Comparison of dipsogenic responses of adult rat offspring as a function of different perinatal programming models.

The perinatal environment interacts with the genotype of the developing organism resulting in a unique phenotype through a developmental or perinatal programming phenomenon. However, it remains unclear how this phenomenon differentially affects particular targets expressing specific drinking responses depending on the perinatal conditions. The main goal of the present study was to compare the dipsogenic responses induced by different thirst models as a function of two perinatal manipulation models, defined by the maternal free access to hypertonic sodium solution and a partial aortic ligation (PAL-W/Na) or a sham-ligation (Sham-W/Na). The programmed adult offspring of both perinatal manipulated models responded similarly when was challenged by overnight water dehydration or after a sodium depletion showing a reduced water intake in comparison to the non-programmed animals. However, when animals were evaluated after a body sodium overload, only adult Sham-W/Na offspring showed drinking differences compared to PAL and control offspring. By analyzing the central neurobiological substrates involved, a significant increase in the number of Fos + cells was found after sodium depletion in the subfornical organ of both programmed groups and an increase in the number of Fos + cells in the dorsal raphe nucleus was only observed in adult depleted PAL-W/Na. Our results suggest that perinatal programming is a phenomenon that differentially affects particular targets which induce specific dipsogenic responses depending on matching between perinatal programming conditions and the osmotic challenge in the latter environment. Probably, each programmed-drinking phenotype has a particular set point to elicit specific repertoires of mechanisms to reestablish fluid balance.

New Spanish semantic feature production norms for older adults.

Semantic feature production norms are a useful tool for researchers to have empirically collected data about the semantic representations of a particular population. As older adults have been shown to have certain differences in their semantic knowledge organization in comparison with younger adults, it is relevant for them to have their own normative data. Thus we present here the first Spanish semantic feature production norms for older adults. They contain information about the feature composition of 400 concrete concepts. We also provide information about some feature and concept variables as well as comparisons between young and old adults on these variables.

Hyperosmolarity-induced vasopressin expression and intrinsic excitability of supraoptic neurons of adult offspring are changed by early maternal separation.

Adverse early life experiences can produce long-lasting changes in neurocircuits. The aim of this study was to investigate the programming effects of early maternal separation on the adult offspring vasopressin system. We hypothesized that subjecting adult rats to 4.5 h of daily maternal separation between postnatal days 1 - 21 will have altered hyperosmolarity-induced Avp expression and the response of supraoptic (SON) neurons to electrical and osmotic stimulation. We measured Avp mRNA and hn-RNA in the SON and in the paraventricular nucleus (PVN) by quantitative PCR, and assessed the intrinsic excitability of magnocellular SON neurons as well as their osmotic responses by the patch-clamp technique. In maternally-separated rats we found that basal and osmolarity-induced Avp mRNA gene expression was upregulated in the SON, whereas osmolarity-induced Avp hn-RNA gene expression was abolished. Similarly, in the PVN of maternally-separated rats the osmolarity-induced Avp mRNA gene expression was blunted. The supraoptic neurons of separated rats also had greater excitability than those of non-separated rats. Our results indicate that early maternal separation has long-term consequences on basal and hyperosmolarity-induced Avp hypothalamic expression as well as on the intrinsic excitability of magnocellular supraoptic neurons.

Brain osmo-sodium sensitive channels and the onset of sodium appetite.

