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PubMed2004

Residual activity of mutant androgen receptors explains wolffian duct development in the complete androgen insensitivity syndrome.

Development of the Wolffian ducts (WD) into epididymides and vasa deferentia is dependent on testosterone. Patients with the complete androgen insensitivity syndrome (CAIS) are therefore not expected to develop these structures. However, WD derivatives have been described in cases of CAIS. It is thought that these may be remnants. This study assesses the degree of WD development in 33 patients with CAIS and investigates whether this development was androgen dependent. Epididymides and vasa deferentia were identified in 70% of patients with substitution mutations in the androgen receptor ligand-binding domain. They were more developed than epididymides and vasa deferentia from 16- to 20-wk-old male fetuses, suggesting that the WD had been stimulated to grow, rather than failed to regress. Receptors with substitutions in the ligand-binding domain were normally expressed and showed residual response to androgens in transactivation assays. Patients with premature stop codons or frameshift mutations, which prevented androgen receptor expression, or DNA-binding domain mutations that abolished transcriptional activity did not have epididymides or vasa deferentia. We hypothesize that mutant receptors with residual activity in vitro respond to high local testosterone concentrations in vivo, thereby stimulating WD development. The classification of androgen insensitivity in such patients should be considered severe rather than complete.

Adolescent↗
PubMed1988

A mutation of the androgen receptor associated with partial androgen resistance, familial gynecomastia, and fertility.

A family is described in which gynecomastia and undervirilization in five men (four of whom have fathered children) were inherited in a manner compatible with an X-linked defect. Three members from whom blood could be obtained had supranormal serum testosterone and normal LH and FSH levels. One man had severe oligospermia with decreased motility, and one had normal sperm density and motility. In fibroblasts cultured from genital skin biopsies from two of the men, the levels of androgen receptor and affinity of binding of receptor to dihydrotestosterone were normal. However, androgen binding in fibroblast monolayers was thermolabile, up-regulation of receptor levels did not occur after prolonged incubation of monolayers with dihydrotestosterone or methyltrienolone, and dissociation rates at 37 C were increased with the synthetic androgen mibolerone. In addition, in cytosol preparations the androgen receptor protein was unstable. This disorder probably represents the most subtle functional abnormality of androgen receptor characterized to date, since it is compatible with normal male phenotypic development and in some affected men with fertility. It follows that infertility is not an invariable feature of androgen resistance as we previously suggested.

Adolescent↗
PubMed2003

Androgen receptor corepressor-19 kDa (ARR19), a leucine-rich protein that represses the transcriptional activity of androgen receptor through recruitment of histone deacetylase.

Androgen receptor (AR) that mediates androgen action is a crucial factor in male reproductive functions. Here, we report a novel AR corepressor ARR19 (androgen receptor corepressor-19 kDa), which has been isolated as a putative androgen-induced gene from murine testis. ARR19 encoding a leucine-rich protein is expressed only in male reproductive organs such as testis and prostate. ARR19 expression in the testis is developmentally regulated. Functional analysis conducted by the transient transfection of mammalian cells shows that ARR19 represses AR transactivation in a dose-dependent manner. Furthermore, yeast two-hybrid and glutathione S-transferase pull-down analyses reveal that ARR19 directly associates with AR through the N-terminal and leucine zipper-containing regions of ARR19 and the DNA binding-hinge domain of AR. Interestingly, ARR19 localized in the cytoplasmic compartment cotranslocates into the nucleus with AR upon androgen exposure. The ARR19 repression of AR transactivation is through the recruitment of histone deacetylase 4 (HDAC4) by ARR19. Overexpression of HDAC4 further inhibits the ARR19-repressed AR transactivation. In addition, ARR19 directly interacts with HDAC4 in vitro. Furthermore, DNA-protein complex immunoprecipitation assays reveal that HDAC4 is recruited to an androgen-regulated promoter through ARR19. Taken together, the results suggest that ARR19 may act as an AR corepressor in vivo and play an important role in male reproductive functions.

Androgen Receptor Antagonists↗
PubMed1997

An androgen response element in a far upstream enhancer region is essential for high, androgen-regulated activity of the prostate-specific antigen promoter.

