RESUMEN

Photon-mediated interactions between quantum systems are essential for realizing quantum networks and scalable quantum information processing. We demonstrate such interactions between pairs of silicon-vacancy (SiV) color centers coupled to a diamond nanophotonic cavity. When the optical transitions of the two color centers are tuned into resonance, the coupling to the common cavity mode results in a coherent interaction between them, leading to spectrally resolved superradiant and subradiant states. We use the electronic spin degrees of freedom of the SiV centers to control these optically mediated interactions. Such controlled interactions will be crucial in developing cavity-mediated quantum gates between spin qubits and for realizing scalable quantum network nodes.

RESUMEN

We demonstrate a quantum nanophotonics platform based on germanium-vacancy (GeV) color centers in fiber-coupled diamond nanophotonic waveguides. We show that GeV optical transitions have a high quantum efficiency and are nearly lifetime broadened in such nanophotonic structures. These properties yield an efficient interface between waveguide photons and a single GeV center without the use of a cavity or slow-light waveguide. As a result, a single GeV center reduces waveguide transmission by 18±1% on resonance in a single pass. We use a nanophotonic interferometer to perform homodyne detection of GeV resonance fluorescence. By probing the photon statistics of the output field, we demonstrate that the GeV-waveguide system is nonlinear at the single-photon level.

RESUMEN

Efficient interfaces between photons and quantum emitters form the basis for quantum networks and enable optical nonlinearities at the single-photon level. We demonstrate an integrated platform for scalable quantum nanophotonics based on silicon-vacancy (SiV) color centers coupled to diamond nanodevices. By placing SiV centers inside diamond photonic crystal cavities, we realize a quantum-optical switch controlled by a single color center. We control the switch using SiV metastable states and observe optical switching at the single-photon level. Raman transitions are used to realize a single-photon source with a tunable frequency and bandwidth in a diamond waveguide. By measuring intensity correlations of indistinguishable Raman photons emitted into a single waveguide, we observe a quantum interference effect resulting from the superradiant emission of two entangled SiV centers.

RESUMEN

We report the observation of stable optical transitions in nitrogen-vacancy (NV) centers created by ion implantation. Using a combination of high temperature annealing and subsequent surface treatment, we reproducibly create NV centers with zero-phonon lines (ZPL) exhibiting spectral diffusion that is close to the lifetime-limited optical line width. The residual spectral diffusion is further reduced by using resonant optical pumping to maintain the NV(-) charge state. This approach allows for placement of NV centers with excellent optical coherence in a well-defined device layer, which is a crucial step in the development of diamond-based devices for quantum optics, nanophotonics, and quantum information science.

RESUMEN

The realization of efficient optical interfaces for solid-state atom-like systems is an important problem in quantum science with potential applications in quantum communications and quantum information processing. We describe and demonstrate a technique for coupling single nitrogen vacancy (NV) centers to suspended diamond photonic crystal cavities with quality factors up to 6000. Specifically, we present an enhancement of the NV center's zero-phonon line fluorescence by a factor of ~ 7 in low-temperature measurements.

Asunto(s)

Nanotecnología , Óptica y Fotónica , Teoría Cuántica , Cristalización , Fluorescencia , Nitrógeno/química

RESUMEN

The uterus is a well-known target of endocrine, paracrine and autocrine acting molecules among which steroid hormones (oestrogens, androgens and progesterone) are of special importance. The uterine tissues (endometrium and myometrium) undergo morphological and physiological changes which are associated with changes in expression of steroid hormone receptors. Androgen receptors (AR) that mediate the action of androgens have already been detected in porcine uteri during the oestrous cycle and early pregnancy. To evaluate the role of AR in uterine physiology, the presence of ARmRNA and AR protein localization in the porcine uterus from day 10 to day 90 of pregnancy and in the uterus from the foetus of day 90 postcoitum (p.c.) and from the neonatal 1-day-old piglet was studied. ARmRNA was detected in the porcine endometrium up to day 18 p.c., while AR protein was detectable in glandular epithelium and stromal cells as through day 90 of pregnancy. AR was also detected in the myometrium on all investigated days of pregnancy; however, on day 90, the immunostaining was present only in a limited number of cells. AR immunostaining was clearly demonstrated in the uterus of the female foetuses on day 90 as well as in the uterus of 1-day-old piglets. The physiological relevance of this finding needs further elucidation.

