Castration and the Growth of Muscles in the Rat1

Kochakian, Charles D.; Tillotson, Carol; Endahl, Gerald L.

doi:10.1210/endo-58-2-226

Cited by 41 publications

(11 citation statements)

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“…In our previous studies, wherein we utilized the highly androgen sensitive SNB neuromuscular system (Fargo and Sengelaub, 2004a,b; 2007), testosterone treatment increased the size of the non-saporin-injected adjacent perineal musculature by approximately 20%. Although androgens are known to have protein anabolic effects on general skeletal muscle tissue (Kochakian, 1975), these effects are small compared to those observed in the perineal muscles (Kochakian et al, 1956; Wainman and Shipounoff, 1941). This, combined with the modest supplemental testosterone treatment we used in the current study, makes the lack of effect of testosterone on quadriceps muscle weight unsurprising.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of testosterone on the morphology and function of somatic motoneurons following the death of neighboring motoneurons

Little

Coons

Sengelaub

2008

J of Comparative Neurology

108

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Motoneuron loss is a significant medical problem, capable of causing severe movement disorders or even death. We have previously shown that partial depletion of motoneurons from sexually dimorphic, highly androgen-sensitive spinal motor populations induces dendritic atrophy in remaining motoneurons, and this atrophy is attenuated by treatment with testosterone. To test whether testosterone has similar effects in more typical motoneurons, we examined potential neuroprotective effects in motoneurons innervating muscles of the quadriceps. Motoneurons innervating the vastus medialis muscle were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, some saporin-injected rats were given implants containing testosterone or left untreated. Four weeks later, motoneurons innervating the ipsilateral vastus lateralis muscle were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. Compared to intact normal males, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons, and this atrophy was attenuated by testosterone treatment. To examine the functional consequences of the induced dendritic atrophy, and its attenuation with testosterone treatment, the activation of remaining quadriceps motoneurons was assessed using peripheral nerve recording. Partial motoneuron depletion resulted in decreased amplitudes of motor nerve activity, and these changes were attenuated by treatment with testosterone, providing a functional correlate to the neuroprotective effects of testosterone treatment on quadriceps motoneuron morphology. Together, these findings suggest that testosterone has neuroprotective effects on morphology and function in both highly androgen-sensitive as well as more typical motoneuron populations, further supporting a role for testosterone as a neurotherapeutic agent in the injured nervous system.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of testosterone on the morphology and function of somatic motoneurons following the death of neighboring motoneurons

Little

Coons

Sengelaub

2008

J of Comparative Neurology

108

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“…Because the weight of the contralateral vastus lateralis muscles was not affected by testosterone treatment, the lack of an androgen effect on the muscles adjacent to the saporin-injected muscles cannot be ascribed to an inhibition of an anabolic effect of testosterone by saporin. Although androgens are known to have protein anabolic effects on general skeletal muscle tissue [18], these effects are small compared to those observed in highly androgen-sensitive, sexually dimorphic muscles (e.g., the perineal muscles, [19,34]). Because the dendritic atrophy in remaining quadriceps motoneurons was attenuated by testosterone treatment while no effects were seen in target muscle weight, it is unlikely that any potential neurotrophic support from the musculature is dependent on muscle size alone.…”

mentioning

confidence: 99%

Neuroprotective effects of testosterone on dendritic morphology following partial motoneuron depletion: Efficacy in female rats

