Food systems for sustainable development: proposals for a profound four-part transformation.

Evidence shows the importance of food systems for sustainable development: they are at the nexus that links food security, nutrition, and human health, the viability of ecosystems, climate change, and social justice. However, agricultural policies tend to focus on food supply, and sometimes, on mechanisms to address negative externalities. We propose an alternative.

Fast non-genomic effects of progesterone-derived neurosteroids on nociceptive thresholds and pain symptoms.

Fast Inhibitory controls mediated by glycine (GlyRs) and GABAA receptors (GABAARs) play an important role to prevent the apparition of pathological pain symptoms of allodynia and hyperalgesia. The use of positive allosteric modulators of these receptors, specifically expressed in the spinal cord, may represent an interesting strategy to limit or block pain expression. In this study, we have used stereoisomers of progesterone metabolites, acting only via non-genomic effects, in order to evaluate the contribution of GlyRs and GABAARs for the reduction of mechanical and thermal heat hypernociception.

The transcription factor DeltaFosB is recruited by inflammatory pain.

DeltaFosB, a stable splice variant of FosB, has been proposed to mediate persistent brain adaptation in response to several chronic perturbations, but it has not yet been considered in the context of sustained pain. Inflammatory pain induces neuronal plasticity that can result in persistent alteration of nociceptive pathways. This neuronal plasticity can partly result from changes in gene expression controlled by transcription factors.

Calibrated forceps: a sensitive and reliable tool for pain and analgesia studies.

Unlabelled: Devices designed for mechanical pain threshold studies are often difficult to implement. The purpose of this study was to investigate a simple tool based on calibrated forceps to induce quantifiable mechanical stimulation in the rat on a linear scale. The most suitable protocol was tested by determining the effects of 3 repetitive measurements on both hind paws, respectively, during long-term (9 days), mid-term (1 day), and short-term (2 hours).

UT-B1 urea transporter is expressed along the urinary and gastrointestinal tracts of the mouse.

Selective transporters account for rapid urea transport across plasma membranes of several cell types. UT-B1 urea transporter is widely distributed in rat and human tissues. Because mice exhibit high urea turnover and are the preferred species for gene engineering, we have delineated UT-B1 tissue expression in murine tissues.

c-Fos and peptide immunoreactivities in the central extended amygdala of morphine-dependent rats after naloxone-precipitated withdrawal.

The central extended amygdala, a forebrain macrostructure, may represent a common substrate for acute drug reward and the dysphoric effects of drug withdrawal. To test its involvement during opiate withdrawal, we studied the distribution of c-Fos immunoreactive neurons, in relation to their neuropeptide content, in brain sections from morphine-dependent or naive rats, killed 90 min after naloxone or saline intraperitoneal injection. Naloxone treatment in naive rats induced a slight increase in c-Fos immunoreactivity in the central amygdaloid nucleus, the lateral bed nucleus of the stria terminalis and the interstitial nucleus of the posterior limb of the anterior commissure.

UT-B1 proteins in rat: tissue distribution and regulation by antidiuretic hormone in kidney.

UT-B1 is the facilitated urea transporter of red blood cells (RBCs) and endothelial cells of descending vasa recta in the kidney. Immunoblotting with a polyclonal antibody against the C-ter sequence of rat UT-B1 revealed UT-B1 as both nonglycosylated (29 kDa) and N-glycosylated (47.5 and 33 kDa) proteins in RBC membranes, kidney medulla, brain, and bladder in rat.

Aquaporins in brain: distribution, physiology, and pathophysiology.

Water homeostasis in the brain is of central physiologic and clinical importance. Neuronal activity and ion water homeostasis are inextricably coupled. For example, the clearance of K+ from areas of high neuronal activity is associated with a concomitant water flux.

Hypervascularization in the magnocellular nuclei of the rat hypothalamus: relationship with the distribution of aquaporin-4 and markers of energy metabolism.

