expression of anabolic androgenic steroid-induced anxiety-like behaviors in the mouse

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