The aim of the present study was to determine whether the TRPV1 channel is involved in the onset of sodium appetite. For this purpose, we used TRPV1-knockout mice to investigate sodium depletion-induced drinking at different times (2/24 h) after furosemide administration combined with a low sodium diet (FURO-LSD). In sodium depleted wild type and TRPV1 KO (SD-WT/SD-TPRV1-KO) mice, we also evaluated the participation of other sodium sensors, such as TPRV4, NaX and angiotensin AT1-receptors (by RT-PCR), as well as investigating the pattern of neural activation shown by Fos immunoreactivity, in different nuclei involved in hydromineral regulation. TPRV1 SD-KO mice revealed an increased sodium preference, ingesting a higher hypertonic cocktail in comparison with SD-WT mice. Our results also showed in SD-WT animals that SFO-Trpv4 expression increased 2 h after FURO-LSD, compared to other groups, thus supporting a role of SFO-Trpv4 channels during the hyponatremic state. However, the SD-TPRV1-KO animals did not show this early increase, and maybe as a consequence drank more hypertonic cocktail. Regarding the SFO-NaX channel expression, in both genotypes our findings revealed a reduction 24 h after FURO-LSD. In addition, there was an increase in the OVLT-NaX expression of SD-WT 24 h after FURO-LSD, suggesting the participation of OVLT-NaX channels in the appearance of sodium appetite, possibly as an anticipatory response in order to limit sodium intake and to induce thirst. Our work demonstrates changes in the expression of different osmo­sodium-sensitive channels at specific nuclei, related to the body sodium status in order to stimulate an adequate drinking.

Acute body sodium depletion induces skin sodium mobilization in female Wistar rats.

NEW FINDINGS: What is the central question of this study? Can Na+ depletion mobilize Na+ from the skin reservoir in ovariectomized rats? Does oestrogen replacement change the amount and the dynamics of skin Na+ storage? Is the reduced salt appetite after Na+ depletion in ovariectomized rats with oestrogen replacement related to changes in the skin Na+ ? What is the main finding and its importance? This work demonstrated that acute body Na+ depletion induced by frusemide mobilized the osmotically inactive skin Na+ reservoir to become osmotically active. Oestrogen treatment decreased the induced Na+ intake in ovariectomized rats but did not modulate the inactive Na+ reservoir in control conditions or its mobilization induced by Na+ depletion. ABSTRACT: Oestradiol, which is an important hormone for water and electrolyte balance, also has a role in the inhibition of induced Na+ appetite. Sodium can be stored in the skin in osmotically active or inactive forms, and this skin Na+ reservoir may be involved in the control of body Na+ levels during physiopathological challenges. In this study, we investigated whether the effect of sodium depletion by frusemide can mobilize Na+ from the skin reservoir and whether oestradiol replacement changes or mobilizes the Na+ reserves in the skin. Ovariectomized Wistar rats were treated with vehicle or oestradiol for 7 days to evaluate the effects of oestrogen on the hydroelectrolyte balance, intake responses and skin Na+ and water content in basal conditions. Furthermore, the effects of oestrogen were evaluated after 24 h frusemide-induced whole-body Na+ depletion. Oestradiol-replaced rats exhibited reduced water intake without any significant changes in salt intake, Na+ excretion or water and Na+ skin content in basal conditions. After sodium depletion, both vehicle- and oestradiol-treated rats exhibited an increase in the osmotically active skin Na+ , which was associated with a decrease of the inactive skin Na+ reservoir. Oestrogen decreased the hypertonic saline intake induced by Na+ depletion, but it was not associated with any significant changes in the skin Na+ reservoir. Thus, sodium depletion is able to change the inactive-active skin Na+ reservoir balance. However, the oestrogenic modulation of sodium appetite after Na+ depletion is probably not related to the action of this hormone in the skin Na+ reservoir balance.

Propiedades psicométricas del addenbrooke´s cognitive examinattion para bajo nivel socioeducativo / Psychometric properties of addenbrooke's cognitive examinattion for low socio-educational level

