Directive Multiband Antenna Based on Rectangular Loop Array and Dumbbell-Shaped Slot Radiator.

In this article, a combination of rectangular loop array and slot radiator for multiband applications is presented. The antenna is configured by arranging, concentrically, a set of rectangular loop radiators excited by electromagnetic coupling provided by a dumbbell slot. The size of the loops is calculated to obtain the desired resonant frequencies, which are almost independent of the adjacent rings. The exciting slot is designed to operate in a wideband frequency range to cover the upper desired resonance. In addition, to obtain directive radiation patterns, a reflector shaped like a box is introduced, giving a stable gain, radiation pattern shape, and port matching at the selected frequencies. The configuration presents great results, since to the authors' knowledge, even a similar configuration given in the open literature presents some disadvantages compared to this one; moreover, not just any structure can be employed as the resonating elements, obtaining multiband behavior at the same time.

Glutamate corelease promotes growth and survival of midbrain dopamine neurons.

Recent studies have proposed that glutamate corelease by mesostriatal dopamine (DA) neurons regulates behavioral activation by psychostimulants. How and when glutamate release by DA neurons might play this role remains unclear. Considering evidence for early expression of the type 2 vesicular glutamate transporter in mesencephalic DA neurons, we hypothesized that this cophenotype is particularly important during development. Using a conditional gene knock-out approach to selectively disrupt the Vglut2 gene in mouse DA neurons, we obtained in vitro and in vivo evidence for reduced growth and survival of mesencephalic DA neurons, associated with a decrease in the density of DA innervation in the nucleus accumbens, reduced activity-dependent DA release, and impaired motor behavior. These findings provide strong evidence for a functional role of the glutamatergic cophenotype in the development of mesencephalic DA neurons, opening new perspectives into the pathophysiology of neurodegenerative disorders involving the mesostriatal DA system.

Role of IL-6 in the etiology of hyperexcitable neuropsychiatric conditions: experimental evidence and therapeutic implications.

Many neuropsychiatric conditions are primed or triggered by different types of stressors. The mechanisms through which stress induces neuropsychiatric disease are complex and incompletely understood. A 'double hit' hypothesis of neuropsychiatric disease postulates that stress induces maladaptive behavior in two phases separated by a dormant period. Recent research shows that the pleiotropic cytokine IL-6 is released centrally and peripherally following physical and psychological stress. In this article, we analyze evidence from clinics and animal models suggesting that stress-induced elevation in the levels of IL-6 may play a key role in the etiology of a heterogeneous family of hyperexcitable central conditions including epilepsy, schizophrenic psychoses, anxiety and disorders of the autistic spectrum. The cellular mechanism leading to hyperexcitable conditions might be a decrease in inhibitory/excitatory synaptic balance in either or both temporal phases of the conditions. Following these observations, we discuss how they may have important implications for optimal prophylactic and therapeutic pharmacological treatment.

Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels.

Somatodendritic (STD) dopamine (DA) release is a key mechanism for the autoregulatory control of DA release in the brain. However, its molecular mechanism remains undetermined. We tested the hypothesis that differential expression of synaptotagmin (Syt) isoforms explains some of the differential properties of terminal and STD DA release. Down-regulation of the dendritically expressed Syt4 and Syt7 severely reduced STD DA release, whereas terminal release required Syt1. Moreover, we found that although mobilization of intracellular Ca(2+) stores is inefficient, Ca(2+) influx through N- and P/Q-type voltage-gated channels is critical to trigger STD DA release. Our findings provide an explanation for the differential Ca(2+) requirement of terminal and STD DA release. In addition, we propose that not all sources of intracellular Ca(2+) are equally efficient to trigger this release mechanism. Our findings have implications for a better understanding of a fundamental cell biological process mediating transcellular signaling in a system critical for diseases such as Parkinson disease.

A sensory subpopulation depends on vesicular glutamate transporter 2 for mechanical pain, and together with substance P, inflammatory pain.

Ablating or functionally compromising sets of sensory neurons has provided important insights into peripheral modality-specific wiring in the somatosensory system. Inflammatory hyperalgesia, cold pain, and noxious mechanosensation have all been shown to depend upon Na(v)1.8-positive sensory neurons. The release of fast-acting neurotransmitters, such as glutamate, and more slowly released neuropeptides, such as substance P (SP), contribute to the diversified responses to external stimuli. Here we show that deleting Vglut2 in Na(v)1.8(Cre)-positive neurons compromised mechanical pain and NGF-induced thermal hyperalgesia, whereas tactile-evoked sensation, thermal, formalin-evoked, and chronic neuropathic pain were normal. However, when Vglut2(f/f);Na(v)1.8(Cre) mice were injected with a SP antagonist before the formalin test, the second phase pain response was nearly completely abolished, whereas in control mice, the pain response was unaffected. Our results suggest that VGLUT2-dependent signaling originating from Na(v)1.8-positive neurons is a principal sensing mechanism for mechanical pain and, together with SP, inflammatory pain. These data define sets of primary afferents associated with specific modalities and provide useful genetic tools with which to analyze the pathways that are activated by functionally distinct neuronal populations and transmitters.