Asunto(s)

Endometrio/metabolismo , Preñez/fisiología , Receptores Androgénicos/análisis , Células del Estroma/metabolismo , Útero/química , Animales , Animales Recién Nacidos , Femenino , Inmunohistoquímica/veterinaria , Embarazo , ARN Mensajero/análisis , Receptores Androgénicos/genética , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa/veterinaria , Porcinos , Distribución Tisular , Útero/metabolismo

RESUMEN

Apoptin, a chicken anemia virus-derived protein, selectively induces apoptosis in transformed but not in normal cells, thus making it a promising candidate as a novel anticancer therapeutic. The mechanism of apoptin-induced apoptosis is largely unknown. Here, we report that contrary to previous assumptions, Bcl-2 and Bcl-xL inhibit apoptin-induced cell death in several tumor cell lines. In contrast, deficiency of Bax conferred resistance, whereas Bax expression sensitized cells to apoptin-induced death. Cell death induction by apoptin was associated with cytochrome c release from mitochondria as well as with caspase-3 and -7 activation. Benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a broad spectrum caspase inhibitor, was highly protective against apoptin-induced cell death. Apoptosis induced by apoptin required Apaf-1, as immortalized Apaf-1-deficient fibroblasts as well as tumor cells devoid of Apaf-1 were strongly protected. Thus, our data indicate that apoptin-induced apoptosis is not only Bcl-2- and caspase dependent, but also engages an Apaf-1 apoptosome-mediated mitochondrial death pathway.

Asunto(s)

Apoptosis , Proteínas de la Cápside/farmacología , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Proteínas/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Proteína bcl-X/metabolismo , Clorometilcetonas de Aminoácidos/farmacología , Factor Apoptótico 1 Activador de Proteasas , Neoplasias de la Mama/metabolismo , Neoplasias de la Mama/patología , Caspasa 3 , Caspasa 7 , Inhibidores de Caspasas , Caspasas/metabolismo , Inhibidores de Cisteína Proteinasa/farmacología , Citocromos c/metabolismo , Activación Enzimática , Femenino , Fibroblastos/citología , Fibroblastos/efectos de los fármacos , Fibroblastos/metabolismo , Humanos , Péptidos y Proteínas de Señalización Intracelular/antagonistas & inhibidores , Péptidos y Proteínas de Señalización Intracelular/genética , Linfoma de Células B/metabolismo , Linfoma de Células B/patología , Masculino , Mitocondrias/metabolismo , Neoplasias de la Próstata/metabolismo , Neoplasias de la Próstata/patología , Proteínas/antagonistas & inhibidores , Proteínas/genética , Proteínas Proto-Oncogénicas c-bcl-2/genética , ARN Interferente Pequeño/farmacología , Células Tumorales Cultivadas , Proteína bcl-X/genética

RESUMEN

The regulation of survival of spinal motoneurons (MNs) has been shown to depend during development and after injury on a variety of neurotrophic molecules produced by skeletal muscle target tissue. Increasing evidence also suggests that other sources of trophic support prevent MNs from undergoing naturally occurring or injury-induced death. We have examined the role of endogenous and exogenous androgens on the survival of developing avian lumbar spinal MNs during their period of programmed cell death (PCD) between embryonic day (E)6 and E11 or after axotomy on E12. We found that although treatment with testosterone, dihydrotestosterone (DHT), or the androgen receptor antagonist flutamide (FL) failed to affect the number of these MNs during PCD, administration of DHT from E12 to E15 following axotomy on E12 significantly attenuated injury-induced MN death. This effect was inhibited by cotreatment with FL, whereas treatment with FL alone did not affect MN survival. Finally, we examined the spinal cord at various times during development and following axotomy on E12 for the expression of androgen receptor using the polyclonal PG-21 antibody. Our results suggest that exogenously applied androgens are capable of rescuing MNs from injury-induced cell death and that they act directly on these cells via an androgen receptor-mediated mechanism. By contrast, endogenous androgens do not appear to be involved in the regulation of normal PCD of developing avian MNs.