INTRODUCCIÓN Las demencias son una de las patologías más frecuentes en neurología. El Addenbrooke's Cognitive Examination (ACE) es una batería breve de cribado en demencias. La validación en Argentina se ha realizado en una población de alto nivel educativo, lo que es una limitación para su aplicación. OBJETIVOS Analizar las propiedades psicométricas del ACE en una muestra de adultos mayores de bajo nivel socioeducativo (NSE) con y sin demencia. MÉTODOS Se revisaron en forma retrospectiva historias clínicas de pacientes evaluados en el Grupo de Apoyo contra el Mal de Alzheimer (GAMA) durante los últimos 4 años. A ellos se les realizó un examen neurocognitivo completo, que incluyó evaluación clínica/neurológica y estudio por imágenes. Se evaluó en forma prospectiva a 35 participantes sin patología neurológica, que conformaron el grupo normativo. Se les administró el ACE, el Cuestionario de Ansiedad de Hamilton y el Inventario de Depresión de Beck II. El NSE de los participantes se calculó utilizando el Índice de Hollingshead. La muestra quedó conformada por 82 participantes (31 con demencia, 26 con DCL, 25 del grupo normativo). RESULTADOS Se observó una aceptable consistencia interna (alfa de Cronbach 0,68). La validez concurrente con el CDR demostró ser alta (r=-0,66; p<0,001). Se realizó un análisis de curva ROC, con un área bajo la curva de 0,930 (IC95%: 0,869-0,992). Una puntuación de 70 del ACE como punto de corte presentó una sensibilidad del 84% y una especificidad del 80%. Discusión En este trabajo se determinaron las propiedades psicométricas del ACE en una población de bajo NSE. Se recomienda un punto de corte de 70, con una aceptable sensibilidad y especificidad. Los resultados obtenidos podrían ser utilizados en pacientes de los estratos sociales más bajos, lo cual es más frecuente en el subsector público de salud de Argentina.

The effect of increased NaCl intake on rat brain endogenous µ-opioid receptor signalling.

Numerous studies demonstrate the significant role of central ß-endorphin and its receptor, the µ-opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high-NaCl intake and brain endogenous MOR functioning. We examined whether short-term (4 days) obligatory salt intake (2% NaCl solution) in rats induces changes in MOR mRNA expression, G-protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G-protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G-protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G-protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload-induced anorexia.

Prenatal binge-like alcohol exposure alters brain and systemic responses to reach sodium and water balance.

The aim of the present work is to analyze how prenatal binge-like ethanol exposure to a moderate dose (2.0 g/kg; group Pre-EtOH) during gestational days (GD) 17-20 affects hydroelectrolyte regulatory responses. This type of exposure has been observed to increase ethanol consumption during adolescence (postnatal day 30-32). In this study we analyzed basal brain neural activity and basal-induced sodium appetite (SA) and renal response stimulated by sodium depletion (SD) as well as voluntary ethanol consumption as a function of vehicle or ethanol during late pregnancy. In adolescent offspring, SD was induced by furosemide and a low-sodium diet treatment (FURO+LSD). Other animals were analyzed in terms of immunohistochemical detection of Fra-like (Fra-LI-ir) protein and serotonin (5HT) and/or vasopressin (AVP). The Pre-EtOH group exhibited heightened voluntary ethanol intake and a reduction in sodium and water intake induced by SD relative to controls. Basal Na and K concentrations in urine were also reduced in Pre-EtOH animals while the induced renal response after FURO treatment was similar across prenatal treatments. However, the correlation between urine volume and water intake induced by FURO significantly varied across these treatments. At the brain level of analysis, the number of basal Fra-LI-ir was significantly increased in AVP magnocellular neurons of the paraventricular nucleus (PVN) and in 5HT neurons in the dorsal raphe nucleus (DRN) in Pre-EtOH pups. In the experimental group, we also observed a significant increase in Fra-LI along the nucleus of the solitary tract (NTS) and in the central extended amygdala nuclei. In summary, moderate Pre-EtOH exposure produces long-lasting changes in brain organization, affecting basal activity of central extended amygdala nuclei, AVP neurons and the inhibitory areas of SA such as the NTS and the 5HT-DRN. These changes possibly modulate the above described variations in basal-induced drinking behaviors and renal regulatory responses.

Sex differences in body fluid homeostasis: Sex chromosome complement influences on bradycardic baroreflex response and sodium depletion induced neural activity.