Prostate-specific antigen (PSA) is expressed at a high level in the luminal epithelial cells of the prostate and is absent or expressed at very low levels in other tissues. PSA expression can be regulated by androgens. Previously, two functional androgen-response elements were identified in the proximal promoter of the PSA gene. To detect additional, more distal control elements, DNasel-hypersensitive sites (DHSs) upstream of the PSA gene were mapped in chromatin from the prostate-derived cell line LNCaP grown in the presence and absence of the synthetic androgen R1881. In a region 4.8 to 3.8 kb upstream of the transcription start site of the PSA gene, a cluster of three DHSs was detected. The middle DNAseI-hypersensitive site (DHSII, at approximately -4.2 kb) showed strong androgen responsiveness in LNCaP cells and was absent in chromatin from HeLa cells. Further analysis of the region encompassing DHSII provided evidence for the presence of a complex, androgen-responsive and cell-specific enhancer. In transient transfected LNCaP cells, PSA promoter constructs containing this upstream enhancer region showed approximately 3000-fold higher activity in the presence than in the absence of R1881. The core region of the enhancer could be mapped within a 440-bp fragment. The enhancer showed synergistic cooperation with the proximal PSA promoter and was found to be composed of at least three separate regulatory regions. In the center, a functionally active, high-affinity androgen receptor binding site (GGAACATATTGTATC) could be identified. Mutation of this element almost completely abolished PSA promoter activity. Transfection experiments in prostate and nonprostate cell lines showed largely LNCaP cell specificity of the upstream enhancer region, although some activity was found in the T47D mammary tumor cell line.

Androgens↗
PubMed1997

Dehydroepiandrosterone activates mutant androgen receptors expressed in the androgen-dependent human prostate cancer xenograft CWR22 and LNCaP cells.

An androgen receptor (AR) gene mutation identified in the androgen-dependent human prostate cancer xenograft, CWR22, changed codon 874 in the ligand-binding domain (exon H) from CAT for histidine to TAT for tyrosine and abolished a restriction site for the endonuclease SfaNI. SfaNI digestion of AR exon H DNA from normal but not from prostate cancer tissue indicated H874Y is a somatic mutation that occurred before the initial tumor transplant. CWR22, an epithelial cell tumor, expresses a 9.6-kb AR mRNA similar in size to the AR mRNA in human benign prostatic hyperplasia. AR protein is present in cell nuclei by immunostaining as in other androgen-responsive tissues. Transcriptional activity of recombinant H874Y transiently expressed in CV1 cells in the presence of testosterone or dihydrotestosterone was similar to that of wild type AR. With dihydrotestosterone at a near physiological concentration (0.01 nM), H874Y and wild type AR induced 2-fold greater luciferase activity than did the LNCaP mutant AR T877A. The adrenal androgen, dehydroepiandrosterone (10 and 100 nM) with H874Y stimulated a 3- to 8-fold greater response than with wild type AR and at 100 nM the response was similar with the LNCaP mutant. H874Y, like the LNCaP cell mutant, was more responsive to estradiol and progesterone than was wild type AR. The antiandrogen hydroxyflutamide (10 nM) had greater agonist activity (4- to 7-fold) with both mutant ARs than with wild type AR. AR mutations that alter ligand specificity may influence tumor progression subsequent to androgen withdrawal by making the AR more responsive to adrenal androgens or antiandrogens.

Androgen Antagonists↗
PubMed1993

Mutant androgen receptor detected in an advanced-stage prostatic carcinoma is activated by adrenal androgens and progesterone.

Structural changes of the androgen receptor (AR) may contribute to the development of resistance to endocrine therapy in prostatic carcinoma. We have isolated AR cDNA fragments from seven tumor specimens derived from patients with advanced metastatic prostatic tumors. In one specimen obtained from a patient who failed to respond to endocrine and cytotoxic therapy we have detected a point mutation in the hormone-binding domain of the receptor. This AR mutation is a guanine-to-adenine transition at nucleotide 2671 that leads to substitution of methionine for the wild type valine at position 715. It is a somatic mutation because it was not present in the AR genomic DNA fragments isolated from prostatic and testicular tissues of the same patient. The mutant AR was recreated in an expression vector and transiently expressed in COS-7 and CV-1 cells. Hormone-binding assays revealed that the mutant receptor does not differ from the wild type receptor in its ability to bind androgen. The dissociation constant for the synthetic androgen mibolerone was 3 nM for both receptors. There was also no significant difference in binding of other steroids and nonsteroidal antiandrogens as revealed by competition binding assays. However, transfection experiments to determine the trans-activation potential of the mutant receptor produced differences in the action of this receptor compared to the wild type receptor. Dihydrotestosterone and the synthetic androgens methyltrienolone (R1881) and mibolerone were equally proficient in conferring trans-activation activity to both the mutant and wild type receptors. Adrenal androgens such as dehydroepiandrosterone and androstenedione, as well as progesterone mediated a higher trans-activation through the mutant than through the wild type receptor. These data demonstrate that the exchange of a single valine into methionine at position 715 in the AR promoters trans-activation not only by testicular but also by adrenal androgens and progesterone. This pattern of ligand-dependent trans-activation may have significance in the process controlling the progression of prostatic carcinoma.