Asunto(s)

Andrógenos/farmacología , Neuronas Motoras/citología , Neuronas Motoras/fisiología , Médula Espinal/embriología , Antagonistas de Andrógenos/farmacología , Animales , Apoptosis/efectos de los fármacos , Axotomía , Muerte Celular , División Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Embrión de Pollo , Dihidrotestosterona/farmacología , Flutamida/farmacología , Región Lumbosacra , Neuronas Motoras/efectos de los fármacos , Receptores Androgénicos/análisis , Médula Espinal/citología , Testosterona/farmacología

RESUMEN

Embryonic lumbar spinal motoneurons (MNs) are characterized by a period of programmed cell death (PCD) that spans several days and occurs in a rostrocaudal gradient. The generation of these MNs also takes place in a temporal-spatial gradient, such that MNs within rostral lumbar segments exit the cell cycle earlier and MNs within progressively caudal regions are born later. In vitro studies have shown that the latest born spinal MNs, presumably through the possession of endogenous "survival properties," are also the last to acquire their trophic dependence. If the birth date and therefore spinal cord location of lumbar spinal MNs influence the spatial-temporal pattern of PCD, then earlier born MNs should die sooner and be located more rostrally than those generated later. Alternatively, if the time at which MNs die during development is unrelated to their prior exit from the cell cycle, those born at various phases should die throughout the period of PCD. We report here that lumbar MNs generated during the earliest part (embryonic day 2-3) of the proliferative period in the developing chick spinal cord tend to die during the earliest stages of the PCD period and that MNs born in successive 12-h intervals die at correspondingly later periods during PCD. Furthermore, the spatial progression of PCD of these subpopulations of MNs occurs in a rostrocaudal gradient. Finally, while MNs do appear to die in a mediolateral gradient during the period of MN PCD, this pattern is only partly accounted for by MNs born in consecutive intervals. These data support the notion that the timing and rostrocaudal location of MNs undergoing PCD reflect their time of exit from the cell cycle.

Asunto(s)

Apoptosis/genética , Ciclo Celular/genética , Neuronas Motoras/metabolismo , Nervios Espinales/embriología , Animales , Bromodesoxiuridina , División Celular , Embrión de Pollo , Embrión no Mamífero/inervación , Inmunohistoquímica , Factores de Tiempo

RESUMEN

Unilateral limb-bud removal (LBR) before the outgrowth of sensory or motor neurons to the leg of chick embryos was used to examine the role of limb (target)-derived signals in the development and survival of lumbar motoneurons and sensory neurons in the dorsal root ganglia (DRG). After LBR, motor and sensory neurons underwent normal initial histological differentiation, and cell growth in both populations was unaffected. Before their death, target-deprived motoneurons also expressed a cell-specific marker, the homeodomain protein islet-1. Proliferation of sensory and motor precursor cells was also unaffected by LBR, and the migration of neural crest cells to the DRG and of motoneurons into the ventral horn occurred normally. During the normal period of programmed cell death (PCD), increased numbers of both sensory and motor neurons degenerated after LBR. However, whereas motoneuron loss increased by 40-50% (90% total), only approximately 25% more sensory neurons degenerated after LBR. A significant number of the surviving sensory neurons projected to aberrant targets in the tail after LBR, and many of these were lost after ablation of both the limb and tail. Treatment with neurotrophic factors (or muscle extract) rescued sensory and motor neurons from cell death after LBR without affecting precursor proliferation of either population. Activity blockade with curare failed to rescue motoneurons after LBR, and combined treatment with curare plus muscle extract was no more effective than muscle extract alone. Treatment with the antioxidant N-acetylcysteine rescued motoneurons from normal cell death but not after LBR. Two specific inhibitors of the interleukin beta1 converting enzyme (ICE) family of cysteine proteases also failed to prevent motoneuron death after LBR. Taken together these data provide definitive evidence that the loss of spinal neurons after LBR cannot be attributed to altered proliferation, migration, or differentiation. Rather, in the absence of limb-derived trophic signals, the affected neurons fail to survive and undergo PCD. Although normal cell death and cell death after target deprivation share many features in common, the intracellular pathways of cell death in the two may be distinct.