VGLUT2-dependent sensory neurons in the TRPV1 population regulate pain and itch.

The natural response to itch sensation is to scratch, which relieves the itch through an unknown mechanism. Interaction between pain and itch has been frequently demonstrated, and the selectivity hypothesis of itch, based on data from electrophysiological and behavioral experiments, postulates the existence of primary pain afferents capable of repressing itch. Here, we demonstrate that deletion of vesicular glutamate transporter (VGLUT) 2 in a subpopulation of neurons partly overlapping with the vanilloid receptor (TRPV1) primary afferents resulted in a dramatic increase in itch behavior accompanied by a reduced responsiveness to thermal pain. The increased itch behavior was reduced by administration of antihistaminergic drugs and by genetic deletion of the gastrin-releasing peptide receptor, demonstrating a dependence on VGLUT2 to maintain normal levels of both histaminergic and nonhistaminergic itch. This study establishes that VGLUT2 is a major player in TRPV1 thermal nociception and also serves to regulate a normal itch response.

VGLUT2 in dopamine neurons is required for psychostimulant-induced behavioral activation.

The "One neuron-one neurotransmitter" concept has been challenged frequently during the last three decades, and the coexistence of neurotransmitters in individual neurons is now regarded as a common phenomenon. The functional significance of neurotransmitter coexistence is, however, less well understood. Several studies have shown that a subpopulation of dopamine (DA) neurons in the ventral tegmental area (VTA) expresses the vesicular glutamate transporter 2 (VGLUT2) and has been suggested to use glutamate as a cotransmitter. The VTA dopamine neurons project to limbic structures including the nucleus accumbens, and are involved in mediating the motivational and locomotor activating effects of psychostimulants. To determine the functional role of glutamate cotransmission by these neurons, we deleted VGLUT2 in DA neurons by using a conditional gene-targeting approach in mice. A DAT-Cre/Vglut2Lox mouse line (Vglut2(f/f;DAT-Cre) mice) was produced and analyzed by in vivo amperometry as well as by several behavioral paradigms. Although basal motor function was normal in the Vglut2(f/f;DAT-Cre) mice, their risk-taking behavior was altered. Interestingly, in both home-cage and novel environments, the gene targeted mice showed a greatly blunted locomotor response to the psychostimulant amphetamine, which acts via the midbrain DA system. Our results show that VGLUT2 expression in DA neurons is required for normal emotional reactivity as well as for psychostimulant-mediated behavioral activation.

Developmental and target-dependent regulation of vesicular glutamate transporter expression by dopamine neurons.

Mesencephalic dopamine (DA) neurons have been suggested to use glutamate as a cotransmitter. Here, we suggest a mechanism for this form of cotransmission by showing that a subset of DA neurons both in vitro and in vivo expresses vesicular glutamate transporter 2 (VGluT2). Expression of VGluT2 decreases with age. Moreover, when DA neurons are grown in isolation using a microculture system, there is a marked upregulation of VGluT2 expression. We provide evidence that expression of this transporter is normally repressed through a contact-dependent interaction with GABA and other DA neurons, thus providing a partial explanation for the highly restricted expression of VGluT2 in DA neurons in vivo. Our results demonstrate that the neurotransmitter phenotype of DA neurons is both developmentally and dynamically regulated. These findings may have implications for a better understanding of the fast synaptic action of DA neurons as well as basal ganglia circuitry.

Estudio de los factores que influyen en la renuncia de los médicos residentes durante su formación / Study of the factor which promote resident's desertion during their formation

Con el objetivo de conocer los factores que influyen en la renuncia de los médicos residentes durante su formación, se realizó un encuesta comparativa retrospectiva. Fueron tomados para el estudio 52 médicos residentes que renunciaron en el periodo de marzo de 1990 a febrero de 1993 y como grupo control 52 médicos residentes que concluyeron satisfactoriamente su residencia. Se analizaron cinco factores de manera compartiva para grupo de médicos que renunción y para el que no renunció: sexo, estado civil, lugar de origen, tipo de contratación y edad, los tres primeros factores no tuvieron un diferencia estadísticamente; sin embargo, en los dos últimos factores se demostró que existe un menor índice de renuncias (p=0.01 y p=0.05, respectivamente) en los médicos que son seleccionados por la Universidad Nacional Autónoma de México (UNAM) y menores de 35 años, por lo que se concluye que los criterios de selección del médico becado debieran ser de mayor rigor