Adrenal Glands↗
PubMed2005

A role of androgen receptor protein in cell growth of an androgen-independent prostate cancer cell line.

Prostate cancer, which develops due to androgen and is initially responsive to androgen deprivation therapy, often comes to acquire androgen deprivation therapy resistance in short order. We investigated the role of androgen receptor (AR) protein in an androgen-independent prostate cancer cell line using AR ligands and AR siRNA. Although the androgen-independent cell line scarcely responded to AR ligands, their growth was attenuated by ablation of AR protein by siRNA.

Androgens↗
PubMed1991

[The effects of anti-androgen TZP4238 (17 alpha-acetoxy-6-chloro-2-oxapregna-4,6-diene-3,20-dione) and its related compounds on the in vitro formation of androgen-receptor complex].

It was reported that a new steroidal anti-androgen, TZP4238 (17 alpha-acetoxy-6-chloro-2-oxapregna-4,6-diene-3,20-dione), was 10 times stronger than chlormadinone acetate (CMA) as the in vivo anti-androgenic potential. To confirm this result, the effect of TZP4238 and CMA on ventral prostates of intact rats, or castrated ones treated by testosterone, was investigated. Our experiments demonstrated that TZP4238 was 3-5 times stronger than CMA. The effects of this compound on the androgen-receptor complex formation in the human and rat prostates were investigated and compared to the other anti-androgen and related compounds. An aliquot of cytosol or KCl extract from rat or human prostate was incubated with [3H]R1881 in the presence of various tested compounds. By means of dextran coated charcoal assay and sucrose density gradient centrifugation analysis, TZP4238 and TZP4239 showed a stronger inhibitory effect than other compounds except dihydrotestosterone. Judging from all these results, it was estimated that TZP4238 was 2-3 times stronger than CMA. The Scatchard plot analysis revealed that the inhibitory effect of TZP4238 was a competitive type. Between CMA and TZP4238, the difference of in vivo anti-androgenic potential was not identical with that of the inhibitory effect on the androgen-receptor complex formation.

Androgen Antagonists↗
PubMed1979

Anti-androgen TSAA-291. VI. Effects of the anti-androgen TSAA-291 and its related compounds on the in vitro formation of 5 alpha-DHT-receptor complex in the cytosol of rat ventral prostates.

Inhibitory effect of a synthetic steroidal anti-androgen TSAA-291 (16 beta-ethyl-17 beta-hydroxy-4-oestren-3-one) on the in vitro formation of 5 alpha-dihydrotestosterone(5 alpha-DHT)-receptor complex was examined. An aliquot of the cytosol from rat ventral prostates was incubated with [3H]5 alpha-DHT in the presence of various amounts of the anti-androgen. By means of dextran-coated charcoal assay and sucrose density-gradient centrifugation analysis, TSAA-291 was demonstrated to inhibit directly, in a competitive manner, the binding of 5 alpha-DHT to a component analogous in its properties to the cytosol androgen receptor. Further, displacing study using a variety of TSAA-291 analogues was undertaken to examine which of the functional groups of TSAA-291 is important for the affinity to the 5 alpha-DHT binding component, and elucidated that 3-hydroxy or 5 alpha-dihydro derivatives of TSAA-291 and others having axial methyl group at C-10 were less potent competitors for [3H]5 alpha-DHT binding than TSAA-291. Furthermore, using other steroids including androgens and anti-androgens, considerable knowledge was obtained about structural requirements for a steroid molecule to displace the bound [3H]5 alpha-DHT, and this displacing activity of the steroids was discussed in terms of their anti-androgenic activity.

Androgen Antagonists↗
PubMed1999

Differential induction of the androgen receptor transcriptional activity by selective androgen receptor coactivators.