Asunto(s)

Neuronas Motoras/citología , Neuronas Aferentes/citología , Médula Espinal/citología , Médula Espinal/embriología , Acetilcisteína/farmacología , Clorometilcetonas de Aminoácidos/farmacología , Animales , Axones/fisiología , Factor Neurotrófico Derivado del Encéfalo/farmacología , Recuento de Células , Muerte Celular/efectos de los fármacos , Muerte Celular/fisiología , Diferenciación Celular/efectos de los fármacos , Diferenciación Celular/fisiología , Supervivencia Celular/efectos de los fármacos , Supervivencia Celular/fisiología , Embrión de Pollo , Inhibidores de Cisteína Proteinasa/farmacología , Depuradores de Radicales Libres/farmacología , Ganglios Espinales/citología , Esbozos de los Miembros/citología , Esbozos de los Miembros/cirugía , Neuronas Motoras/efectos de los fármacos , Neuronas Motoras/ultraestructura , Factores de Crecimiento Nervioso/farmacología , Neuronas Aferentes/efectos de los fármacos , Neuronas Aferentes/ultraestructura , Neurotrofina 3 , Oligopéptidos/farmacología

RESUMEN

Only male zebra finches sing, and several brain regions implicated in song behavior exhibit marked sex differences in neuron number. In one region, the high vocal center (HVC), this dimorphism develops because the incorporation of new neurons is greater in males than in females during the first several weeks after hatching. Although estrogen (E2) exposure stimulates neuron addition in females, it is not known where (E2) acts, or to what extent sexual differentiation influences the production, specification, or survival of HVC neurons. In the present study we first reassessed sex and (E2)-induced differences in cell degeneration within the HVC using the TUNEL technique to identify cells undergoing DNA fragmentation indicative of apoptosis. HVC neuron number, as well as the density and number of TUNEL-labeled and pyknotic cells within the HVC were measured in normal 20- and 30-day-old males and females, and in 30-day-old females implanted with E2 on posthatch day 18. Although HVC neuron number was greater in males than in females, and was masculinized in E2 females, no group differences were evident in the absolute number of dying cells. These results indicate that sex differences in cell survival within the HVC do not entirely account for sexually dimorphic neuron addition to this region. Rather, sexual differentiation acts on some HVC neurons before they complete their migration and/or early differentiation. Although the migratory route of HVC neurons is not known, a large number of E2 receptor-containing cells (ER cells) reside just ventromedial to the HVC and adjacent to the proliferative ventricular zone. Next, we investigated whether these ER cells contribute to early-arising sex differences in HVC neuron addition. By combining [3H]thymidine autoradiography with immunocytochemistry for ERs, we first established that ER-expressing cells are not generated during posthatch sexually dimorphic HVC neuron addition, and thus are not young HVC neurons that transiently express ERs during their migration. Furthermore, in 25-day-old birds we found no sex difference in the density of pyknotic cells among this group of ER cells, suggesting that these cells do not promote the differential survival of HVC neuronal precursors migrating through this region. Rather, ER cells or other cell populations may establish sex differences in HVC neuron number by creating dimorphisms in cellular specification.