In the magnocellular nuclei of the hypothalamus, there is a rich vascular network for which the function remains to be established. In the supraoptic nucleus, the high vascular density may be one element, which together with the water channel aquaporin-4 expressed in the astrocytes, is related to a role in osmoreception. We tested the osmoreception hypothesis by studying the correlation between vascular and cellular densities in the paraventricular nucleus and the supraoptic nucleus.

Presence of aquaporin-4 and muscarinic receptors in astrocytes and ependymal cells in rat brain: a clue to a common function?

Using combined double immunofluorescence and laser confocal microscopy, we studied the common cellular localization of cholinergic muscarinic receptors (mAChRs) and aquaporin-4 water channels (AQP4) in the cortex, the corpus callosum and in ependymal cells of the rat brain. In the cortex, AQP4 staining was restricted to the perivascular end-feet of astrocytes. It was more widely distributed on the astrocytes of the corpus callosum.

7-Nitroindazole, a selective inhibitor of nNOS, increases hippocampal extracellular glutamate concentration in status epilepticus induced by kainic acid in rats.

The glutamate extracellular concentration is controlled by metabolic and neuronal pathways via release and uptake mechanisms. Stimulation of glutamate receptors induces neuronal nitric oxide (NO) release, which in turn modulates glutamate transmission. In this study, the influence of neuronally derived NO on hippocampal glutamate extracellular concentration was investigated in conditions of intense metabolic activation, i.

Distribution of muscarinic receptors on the endothelium of cortical vessels in the rat brain.

Functional and pharmacological studies have suggested that there are muscarinic receptors (mAChRs) on the endothelial cells of major cerebral arteries, while recent immunological studies indicate that there are no mAChRs on the endothelium of brain capillaries. This difference may be because the distribution of mAChR on the endothelium varies with the type of vessel. This paper examines the distribution of mAChR on the vascular endothelium along intraparenchymal blood vessels in the rat brain by immunolabelling and laser confocal microscopy.

Regional study of the co-localization of neuronal nitric oxide synthase with muscarinic receptors in the rat cerebral cortex.

There is increasing evidence that nitric oxide is an important molecular messenger involved in a wide variety of biological processes including the regulation of the cerebral circulation. For instance, it has been implicated in the vascular response to nucleus basalis magnocellularis stimulation, a structure which is widely recognized as the predominant source of cholinergic fibres projecting to the neocortex. The present investigation was carried out to determine if muscarinic receptors are present on cortical neurons expressing neuronal nitric oxide synthase (nitric oxide-producing enzyme).

Microvessels isolated from brain: localization of muscarinic sites by radioligand binding and immunofluorescent techniques.

The present investigation was carried out to determine the extent to which muscarinic acetylcholine receptors (mAChRs) in vascular and perivascular structures were colocalized with glial fibrillary acidic protein (GFAP)-positive structures. To this aim, an immunocytochemical approach on free-floating cryosections and isolated microvessels obtained from rat brain was performed to study the possible colocalization of immunostaining with the anti-mAChR protein antibody (M35) and an anti-GFAP antibody. Double-labeling experiments were carried out by fluorescent techniques.

Effects of a glutamate uptake inhibitor on glutamate release induced by veratridine and ischemia.

It has been postulated that a reversal of glutamate reuptake ("uptake reverse") may contribute to glutamate release during cerebral ischemia. We tested this hypothesis by studying the effect of threo-3-hydroxy-DL-aspartic acid (THA), a glutamate uptake inhibitor, on extracellular glutamate accumulation measured by microdialysis during 4-vessel ischemia (20 min). The inhibitory effect of THA on sodium-dependent glutamate uptake was measured in vitro on rat hippocampal slices (Ki = 45 +/- 11 microM).

Effects of an A1 adenosine receptor agonist on the neurochemical, behavioral and histological consequences of ischemia.

Untreated rats and rats given the A1 receptor adenosine agonist, R-phenylisopropyladenosine (R-PIA), were subjected to four vessel ischemia. The effect of R-PIA on hippocampal amino acid release, hippocampal neuronal damage, exploratory behavior, learning capacity and global neurological score were evaluated. R-PIA decreased by half the glutamate released during ischemia and improved the global neurological scores 3, 24, 48, 78 h and 7 days after ischemia.