Several new androgen receptor (AR) cofactors, associated to the ligand binding domain of AR, have been identified by our group and named AR associated protein (ARA)70, ARA55, and ARA54. Our previous reports have suggested that the cofactor ARA70 can confer the androgenic effect from 17 beta-estradiol (E2) and antiandrogen to AR. It is of interest for us to compare and determine if the specificity of sex hormones and antiandrogens could be modulated by different coactivators. Our results indicate that ARA70 is the best coactivator to confer the androgenic activity on E2. Only ARA70 and ARA55 could increase significantly the androgenic activity of hydroxyflutamide, a widely used antiandrogen for the treatment of prostate cancer. Furthermore, as compared to the relative specificity of these coactivators to AR in the prostate cancer DU145 cells, our results suggest that ARA70 has a relatively higher specificity. Together, our data suggest that the specificity of sex hormones and antiandrogens can be modulated by some selective AR coactivators. These findings may not only help us to better understand the specificity of the sex hormones and antiandrogens, but also to facilitate the development of better antiandrogens or androgens to fight the androgen-related diseases, such as prostate cancer.

Androgens↗
PubMed1996

The first detection of complete androgen insensitivity with no mutation in the coding sequence of the androgen receptor gene.

We have analyzed the entire nucleotide sequences of complementary DNAs of the androgen receptor gene in two siblings (patients 8044 and 8047) with complete androgen insensitivity. Plasma testosterone was in the normal male range, however, androgen binding capacity was undetectable as measured in skin fibroblasts in both patients. 5alpha-reductase activity was normal in both cases confirming that this enzyme is not involved in the mechanism of androgen insensitivity. Northern blot analysis indicated that mRNA of the AR was normal in size. In addition, no mutation was found in the entire nucleotide sequences of complementary DNAs of the androgen receptor gene. Together, our results reveal an unusual insight into the molecular basis of androgen resistance, and the molecular heterogeneity in this clinical spectrum.

Adolescent↗
PubMed1996

The suppressive effects of testosterone on growth in young chickens appears to be mediated via a peripheral androgen receptor; studies of the anti-androgen ICI 176,334.

ICI 176,334 is a nonsteroidal anti-androgen that has been shown to selectively block peripheral androgen receptors in rats and is presumed to do so in chickens. In chickens, androgens stimulate secondary sexual characteristics (e.g., comb), but inhibit growth and the immune tissues. The present study examined the effect of dietary ICI 176,334 (5 or 25 mg/kg body weight) on growth in chickens in the presence or absence of testosterone treatment (as 1-cm long silastic implants). Treatments began at 2 wk of age and continued through 6 wk of age. Testosterone alone reduced body growth (average daily gain and shank-toe length, together with weights of the body, skeletal muscle, and the bursa of Fabricius, an immune tissue), and stimulated comb development. At the low dose (5 mg/kg), ICI 176,334 alone had no effect on body growth or organ weight with the exception that comb weight was reduced. At the high dose (25 mg/kg), ICI 176,334 decreased growth (body weight, average daily gain, and shank-toe length) and organ weights (breast muscle, bursa of Fabricius, testis, and comb weights). This effect may represent a toxicity. As might be expected with an anti-androgen, ICI 176,334 (at either 5 or 25 mg/kg) completely suppressed the stimulation of comb growth evoked by testosterone. Similarly, ICI 176,334 (5 mg/kg) overcame, albeit partially, the growth-suppressive effects of testosterone (on body weight, average daily gain, shank-toe length, and breast muscle weight) and also had inhibitory effects on the weights of the testis and bursa of Fabricius. The anti-androgen, ICI 176,334, did not influence the reduction in circulating concentrations of luteinizing hormone occurring after testosterone treatment. The present data are consistent with the growth-suppressive effects of testosterone in chickens being mediated via a peripheral androgen receptor. No effects of either testosterone or ICI 176,334 were observed on circulating concentrations of insulin-like growth factor-I despite the marked changes in growth rate.

Androgen Antagonists↗
PubMed2001

A mechanism for androgen receptor-mediated prostate cancer recurrence after androgen deprivation therapy.