Asunto(s)

Apoptosis , Encéfalo/citología , Encéfalo/fisiología , Neuronas/citología , Neuronas/fisiología , Vocalización Animal/fisiología , Animales , Aves , Encéfalo/efectos de los fármacos , División Celular , Fragmentación del ADN , Estradiol/farmacología , Femenino , Masculino , Degeneración Nerviosa , Neuronas/efectos de los fármacos , Receptores de Estrógenos/análisis , Caracteres Sexuales

RESUMEN

Virtually all cell populations in the vertebrate nervous system undergo massive "naturally-occurring" or "programmed" cell death (PCD) early in development. Initially neurons and glia are overproduced followed by the demise of approximately one-half of the original cell population. In this review we highlight current hypotheses regarding how large-scale PCD contributes to the construction of the developing nervous system. More germane to the theme of this symposium, we emphasize that the survival of cells during PCD depends critically on their ability to access "trophic" molecular signals derived primarily from interactions with other cells. Here we review the cell-cell interactions and molecular mechanisms that control neuronal and glial cell survival during PCD, and how the inability of such signals to suppress PCD may contribute to cell death in some diseases such as spinal muscular atrophy. Finally, by using neurotrophic factors (e.g. CNTF, GDNF) and genes that control the cell death cascade (e.g. Bcl-2) as examples, we underscore the importance of studying the mechanisms that control neuronal and glial cell survival during normal development as a means of identifying molecules that prevent pathology-induced cell death. Ultimately this line of investigation could reveal effective strategies for arresting neuronal and glial cell death induced by injury, disease, and/or aging in humans.

Asunto(s)

Apoptosis , Sistema Nervioso/embriología , Sistema Nervioso/crecimiento & desarrollo , Neuroglía/fisiología , Neuronas/fisiología , Envejecimiento , Animales , Supervivencia Celular , Desarrollo Embrionario y Fetal , Humanos , Modelos Neurológicos , Enfermedades del Sistema Nervioso/patología , Enfermedades del Sistema Nervioso/fisiopatología , Neuroglía/citología , Neuronas/citología , Vertebrados

RESUMEN

Only male zebra finches (Poephila guttata) sing, and nuclei implicated in song behavior exhibit marked sex differences in neuron number. In the robust nucleus of the anterior neostriatum (RA), these sex differences develop because more neurons die in young females than in males. However, it is not known whether the sexually dimorphic survival of RA neurons is a primary event in sexual differentiation or a secondary response to sex differences in the number of cells interacting trophically with RA neurons. In particular, since sexual differentiation of the RA parallels the development of dimorphisms in the numbers of neurons providing afferent input from the lateral magnocellular nucleus of the anterior neostriatum (IMAN) and the high vocal center (HVC), it has been hypothesized that sex differences in the size of these afferent populations trigger differential RA neuron survival and growth. To test this hypothesis, we lesioned either the IMAN or both the IMAN and HVC unilaterally in 12-day-old male and female zebra finches. Subsequently, RA cell death and RA neuron number and size were measured. Unilateral IMAN lesions increased cell death and decreased neuron number and size within the ipsilateral RA of both sexes. However, even in the IMAN-lesioned hemisphere, these effects were less pronounced in males than in females, so that by day 25 the volume, number, and size of neurons were sexually dimorphic in both the contralateral and ipsilateral RA. Similarly, the absence of both IMAN and HVC afferents did not prevent the emergence of sex differences in the number and size of RA neurons by 25 days posthatching. We conclude that these sex differences within the RA are not a secondary response to dimorphisms in the numbers of IMAN or HVC neurons providing afferent input.

Asunto(s)

Aves/anatomía & histología , Neostriado/crecimiento & desarrollo , Neuronas/citología , Caracteres Sexuales , Vías Aferentes/fisiología , Animales , Recuento de Células , División Celular/fisiología , Supervivencia Celular/fisiología , Femenino , Masculino , Neostriado/citología