Clinical and basic findings indicate that angiotensin II (ANG II) differentially modulates hydroelectrolyte and cardiovascular responses in male and female. But are only the activational and organizational hormonal effects to blame for such differences? Males and females not only differ in their sex (males are born with testes and females with ovaries) but also carry different sex chromosome complements and are thus influenced throughout life by different genomes. In this review, we discuss our recent studies in order to evaluate whether sex chromosome complement is in part responsible for gender differences previously observed in ANG II bradycardic-baroreflex response and sodium depletion-induced sodium appetite and neural activity. To test the hypothesis that XX or XY contributes to the dimorphic ANG II bradycardic-baroreflex response, we used the four core genotype mouse model, in which the effects of gonadal sex (testes or ovaries) and sex chromosome complement (XX or XY) are dissociated. The results indicate that ANG II bradycardic-baroreflex sexual dimorphic response may be ascribed to differences in sex chromosomes, indicating an XX-sex chromosome complement facilitatory bradycardic-baroreflex control of heart rate. Furthermore, we evaluated whether genetic differences within the sex chromosome complement may differentially modulate the known sexually dimorphic sodium appetite as well as basal or induced brain activity due to physiological stimulation of the renin-angiotensin system by furosemide and low-sodium treatment. Our studies demonstrate an organizational hormonal effect on sexually dimorphic induced sodium intake in mice, while at the brain level (subfornical organ and area postrema) we showed a sex chromosome complement effect in sodium-depleted mice, suggesting a sex chromosome gene participation in the modulation of neural pathways underlying regulatory response to renin-angiotensin stimulation.

A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality.

UNLABELLED: Previous results from our laboratory showed that angiotensin II AT1 receptors (AT1-R) are involved in the neuroadaptative changes induced by amphetamine. The aim of the present work was to study functional and neurochemical responses to angiotensin II (ANG II) mediated by AT1-R activation in animals previously exposed to amphetamine. For this purpose male Wistar rats (250-320 g) were treated with amphetamine (2.5mg/kg/day intraperitoneal) or saline for 5 days and implanted with intracerebroventricular (i.c.v.) cannulae. Seven days after the last amphetamine administration the animals received ANG II (400 pmol) i.c.v. One group was tested in a free choice paradigm for sodium (2% NaCl) and water intake and sacrificed for Fos immunoreactivity (Fos-IR) determinations. In a second group of rats, urine and plasma samples were collected for electrolytes and plasma renin activity determination and then they were sacrificed for Fos-IR determination in Oxytocinergic neurons (Fos-OT-IR). RESULTS: Repeated amphetamine exposure (a) prevented the increase in sodium intake and Fos-IR cells in caudate-putamen and accumbens nucleus induced by ANG II i.c.v. (b) potentiated urinary sodium excretion and Fos-OT-IR in hypothalamus and (c) increased the inhibitory response in plasma renin activity, in response to ANG II i.c.v. Our results indicate a possible functional desensitisation of AT1-R in response to ANG II, induced by repeated amphetamine exposure. This functional AT1-R desensitisation allows to unmask the effects of ANG II i.c.v. mediated by oxytocin. We conclude that the long lasting changes in brain AT1-R functionality should be considered among the psychostimulant-induced neuroadaptations.

Prenatal ethanol exposure alters ethanol-induced Fos immunoreactivity and dopaminergic activity in the mesocorticolimbic pathway of the adolescent brain.

Prenatal ethanol exposure (PEE) promotes alcohol intake during adolescence, as shown in clinical and pre-clinical animal models. The mechanisms underlying this effect of prenatal ethanol exposure on postnatal ethanol intake remain, however, mostly unknown. Few studies assessed the effects of moderate doses of prenatal ethanol on spontaneous and ethanol-induced brain activity on adolescence. This study measured, in adolescent (female) Wistar rats prenatally exposed to ethanol (0.0 or 2.0g/kg/day, gestational days 17-20) or non-manipulated (NM group) throughout pregnancy, baseline and ethanol-induced cathecolaminergic activity (i.e., colocalization of c-Fos and tyrosine hydroxylase) in ventral tegmental area (VTA), and baseline and ethanol-induced Fos immunoreactivity (ir) in nucleus accumbens shell and core (AcbSh and AcbC, respectively) and prelimbic (PrL) and infralimbic (IL) prefrontal cortex. The rats were challenged with ethanol (dose: 0.0, 1.25, 2.5 or 3.25g/kg, i.p.) at postnatal day 37. Rats exposed to vehicle prenatally (VE group) exhibited reduced baseline dopaminergic tone in VTA; an effect that was inhibited by prenatal ethanol exposure (PEE group). Dopaminergic activity in VTA after the postnatal ethanol challenge was greater in PEE than in VE or NM animals. Ethanol-induced Fos-ir at AcbSh was found after 1.25g/kg and 2.5g/kg ethanol, in VE and PEE rats, respectively. PEE did not alter ethanol-induced Fos-ir at IL but reduced ethanol-induced Fos-ir at PrL. These results suggest that prenatal ethanol exposure heightens dopaminergic activity in the VTA and alters the response of the mesocorticolimbic pathway to postnatal ethanol exposure. These effects may underlie the enhanced vulnerability to develop alcohol-use disorders of adolescents with a history of in utero ethanol exposure.