The development and growth of prostate cancer depends on the androgen receptor and its high-affinity binding of dihydrotestosterone, which derives from testosterone. Most prostate tumors regress after therapy to prevent testosterone production by the testes, but the tumors eventually recur and cause death. A critical question is whether the androgen receptor mediates recurrent tumor growth after androgen deprivation therapy. Here we report that a majority of recurrent prostate cancers express high levels of the androgen receptor and two nuclear receptor coactivators, transcriptional intermediary factor 2 and steroid receptor coactivator 1. Overexpression of these coactivators increases androgen receptor transactivation at physiological concentrations of adrenal androgen. Furthermore, we provide a molecular basis for this activation and suggest a general mechanism for recurrent prostate cancer growth.

Aged↗
PubMed2002

Raloxifene, a selective estrogen receptor modulator, induces apoptosis in androgen-responsive human prostate cancer cell line LNCaP through an androgen-independent pathway.

Raloxifene, a selective estrogen receptor (ER) modulator, is a mixed estrogen agonist/antagonist that has been shown to prevent osteoporosis and breast cancer in women. Because the prostate contains a high level of ER-beta, the present study investigated the effect of raloxifene in the androgen-sensitive human prostate cancer cell line LNCaP. Previously, it has been demonstrated that LNCaP cells express ER-beta but not ER-alpha and that tamoxifene induces apoptosis in these cells. After treatment with raloxifene, a dramatic increase in cell death occurred in a dose-dependent manner (10(-9) to 10(-6) M range). Using the terminal deoxynucleotidyl transferase-mediated nick end labeling apoptotic assay, we demonstrated that the nuclear fragmentation was due to apoptosis. The dramatic change in cellular morphology after treatment with raloxifene was no longer observed when cells were pretreated with a pan-caspase inhibitor, Z-VAD-FMK, and a specific caspase-9 inhibitor, Z-LEHD-FMK. Furthermore, immunoblot demonstrated an activation of caspase-9 in LNCaP cells. Because LNCaP cells contain a mutated androgen receptor that allows cellular proliferation in the presence of antiandrogens, prostate-specific antigen assay and transfection with a reporter construct containing luciferase gene under the control of androgen response element (pARE) were carried out. The results demonstrated that raloxifene does not significantly alter androgen receptor activity in LNCaP cells. Taken together, these results demonstrate that raloxifene, a selective ER modulator, induces apoptosis in the androgen-sensitive human prostate cancer cell line LNCaP through an androgen-independent pathway.

Androgens↗
PubMed1989

Androgen dependency of a tumor produced by a cell line derived from androgen-responsive Shionogi carcinoma 115.

An androgen-dependent tumor (SCC8 tumor) was obtained by inoculating an androgen-responsive cell line derived from the androgen-responsive Shionogi carcinoma 115 (SC115) into mice and then treating the mice with testosterone propionate (TP) at a pharmacological dose (400 micrograms/day). The SCC8 tumor differed in histological appearance from the SC115 tumor and its growth was less stimulated by androgen than that of the SC115 tumor. However, its growth was completely androgen dependent; SCC8 tumors did not develop in castrated mice and regressed when TP treatment was discontinued. The decreased sensitivity of the SCC8 tumor seemed to be attributable in part to its rapid metabolism of testosterone to metabolites with lower androgenic actions. The effects of TP at doses of 0, 100, 200, and 400 micrograms/day on cell division and cell death in SCC8 tumors of medium size were examined by measurements of the mitotic index and the retention of 5-[125I]iodo-2'-deoxyuridine incorporated into the whole tumor. TP increased the mitotic index dose dependently and at all doses reduced the decrease in the retention of 5-[125I]iodo-2'-deoxyuridine. These results suggest that steroids may not only stimulate cell division but also reduce cell death in steroid-dependent tumors.

Androgens↗
PubMedDate not supplied

Molecular analysis of the androgen receptor in ten prostate cancer specimens obtained before and after androgen ablation.