RESUMEN

Only male zebra finches sing and several telencephalic song control regions exhibit sex differences in neuron number that presumably reflect effects of estrogen (E2) exerted during the first few posthatch weeks. That is, implanting females with E2 during this time masculinizes neuron number and instills the capacity for vocal behavior. In certain song regions, E2 masculinizes neuron number by preventing the naturally-occurring death of neurons, long after their production, migration and process outgrowth are complete. However, in the Higher Vocal Center (HVC), the cellular mechanisms by which E2 establishes sex differences in neuron number are poorly understood. In contrast with other song regions, HVC neurogenesis overlaps with sexual differentiation and the incorporation of new neurons is greater in young males and E2-treated females, than in normal females. However, it is not known whether E2 promotes the addition of HVC neurons by stimulating their production, specification, and/or survival. To address this issue we injected males and females with [3H]thymidine on days 15 and 16 to label a small group of sexually dimorphic HVC neuronal cohorts born during sexual differentiation. Afterwards, on day 17, females were implanted with Silastic pellets filled with estradiol benzoate (EB) or left empty. We report here that EB exposure on day 17 masculinized (increased) the number of neurons in the HVC at day 35 that were labeled by [3H]thymidine injections on days 15/16. Thus, EB was able to increase cell number among at least some HVC neuronal cohorts after their final division, implying estrogenic regulation of post-mitotic events.(ABSTRACT TRUNCATED AT 250 WORDS)

Asunto(s)

Aves/fisiología , Encéfalo/efectos de los fármacos , Estrógenos/farmacología , Mitosis/efectos de los fármacos , Vocalización Animal/efectos de los fármacos , Animales , Encéfalo/citología , Encéfalo/fisiología , Recuento de Células , Supervivencia Celular , Femenino , Masculino , Neuronas/efectos de los fármacos , Diferenciación Sexual , Timidina/metabolismo , Vocalización Animal/fisiología

RESUMEN

In zebra finches, only males sing and brain regions controlling song exhibit sex differences in neuron number that stem from actions of estrogen during a critical developmental period. In certain song nuclei, these dimorphisms emerge long after neurogenesis and migration are complete, and estrogen promotes masculinization by preventing the death of well-differentiated neurons. But in another region, the higher vocal center (HVC), cellular mechanisms underlying sex differences in neuron number are not so well understood. In the HVC, neurogenesis continues throughout the post-hatch period of sexual differentiation, and sex differences arise during this time because neuron number increases in males but not females. We used [3H]thymidine autoradiography to establish when sex differences in neuron number first develop among a small group of HVC neuronal cohorts. We report that HVC neurons labeled by [3H]thymidine on days 15 and 16 after hatching are sexually dimorphic in number within 10 days of their birth, even before all cells in this cohort complete their migration and/or differentiation. This suggests that the cellular mechanisms contributing to sex differences in neuron number in the HVC may differ from those in other sexually dimorphic neural regions of the vertebrate nervous system. In addition, we found that although many thymidine-labeled HVC neurons ultimately project to the robust nucleus of the archistriatum (RA), a sexually dimorphic target, sex differences in their number develop before this efferent projection is established. These results have important implications regarding the site(s) of hormone action, since they suggest that sexual differentiation acts on certain HVC neurons before they establish their efferent projections, and perhaps even before they arrive within the HVC.

Asunto(s)

Aves/crecimiento & desarrollo , Encéfalo/crecimiento & desarrollo , Neuronas/fisiología , Caracteres Sexuales , Animales , Autorradiografía , Encéfalo/citología , Femenino , Masculino , Prosencéfalo/crecimiento & desarrollo , Prosencéfalo/fisiología , Timidina/metabolismo , Vocalización Animal/fisiología

RESUMEN

In zebra finches, only males sing, and the neural regions controlling song exhibit prominent, hormone-induced sex differences in neuron number. In order to understand how sexual differentiation regulates neuron number within one song nucleus, the lateral magnocellular nucleus of the anterior neostriatum (IMAN), we studied the development of sex differences among IMAN neurons that project to the robust nucleus of the archistriatum (RA). The IMAN is implicated in song learning, and previous ontogenetic studies have indicated that males lose over 50% of their IMAN neurons during the juvenile song learning period. Based on developmental changes in both the extent of androgen accumulation within the IMAN and its appearance in Nissl-stained tissue, it had been hypothesized that IMAN neuron loss was even greater in young females, resulting in sex differences in neuron number. However, this hypothesis has not been tested directly because the Nissl-stained boundaries of the IMAN sometimes are ambiguous in young animals, and are not evident at all in adult females. To circumvent these problems, we employed the retrograde tracer fast blue to study the development of IMAN neurons defined on the basis of their projections to the RA. We find that the number of these IMAN-RA projection neurons is much greater in adult males than in females, and that this sex difference develops during the juvenile period of sexual differentiation and song learning because a significant number of these neurons are lost in females but not in males. With respect to sexual differentiation, we conclude that masculinization (which is stimulated by the hormone estradiol) promotes the retention of IMAN-RA projection neurons. In addition, our results indicate that any loss of IMAN neurons that may occur in young males does not include cells projecting to the RA.

