Thyroxine reduces the production rate of BrdU-labeled cells in the ventricular zone of the adult canary brain

Arai, Okio; Saito, Nozomu

doi:10.1016/0304-3940(95)11989-a

Cited by 12 publications

(8 citation statements)

References 16 publications

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“…However, we cannot rule out the possibility that chronic, but not acute, hormone treatment reduced cell proliferation-a hypothesis that we did not test. Arai and Saito (1995) reported that a much larger dose of T 4 (1 mg) in adult canaries caused a decrease in VZ cell labeling with bromodeoxyuridine. Species, hormone dosage, and other methodological differences between the present study and that of Arai and Saito preclude direct comparisons.…”

Section: Discussionmentioning

confidence: 98%

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Tekumalla¹,

Tontonoz²,

Hesla³

et al. 2002

J. Neurobiol.

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Widespread telencephalic neuronal replacement occurs throughout life in birds. We explored the potential relationship between thyroxine (T4) and cell turnover in the adult male zebra finch. We found that many cells in the zebra finch brain, including long-projection neurons in the high vocal center (HVC), stained positively with an antibody to thyroid hormone receptors (TR). Labeling was generally weak in the ventricular zone (VZ) that gives rise to new neurons but some proliferative VZ cells and/or their progeny, identified by [3H]-thymidine labeling, co-labeled with anti-TR antibody. Acute T4 treatment dramatically increased the number of pyknotic and TUNEL-positive cells in HVC and other telencephalic regions. In contrast, degenerating cells were never observed in the archistriatum or sub-telencephalic regions, suggesting that excess T4 augments cell death selectively in regions that show naturally occurring neuronal turnover. VZ mitotic activity was not altered shortly after acute T4 treatment at a dosage that stimulated cell death, although [3H]-labeling intensity per cell was slightly reduced. Moreover, the incorporation rates for neurons formed shortly before or after acute hormone treatment were no different from control values. Chronic T4 treatment resulted in a reduction in the total number of HVC neurons. Thus, hyperthyroidism augmented neuronal death, which was not compensated for by neuronal replacement. Collectively, these results indicate that excess T4 affects adult neuronal turnover in birds, and raises the possibility that thyroxine plays an important role in the postnatal development of the avian brain and vocal behavior.

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Section: Discussionmentioning

confidence: 98%

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Tekumalla¹,

Tontonoz²,

Hesla³

et al. 2002

J. Neurobiol.

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“…injections into a pectoral muscle of the thymidine analog 5 0 -bromo-2 0 -deoxy-uridine (BrdU; Sigma Chemical, St. Louis, MO; 10 mg/mL in 0.9% NaCl) at a dose of 50 mg/kg three times daily at 4 h intervals for 2 days to label dividing cells (Arai and Saito, 1995). Birds were sacrificed 28 days later.…”

Section: Experimental Treatments and Surgerymentioning

confidence: 99%

Hormonal and environmental control of song control region growth and new neuron addition in adult male house finches, Carpodacus mexicanus

Strand

Deviche

2007

Developmental Neurobiology

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In songbirds, testosterone (T) mediates seasonal changes in the sizes and neuroanatomical characteristics of brain regions that control singing (song control regions; SCRs). One model explaining the mechanisms of the growth of one SCR, the HVC, postulates that in the spring increasing photoperiod and circulating T concentrations enhance new neuron survival, thus increasing total neuron number. However, most research investigating the effects of T on new neuron survival has been done in autumn. The present study investigated the effects of photoperiod and T treatment on SCR growth and new neuron survival in the HVC in photosensitive adult male House Finches, Carpodacus mexicanus, under simulated spring-like conditions. Birds were castrated, given T-filled or empty Silastic capsules and maintained on short days (SD; 8L:16D) or long days (LD; 16L:8D). To mark new cells, birds received bromodeoxyuridine injections 11 days after experimental manipulations began and were sacrificed 28 days later. Testosterone treatment increased the sizes of two SCRs, the HVC and Robust nucleus of the arcopallium (RA). Exposure to LD did not affect HVC volume, but did increase RA volume. Testosterone treatment increased the total number of HVC neurons, but did not affect the number of new HVC neurons. Thus, T initiates SCR growth and increases neuron survival, but effects of T on new neuron incorporation may be limited in photosensitive birds under spring-like conditions. These results provide new insight into the effects of photoperiod and T treatment on vernal SCR growth and new neuron incorporation and support current models explaining this growth.

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“…[32][33][34][35] for review) as do estradiol-17␤ implants (36). Besides the gonadal hormones, an increase in thyroxine can reduce mitotic activity (37) as well as cell survival (38) in adult songbirds. Interestingly, the complexity of social interactions in the highly social zebra finch also leads to an increase in the survival of adult-generated neurons in the nidopallium caudale, area X, and HVC (39 -41).…”

mentioning

confidence: 99%

Opioid modulation of cell proliferation in the ventricular zone of adult zebra finches (Taenopygia guttata)

et al. 2010

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Besides modulating pain, stress, physiological functions, motivation, and reward, the opioid system has been implicated in developmental and adult mammalian neurogenesis and gliogenesis. In adult male songbirds including zebra finches, neurons generated from the ventricular zone (VZ) of the lateral ventricles are incorporated throughout the telencephalon, including the song control nuclei, HVC, and area X. Although the endogenous opioid met-enkephalin is present in neurons adjacent to the VZ and is upregulated in song control regions during singing, it is not known whether the opioid system can modulate adult neurogenesis/gliogenesis in zebra finches. We used quantitative RT-PCR and in situ hybridization to demonstrate that μ- and δ-opioid receptors are expressed by the VZ of adult male zebra finches. Treating cultured VZ cells from male birds with the opioid antagonist naloxone led to an increase in cell proliferation measured by 5-bromo-2-deoxyuridine incorporation, whereas administering met-enkephalin had the opposite effect, compared with saline-treated cultures. Systemically administering naloxone (2.5 mg/kg body wt) to adult male zebra finches for 4 d also led to a significant increase in cell proliferation in the ventral VZ of these birds, compared with saline-treated controls. Our results show that cell proliferation is augmented by naloxone in the VZ adjacent to the anterior commissure, suggesting that the endogenous opioids modulate adult neurogenesis/gliogenesis by inhibiting cell proliferation in songbirds.

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Thyroxine reduces the production rate of BrdU-labeled cells in the ventricular zone of the adult canary brain

Cited by 12 publications

References 16 publications

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Effects of excess thyroid hormone on cell death, cell proliferation, and new neuron incorporation in the adult zebra finch telencephalon

Hormonal and environmental control of song control region growth and new neuron addition in adult male house finches, Carpodacus mexicanus

Opioid modulation of cell proliferation in the ventricular zone of adult zebra finches (Taenopygia guttata)

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