Wilson

Coons

Sengelaub

2009

Neuroscience Letters

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Motoneuron loss is a significant medical problem, capable of causing severe movement disorders and even death. We have previously demonstrated that partial depletion of motoneurons induces dendritic atrophy in remaining motoneurons, with a concomitant reduction in motor activation. Treatment of male rats with testosterone attenuates the regressive changes following partial motoneuron depletion. To test whether testosterone has similar effects in females, we examined potential neuroprotective effects in motoneurons innervating muscles of the quadriceps of female rats. Motoneurons were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, some saporin-injected rats were given implants containing testosterone or left untreated. Four weeks later, surviving motoneurons were labeled with cholera toxin-conjugated HRP, and dendritic arbors were reconstructed in 3 dimensions. Compared to normal females, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons, and this atrophy was greatly attenuated by testosterone treatment. These findings suggest that testosterone has neuroprotective effects on morphology in both males and females, further supporting a role for testosterone as a neurotherapeutic agent in the injured nervous system. Keywords steroids; neuroprotection; morphology; dendrites Motoneuron diseases such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophies (e.g., spinal and bulbar muscular atrophy) are characterized by progressive loss of motoneurons [3,17]. Similarly, damage to spinal nerves resulting in laceration and avulsion of spinal roots can lead to the death of motoneurons and preganglionic autonomic neurons in the spinal cord, resulting in autonomic and motor dysfunction [16]. However, the death of motoneurons is not the only outcome, and after such insults surviving motoneurons undergo dendritic retraction and atrophy [e.g., 2,28] as well as functional and biochemical changes [e.g., 1,33]. We have been examining the effects of motoneuron loss on the structure and function of surviving motoneurons using a rat model of motoneuron death. Partial depletion of motoneurons results in substantial somal and dendritic atrophy [10][11][12]23] and reduced excitability [9,23] in the remaining motoneurons.

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“…Skeletal muscle is a sex steroid‐sensitive tissue and it expresses receptors for both androgens and estrogens (Svensson et al, ). Testosterone, dihydrotestosterone and estradiol affect growth, strength, metabolism, and antioxidants in the skeletal muscle (Aizawa et al, ; Baltgalvis et al, ; Bhasin et al, ; Dube et al, ; Hamdi & Mutungi, ) Although androgens are known to have protein anabolic effects on general skeletal muscle tissue, these effects vary and are small compared to those observed in perineal muscles such as the Pcm of male and female rats (Wainman and Shipounoff, ; Kochakian et al, ; Alvarado et al, ; Lara‐Garcia et al, ;).…”

Section: Discussionmentioning

confidence: 99%

Hormonal Treatment Effects on the Cross‐sectional Area of Pubococcygeus Muscle Fibers After Denervation and Castration in Male Rats

Lara-García

Alvarado

Cuevas

et al. 2017

The Anatomical Record

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We explore the interaction of muscle innervation and gonadal hormone action in the pubococcygeus muscle (Pcm) after castration and hormone replacement. Male Wistar rats were castrated and the Pcm was unilaterally denervated; after 2 or 6 weeks, the cross-sectional area (CSA) of Pcm fibers was assessed. Additional groups of castrated rats were used to examine the effects of hormone replacement. At 2 weeks post surgeries, rats were implanted with Silastic capsules containing either dihydrotestosterone (DHT), estradiol benzoate (EB) or both hormones, and the CSA of Pcm fibers was assessed after 4 weeks of hormone treatment. At 2 weeks post surgeries, gonadectomy without hormone replacement resulted in reductions in the CSA of Pcm fibers, and denervation combined with castration increased the magnitude of this effect; further reductions in CSA were present at 6 weeks post surgeries, but again denervation combined with castration increased the magnitude of this effect. Hormone replacement with DHT resulted in hypertrophy in the CSA of nondenervated muscles compared to those of intact normal males, but this effect was attenuated in denervated muscles. Hormone replacement with EB treatment prevented further castration-induced reductions in CSA of nondenervated muscles, but denervation prevented this effect. Similar to that seen with treatment with EB alone, combined treatment with both DHT and EB prevented further reductions in CSA of Pcm fibers in nondenervated muscles, but again denervation attenuated this effect. Thus, while hormone replacement can reverse or prevent further castration-induced atrophy of Pcm fibers, these effects are dependent on muscle innervation. Anat Rec, 300:1327-1335, 2017. © 2017 Wiley Periodicals, Inc.

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Castration and the Growth of Muscles in the Rat1

Cited by 41 publications

References 0 publications

Neuroprotective effects of testosterone on the morphology and function of somatic motoneurons following the death of neighboring motoneurons

Neuroprotective effects of testosterone on the morphology and function of somatic motoneurons following the death of neighboring motoneurons

Neuroprotective effects of testosterone on dendritic morphology following partial motoneuron depletion: Efficacy in female rats

Hormonal Treatment Effects on the Cross‐sectional Area of Pubococcygeus Muscle Fibers After Denervation and Castration in Male Rats

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