Regional variability in DNA fragmentation after global ischemia evidenced by combined histological and gel electrophoresis observations in the rat brain.

We have studied whether the delayed cell death induced by transient forebrain ischemia is associated with an internucleosomal cleavage of DNA into oligonucleosome-sized fragments. The integrity of genomic DNA in various brain regions after a 20-min four-vessel ischemia was examined using gel electrophoresis. We found typical ladders of oligonucleosomal DNA fragments in the striatum and in the Ammon's horn.

Adenosine modulation of amino acid release in rat hippocampus during ischemia and veratridine depolarization.

This study was undertaken to determine whether endogenous adenosine modulates 'in vivo' neurotransmitter amino acid release via its presynaptic receptors. Two conditions were compared: neuronal depolarization by local infusion of veratridine (600 microM), and transient global ischemia by four-vessel occlusion. Both stimuli were applied for 20 min.

Effect of two different routes of administration of R-PIA on glutamate release during ischemia.

Considering that adenosine decreases glutamate release from brain slices by stimulating presynaptic A1 receptors, we have attempted to modulate glutamate release in vivo during global ischemia with an agonist (R-phenylisopropyladenosine, R-PIA) of A1 receptors. Extracellular hippocampal glutamate was sampled by microdialysis and measured by HPLC. Conscious rats were submitted to transient global ischemia for 20 min.

Muscarinic binding of pial vessels and arachnoid membrane.

The muscarinic sites in arachnoid and pial vessels were compared by analysis of the binding of quinuclidinyl benzilate (QNB) to membrane preparations. Saturation analysis indicated that the process was saturable, high affinity, and related to protein concentration in both structures. Although the affinities in the two structures [KD = 0.

Effect of monoamine oxidase inhibition on the regional cerebral blood flow response to circulating noradrenaline.

The effect of an acute i.v. infusion of noradrenaline (NA) on regional cerebral blood flow (rCBF) was investigated in the awake rat using [14C]iodoantipyrine as diffusible tracer.

Cerebrovascular changes elicited by electrical stimulation of the centromedian-parafascicular complex in rat.

Electrical stimulation of the centromedian-parafascicular complex (CM-Pf) in anesthetized (chloralose) and paralyzed (tubocurarine) rats elicits a widespread cerebrovascular dilatation. Regional cerebral blood flow (rCBF) was measured in dissected tissue samples of 10 brain regions (medulla, pons, cerebellum, inferior colliculus, superior colliculus, frontal parietal and occipital cortices, caudate-putamen and corpus callosum) by [14C]iodoantipyrine method. In unstimulated and sham-operated rats rCBF ranged from 40 +/- 3 (ml/100 g/min) in corpus callosum to 86 +/- 6 (ml/100 g/min) in inferior colliculus.

Local cerebral blood flow in gently restrained rats: effects of propranolol and diazepam.

The cerebrovascular consequences of the gentle restraint commonly used for the measurement of local cerebral blood flow (LCBF) in conscious rats has been tested by using two drugs, propranolol and diazepam. Propranolol induced small LCBF decreases in 7 structures suggesting that the cerebral circulation was partially controlled by the activation of intra or extracerebral aminergic pathways in this protocol. Sedative doses of diazepam reduced LCBF in most of the structures but anxiolytic doses increased it in 4 structures.

Stress and local cerebral blood flow: studies on restrained and unrestrained rats.

The degree of stress has been compared between two protocols used for the measurement of local cerebral blood flow (LCBF) in conscious rats. The first method involved acute surgical procedures (cannulation of both femoral veins and arteries) under halothane anesthesia. It was followed by a recovery period (2-3 h) during which the rat was before LCBF measurement.

Adrenergic receptors on cerebral microvessels in control and parkinsonian subjects.

The binding of adrenergic ligands (3H-prazosin, 3H-clonidine, 3H-dihydroalprenolol) was studied on a preparation of cerebral microvessels in the prefrontal cortex and putamen of control and Parkinsonian subjects. The adrenergic receptor density in microvessels of control patients was less than 0.5% and 3.