Androgens modulate endplate size and ACh receptor density at synapses in rat levator ani muscle

Bleisch, William V.; Harrelson, Allan

doi:10.1002/neu.480200403

Cited by 33 publications

(27 citation statements)

References 42 publications

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“…A positive correlation between androgen levels and muscle fiber size has also been shown in sexually dimorphic, androgen-sensitive muscles in other vertebrate classes. Castration causes a decrease in fiber size that is reversible with testosterone treatment in rat bulbocavernosus muscles (Bleisch and Harrelson, 1989;Balice-Gordon et al, 1990), songbird syringeal muscles (Luine et al, 1980), and guinea pig temporalis muscles (Papanicolau and Falk, 1938;Kochakian et al, 1956).…”

Section: Effects Of Testosterone On Muscle Fiber Propertiesmentioning

confidence: 93%

Differential sensitivity to androgens within a sexually dimorphic muscle of male frogs (Xenopus laevis)

Regnier

Herrera

1993

J. Neurobiol.

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Male frogs use their forelimb flexor muscles to clasp females during the mating behavior known as amplexus. We investigated the effects of testosterone on a principal forelimb flexor, the flexor carpi radialis muscle (FCR), using morphological and histochemical techniques. Male Xenopus laevis were surgically manipulated to produce high or low levels of circulating testosterone for an 8-week period. After this treatment, measurement of fibers in muscle cross-sections revealed that average fiber size was positively correlated with testosterone level. This effect was not the same for all muscle fibers, however. Fibers in the shoulder region were more sensitive to testosterone than fibers in other regions of the muscle. Histochemical staining of cross-sections showed that the patterns of staining for myosin ATPase or succinic dehydrogenase (SDH) were not influenced by testosterone levels, but total SDH activity was increased by testosterone treatment. When sensitivity to testosterone was correlated with ATPase activity, fibers with high ATPase activity were found to be more sensitive to testosterone than fibers with low activity, regardless of position within the muscle. Most fibers with high ATPase activity were located in the shoulder region of the muscle. These fibers are innervated by different motor axons than are fibers in the elbow region of the muscle, and contractions of shoulder (but not elbow) region fibers, elicited by stimulation of motor axons, are slowed by testosterone treatment (Regnier and Herrera, 1993, J. Physiol. 461:565-581).

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Section: Effects Of Testosterone On Muscle Fiber Propertiesmentioning

confidence: 93%

Differential sensitivity to androgens within a sexually dimorphic muscle of male frogs (Xenopus laevis)

Regnier

Herrera

1993

J. Neurobiol.

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“…In addition, there is strong evidence for the fact that testosterone via its receptor may regulate the coupling mechanisms between Ca v2.2 channels and neurotransmitter release at the neuromuscular junctions of bulbocavernosus and levator ani muscles motoneurons (Nudler et al, 2005). Earlier results have shown that testosterone deprivation reduces the junctional acetylcholine receptor density and androgens modulate endplate size and acetylcholine ACh receptor density at synapses in rat levator ani muscle (Bleisch and Harrelson, 1989;Bleisch et al, 1982;Souccar et al, 1991). Finally, in Xenopus laevis, females have stronger laryngeal synapses than males, and synapse strength is estrogen dependent and the laryngeal neuromuscular synapse is the final effector for sexually differentiated song production.…”

Section: Genetic and Age-linked Alterations In Lactate Homeostasis Unmentioning

confidence: 99%

Lactate dyscrasia: a novel explanation for amyotrophic lateral sclerosis

Meethal

Atwood

2012

Neurobiology of Aging

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Amyotrophic lateral sclerosis (ALS; Lou Gehrig's disease) is a progressive debilitating neurodegenerative disease with no cure. We propose a novel molecular model for the pathogenesis of ALS that involves an adenosine triphosphate (ATP)-dependent muscle neuronal lactate shuttle (MNLS) at the neuromuscular junction (NMJ) to regulate the flow of lactate from muscle to neurons and vice versa. Failure of the MNLS due to respiratory chain dysfunction is proposed to result in lactate toxicity and degeneration of nerve endings at the NMJ leading to nerve terminus dysjunction from the muscle cell. At a critical threshold where denervation outpaces reinnervation, a vicious cycle is established where the remaining innervated muscle fibers are required to work harder to compensate for normal function, and in so doing produce toxic lactate concentrations which induces further denervation and neuronal death. This mechanism explains the exponential progression of ALS leading to paralysis. The molecular events leading to the dysregulation of the MNLS and the dismantling of NMJ are explained in the context of known ALS familial mutations and age-related endocrine dyscrasia. Combination drug therapies that inhibit lactate accumulation at the NMJ, enhance respiratory chain function, and/or promote reinnervation are predicted to be effective therapeutic strategies for ALS. Published by Elsevier Inc.

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“…These anabolic effects of androgens involve changes in perineal muscle fiber size, without a change in fiber number (Venable, 1966). Androgens in adulthood also maintain BC/LA neuromuscular junction size (Bleisch and Harrelson, 1989;Balice-Gordon et al, 1990;Lubischer and Bebinger, 1999), acetylcholine receptor number (Bleisch et al, 1982;Bleisch and Harrelson, 1989), and peripheral nerve activity (Fargo et al, 2003).…”

Section: Hormone Dependence Of the Bc/la Muscles In Adulthoodmentioning

confidence: 99%

The spinal nucleus of the bulbocavernosus: Firsts in androgen-dependent neural sex differences

Sengelaub

Forger

2008

Hormones and Behavior

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Cell number in the spinal nucleus of the bulbocavernosus (SNB) of rats was the first neural sex difference shown to differentiate under the control of androgens, acting via classical intracellular androgen receptors. SNB motoneurons reside in the lumbar spinal cord and innervate striated muscles involved in copulation, including the bulbocavernosus (BC) and levator ani (LA). SNB cells are much larger and more numerous in males than in females, and the BC/LA target muscles are reduced or absent in females. The relative simplicity of this neuromuscular system has allowed for considerable progress in pinpointing sites of hormone action, and identifying the cellular bases for androgenic effects. It is now clear that androgens act at virtually every level of the SNB system, in development and throughout adult life. In this review we focus on effects of androgens on developmental cell death of SNB motoneurons and BC/LA muscles; the establishment and maintenance of SNB motoneuron soma size and dendritic length; BC/LA muscle morphology and physiology; and behaviors controlled by the SNB system. We also describe new data on neurotherapeutic effects of androgens on SNB motoneurons after injury in adulthood.

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Androgens modulate endplate size and ACh receptor density at synapses in rat levator ani muscle

Cited by 33 publications

References 42 publications

Differential sensitivity to androgens within a sexually dimorphic muscle of male frogs (Xenopus laevis)

Differential sensitivity to androgens within a sexually dimorphic muscle of male frogs (Xenopus laevis)

Lactate dyscrasia: a novel explanation for amyotrophic lateral sclerosis

The spinal nucleus of the bulbocavernosus: Firsts in androgen-dependent neural sex differences

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