Early free access to hypertonic NaCl solution induces a long-term effect on drinking, brain cell activity and gene expression of adult rat offspring.

Exposure to an altered osmotic environment during a pre/postnatal period can differentially program the fluid intake and excretion pattern profile in a way that persists until adulthood. However, knowledge about the programming effects on the underlying brain neurochemical circuits of thirst and hydroelectrolyte balance, and its relation with behavioral outputs, is limited. We evaluated whether early voluntary intake of hypertonic NaCl solution may program adult offspring fluid balance, plasma vasopressin, neural activity, and brain vasopressin and angiotensinergic receptor type 1a (AT1a)-receptor gene expression. The manipulation (M) period covered dams from 1 week before conception until offspring turned 1-month-old. The experimental groups were (i) Free access to hypertonic NaCl solution (0.45 M NaCl), food (0.18% NaCl) and water [M-Na]; and (ii) Free access to food and water only [M-Ctrol]. Male offspring (2-month-old) were subjected to iv infusion (0.15 ml/min) of hypertonic (1.5M NaCl), isotonic (0.15M NaCl) or sham infusion during 20 min. Cumulative water intake (140 min) and drinking latency to the first lick were recorded from the start of the infusion. Our results indicate that, after systemic sodium overload, the M-Na group had increased water intake, and diminished neuronal activity (Fos-immunoreactivity) in the subfornical organ (SFO) and nucleus of the solitary tract. They also showed reduced relative vasopressin (AVP)-mRNA and AT1a-mRNA expression at the supraoptic nucleus and SFO, respectively. The data indicate that the availability of a rich source of sodium during the pre/postnatal period induces a long-term effect on drinking, neural activity, and brain gene expression implicated in the control of hydroelectrolyte balance.

Temporal dissociation between sodium depletion and sodium appetite appearance: Involvement of inhibitory and stimulatory signals.

Our aim was to analyze the participation of inhibitory and stimulatory signals in the temporal dissociation between sodium depletion (SD) induced by peritoneal dialysis (PD) and the appearance of sodium appetite (SA), particularly 2h after PD, when the rats are hypovolemic/natremic but SA is not evident. We investigated the effects of bilateral injections of the serotonin (5-HT) receptor antagonist, methysergide, into the lateral parabrachial nucleus (LPBN) on hypertonic NaCl and water intake 2h vs. 24h after PD. We also studied plasma renin activity (PRA) and aldosterone (ALDO) concentration 2h vs. 24h after PD. Additionally, we combined the analysis of brain Fos immunoreactivity (Fos-ir) with the detection of double immunoreactivity in 5HT and oxytocinergic (OT) cells 2h after PD. Bilateral LPBN injections of methysergide (4µg/200nl at each site) increased NaCl intake when tested 2h after PD compared to controls. We found a significant increase in PRA and ALDO concentration after PD but no differences between 2 and 24h after PD. We also found for the first time a significant increase 2h after PD in the number of Fos-ir neurons in the brainstem nuclei that have been shown to be involved in the inhibition of SA. In summary, the results show that 5HT-mechanisms in the LPBN modulate sodium intake during the delay of SA when the renin angiotensin aldosterone system (RAAS) is increased. In addition, the activation of brainstem areas previously associated with the satiety phase of SA is in part responsible for the temporal dissociation between SD and behavioral arousal.

The long-term outcome of patients treated operatively and non-operatively for scoliosis deformity secondary to spina bifida.