Asunto(s)

Aves/fisiología , Aprendizaje/fisiología , Neuronas/fisiología , Vocalización Animal/fisiología , Envejecimiento/fisiología , Animales , Cuerpo Estriado/citología , Cuerpo Estriado/crecimiento & desarrollo , Cuerpo Estriado/fisiología , Femenino , Histocitoquímica , Masculino , Vías Nerviosas/fisiología , Caracteres Sexuales , Coloración y Etiquetado

RESUMEN

In zebra finches early auditory experience is critical for normal song development. Young males first listen to and memorize a suitable song model and then use auditory feedback from their own vocalizations to mimic that model. During these two phases of vocal learning, song-related brain regions exhibit large, hormone-induced changes in volume and neuron number. Overlap between these neural changes and auditory-based vocal learning suggests that processing and acquiring auditory input may influence cellular processes that determine neuron number in the song system. We addressed this hypothesis by measuring neuron density, nuclear volume, and neuron number within the song system of normal male zebra finches and males deafened prior to song learning (10 days of age). Measures were obtained at 25, 50, 65, and 120 days of age, and included four song nuclei: the hyperstriatum ventralis pars caudalis or higher vocal center (HVc), Area X, the robust nucleus of the archistriatum (RA), and the lateral magnocellular nucleus of the anterior neostriatum (IMAN). In both HVc and Area X, nuclear volume and neuron number increased markedly with age in both normal and deafened birds. The volume of RA also increased with age and was not affected by early deafening. In IMAN, deafening also did not affect the overall age-related loss of neurons, although at 25 days neuron number was slightly less in deafened than in normal birds. We conclude that while the addition and loss of neurons in the developing song system may provide plasticity essential for song learning, these changes do not reflect learning.(ABSTRACT TRUNCATED AT 250 WORDS)

Asunto(s)

Aves/fisiología , Encéfalo/fisiología , Neuronas/fisiología , Vocalización Animal/fisiología , Estimulación Acústica , Envejecimiento/fisiología , Animales , Encéfalo/citología , Encéfalo/crecimiento & desarrollo , Cuerpo Estriado/citología , Cuerpo Estriado/fisiología , Sordera/fisiopatología , Aprendizaje/fisiología , Masculino

Asunto(s)

Publicidad , Servicios de Salud Dental/estadística & datos numéricos , Aceptación de la Atención de Salud , Adulto , Anciano , Servicios de Salud Dental/provisión & distribución , Humanos , Persona de Mediana Edad , Encuestas y Cuestionarios

RESUMEN

This study was designed to discover the nature of concerns that adult patients have toward their orthodontic therapy. I had observed, after many years of treating this age group, that concerns brought to my office by prospective and active patients were similar. All patients, however, felt that their attitudes and feelings were unique. Initially, the investigation was carried out in the presence of a psychologist during evening meetings. This was then followed by giving questionnaires to thirty-five patients. The first questionnaire was distributed to patients who had decided to undergo therapy but had not yet started. The second was given to that same group of patients upon completion, or imminent completion, of their treatment. Thirty-three patients returned both questionnaires. The principal conclusion was that negative concerns and fears that the patients had about their course of treatment were soon dissipated. Perseverance toward the treatment goal was an overriding characteristic of every patient, and satisfaction with the end result was uniformly favorable. These patients would encourage all others to undergo treatment if it was required.

Asunto(s)

Actitud , Ortodoncia Correctiva , Aceptación de la Atención de Salud , Adolescente , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Motivación , Ortodoncia Correctiva/psicología

Asunto(s)

Administración Financiera , Seguro Odontológico/economía , Capitación , Costos y Análisis de Costo , Seguro Odontológico/organización & administración