Hormonal or androgen-ablation (AA) therapy is the predominant form of systemic treatment for metastatic prostate cancer. Although an initial response to AA is observed in 70%-80% of patients with advanced disease, most tumors eventually progress to androgen-independent growth, and only a minority of affected individuals are alive 5 years following initiation of treatment. Because AA induces a dramatic change in the hormonal milieu of the patient and because these tumors maintain the ability to proliferate, it is possible that this treatment selects a population of cells with mutated androgen receptors (ARs) that sustain growth despite the absence of circulating androgen. To test this hypothesis we investigated the molecular structure of the AR in 10 prostate cancer specimens obtained before and after AA. Tumors (coded A through L) were microdissected to uniquely enrich genomic DNA from cancer cells. Exons 1-8 of the AR were screened by polymerase chain reaction, single-stranded conformational polymorphism, and sequence analysis. A mutation consisting of an expansion of the polyglutamine (poly-Q) repeat from 20 (found in 100% of the sequences of specimens obtained before AA) to 26 (found in 70% of the sequences of specimens obtained after AA) was detected in patient F. The 26 glutamine (Q26) AR readily translocated to the nucleus upon addition of androgen, and did not show significant differences in its ability to bind (3)[H]-dihydrotestosterone compared to its wild-type counterpart. Nevertheless, analysis of transcriptional activity showed that the Q66 AR was transcriptionally 30%-50% less active than the wild-type molecule. Because clones of AR with an expanded poly-Q tract were detected only in the specimen from patient F obtained after AA, we conclude that in specific circumstances, AA treatments can select variant forms of the AR in the prostate of patients affected by prostate cancer. Further experiments are needed to conclusively determine whether the Q26 clone was responsible for sustaining survival of prostate cancer cells in the androgen-depleted milieu of this patient.

Animals↗
PubMed1978

The possible influence of temporal factors in androgenic responsiveness of urogenital tissue recombinants from wild-type and androgen-insensitive (Tfm) mice.

Tissue recombinants of epithelium and stroma from embryonic and neonatal urogenital rudiments derived from wild-type and feminized (Tfm/Y) mice sere grown as grafts in intact male hosts and analyzed morphologically for androgenic response. When mesenchyme of embryonic wild-type urogenital sinus (UGS) was associated with epithelium from embryonic wild-type bladder (B), the epithelium developed into glandular structures resembling prostate. In the reciprocal recombinant (B mesenchyme + UGS epithelium) the response was mixed, half of the recombinants exhibited bladder morphology and half exhibited prostatic-like morphology. Vaginal-like histogenesis occurred in UGS recombinants of androgen-insensitive Tfm/Y mesenchyme and wild-type epithelium, while prostatic morphology developed in reciprocal recombinants of wild-type mesenchyme and Tfm/Y epithelium. These observations demonstrate (1) that the presence of wild-type mesenchyme appears essential for expression of androgen-dependent morphogenesis during embryonic periods; and (2) that Tfm/Y epithelium is capable of participating in an androgenic response. Conversely, in similar recombinants prepared with neonatal tissues, the presence of wild-type urogenital stroma may not be required for expression of certain androgen-dependent phenomena since maintenance of the height and cytodifferentiation of ductus deferens epithelium occurs even when this epithelium is associated with Tfm/Y urogenital stroma. It appears, therefore, that the requirement of urogenital epithelium for wild-type (androgen sensitive) stroma may vary temporally.

Androgens↗
PubMed2002

Evidence for species differences in the pattern of androgen receptor distribution in relation to species differences in an androgen-dependent behavior.

Chickens (Gallus gallus domesticus) and Japanese quail (Coturnix japonica), two closely related gallinaceous bird species, exhibit a form of vocalization-crowing-which differs between the species in two components: its temporal acoustic pattern and its accompanying postural motor pattern. Previous work utilizing the quail-chick chimera technique demonstrated that the species-specific characteristics of the two crow components are determined by distinct brain structures: the midbrain confers the acoustic pattern, and the caudal hindbrain confers the postural pattern. Crowing is induced by androgens, acting directly on androgen receptors. As a strategy for identifying candidate neurons in the midbrain and caudal hindbrain that could be involved in crow production, we performed immunocytochemistry for androgen receptors in these brain regions in both species. We also investigated midbrain-to-hindbrain vocal-motor projections. In the midbrain, both species showed prominent androgen receptor immunoreactivity in the nucleus intercollicularis, as had been reported in previous studies. In the caudal hindbrain, we discovered characteristic species differences in the pattern of androgen receptor distribution. Chickens, but not quail, showed strong immunoreactivity in the tracheosyringeal division of the hypoglossal nucleus, whereas quail, but not chickens, possessed strong immunoreactivity in a region of the ventrolateral medulla. Some of these differences in hindbrain androgen receptor distribution may be related to the species differences in the postural component of crowing behavior. The results of the present study imply that the spatial distribution of receptor proteins can vary even between closely related species. Such variation in receptor distribution could underlie the evolution of species differences in behavior.

Animals↗