The purpose of this study was to evaluate the long-term outcome of adults with spina bifida cystica (SBC) who had been treated either operatively or non-operatively for scoliosis during childhood. We reviewed 45 patients with a SBC scoliosis (Cobb angle ≥ 50º) who had been treated at one of two children's hospitals between 1991 and 2007. Of these, 34 (75.6%) had been treated operatively and 11 (24.4%) non-operatively. After a mean follow-up of 14.1 years (standard deviation (sd) 4.3) clinical, radiological and health-related quality of life (HRQOL) outcomes were evaluated using the Spina Bifida Spine Questionnaire (SBSQ) and the 36-Item Short Form Health Survey (SF-36). Although patients in the two groups were demographically similar, those who had undergone surgery had a larger mean Cobb angle (88.0º (sd 20.5; 50.0 to 122.0) ; : versus 65.7º (sd 22.0; 51.0 to 115.0); p < 0.01) and a larger mean clavicle-rib intersection difference (12.3 mm; (sd 8.5; 1 to 37); versus 4.1 mm, (sd 5.9; 0 to 16); p = 0.01) than those treated non-operatively. Both groups were statistically similar at follow-up with respect to walking capacity, neurological motor level, sitting balance and health-related quality of life (HRQOL) outcomes. Spinal fusion in SBC scoliosis corrects coronal deformity and stops progression of the curve but has no clear effect on HRQOL.

Vascular imaging in diabetes.

Diabetes is a global epidemic affecting individuals of all socioeconomic backgrounds. Despite intensive efforts, morbidity and mortality secondary to the micro- and macrovascular complications remain unacceptably high. As a result, the use of imaging modalities to determine the underlying pathophysiology, early onset of complications, and disease progression has become an integral component of the management of such individuals. Echocardiography, stress echocardiography, and nuclear imaging have been the mainstay of noninvasive cardiovascular imaging tools to detect myocardial ischemia, but newer modalities such as cardiac MRI, cardiac CT, and PET imaging provide incremental information not available with standard imaging. While vascular imaging to detect cerebrovascular and peripheral arterial disease non-invasively has traditionally used ultrasound, CT- and MRI-based techniques are increasingly being employed. In this review, we will provide an outline of recent studies utilizing non-invasive imaging techniques to assist in disease diagnosis as well as monitoring disease progression. In addition, we will review the evidence for newer modalities such as MR spectroscopy, 3D intravascular ultrasound, and optical coherence tomography that provide exquisite detail of metabolic function and coronary anatomy not available with standard imaging, but that have not yet become mainstream.

Co nanostructures in ordered templates: comparative FORC analysis.

A comparative study on the structural and magnetic properties of highly ordered hexagonal arrays of Co nanoholes, nanowires, nanopillars and nanotubes, with tuned pore/wire/tube diameters, is here presented. The magnetic interactions and their dependence on the geometric features of the arrays were studied using first-order reversal curves (FORCs). For all nanostructures we observe an increase of the magnetostatic interactions with the templates' pore diameter, with the higher (smaller) values found for the nanowire (nanohole) arrays. For the smallest diameters studied (35 nm), all types of arrays could be considered as almost isolated nanostructures, where local interactions prevail. In particular, both nanotube and nanohole arrays exhibit considerable local magnetostatic interactions coming from the stray fields within each void or empty core. On the other hand, the coercivity is found to decrease with diameter for the elongated nanostructures, while it increases with the pore diameter for the nanohole arrays. This behavior is associated with the magnetization reversal mechanisms present in each array. This work highlights a versatile route to tailor the size, geometrical arrangement and magnetostatic interactions of ordered arrays and demonstrates their importance for the tuning of the magnetic behavior of nanometric devices.

Mapping and signaling of neural pathways involved in the regulation of hydromineral homeostasis.

Several forebrain and brainstem neurochemical circuitries interact with peripheral neural and humoral signals to collaboratively maintain both the volume and osmolality of extracellular fluids. Although much progress has been made over the past decades in the understanding of complex mechanisms underlying neuroendocrine control of hydromineral homeostasis, several issues still remain to be clarified. The use of techniques such as molecular biology, neuronal tracing, electrophysiology, immunohistochemistry, and microinfusions has significantly improved our ability to identify neuronal phenotypes and their signals, including those related to neuron-glia interactions. Accordingly, neurons have been shown to produce and release a large number of chemical mediators (neurotransmitters, neurohormones and neuromodulators) into the interstitial space, which include not only classic neurotransmitters, such as acetylcholine, amines (noradrenaline, serotonin) and amino acids (glutamate, GABA), but also gaseous (nitric oxide, carbon monoxide and hydrogen sulfide) and lipid-derived (endocannabinoids) mediators. This efferent response, initiated within the neuronal environment, recruits several peripheral effectors, such as hormones (glucocorticoids, angiotensin II, estrogen), which in turn modulate central nervous system responsiveness to systemic challenges. Therefore, in this review, we shall evaluate in an integrated manner the physiological control of body fluid homeostasis from the molecular aspects to the systemic and integrated responses.

Mapping and signaling of neural pathways involved in the regulation of hydromineral homeostasis

Several forebrain and brainstem neurochemical circuitries interact with peripheral neural and humoral signals to collaboratively maintain both the volume and osmolality of extracellular fluids. Although much progress has been made over the past decades in the understanding of complex mechanisms underlying neuroendocrine control of hydromineral homeostasis, several issues still remain to be clarified. The use of techniques such as molecular biology, neuronal tracing, electrophysiology, immunohistochemistry, and microinfusions has significantly improved our ability to identify neuronal phenotypes and their signals, including those related to neuron-glia interactions. Accordingly, neurons have been shown to produce and release a large number of chemical mediators (neurotransmitters, neurohormones and neuromodulators) into the interstitial space, which include not only classic neurotransmitters, such as acetylcholine, amines (noradrenaline, serotonin) and amino acids (glutamate, GABA), but also gaseous (nitric oxide, carbon monoxide and hydrogen sulfide) and lipid-derived (endocannabinoids) mediators. This efferent response, initiated within the neuronal environment, recruits several peripheral effectors, such as hormones (glucocorticoids, angiotensin II, estrogen), which in turn modulate central nervous system responsiveness to systemic challenges. Therefore, in this review, we shall evaluate in an integrated manner the physiological control of body fluid homeostasis from the molecular aspects to the systemic and integrated responses.

Magnetic properties of Co nanopillar arrays prepared from alumina templates.

The preparation of magnetic nanopillars from anodic alumina templates represents a cheap way to obtain extensive ordered arrays, and thus is very appealing for nanotechnology applications. In this paper we report the preparation of arrays of Co nanopillars with 120 nm height and varying diameter. The high anisotropy of Co offers an additional possibility to control their magnetic properties. The magnetic properties of arrays of Co nanopillars are studied both experimentally and by micromagnetic simulations. Experiment and modeling show crucial changes of hysteresis loops when the diameter is increased. Magnetic data are interpreted considering the change of crystalline structure as well as the influence of geometry. The micromagnetic simulations explain the measured magnetic properties by the role of magnetocrystalline anisotropy and the combined influence of the shape anisotropy and the interactions. They also show the change in the reversal mode with the increased diameter from vortex propagation to curling when the field is applied parallel to the nanopillar axis, and from coherent rotation to curling when it is applied perpendicular.

Magnetic properties of (Fe, Co)-Pd nanowire arrays.

Ordered arrays of ferromagnetic nanowires with (Fe, Co)-Pd compositions have been fabricated from chloride based electrochemical baths by means of template-assisted electrodeposition into self-assembled nanopores of anodic alumina membranes. The nanowires have a diameter and inter-spacing distance of 72 nm and 105 nm, respectively, and around 0.6-1.6 microm in length. Their microstructure and basic magnetic properties are reported. Coercivity, remanence and respective angular dependences on the applied field up to +/- 3 T have been determined from room temperature hysteresis loops measured in a VSM. The study has been performed paying particular attention to the influence of increasing from about 27 up to 63 percent the Pd content in the nanowire alloy.