Decreased social interaction in aged rats may not reflect changes in anxiety-related behaviour

There is evidence that ageing both in humans and animals is accompanied by changes in emotional behaviour. Behavioural studies in rats point to an increase in emotional reactivity and/or anxiety-related behaviour with age. Here we studied social interaction in young adult (3 months) and aged (30 months old) rats using an established test system for anxiety-related behaviour. Using Fos expression as a marker of neuronal activation, we aimed to investigate whether age-related differences in anxiety would be reflected by changes in neuronal activity in brain regions known to be sensitive to fear- and anxiety-related stimuli. Aged rats spent significantly less time (75%) in active social interaction than young rats, without concomitant changes in general locomotor activity. Social interaction enhanced Fos expression both in young and aged rats in several anxiety-related brain areas. Lower Fos response in aged versus young rats was noted in the dorsomedial, dorsolateral and ventrolateral part of the periaqueductal grey, the medial and basolateral amygdala and parvocellular region of the paraventricular hypothalamic nucleus, while no differences in Fos expression were observed in the other regions examined, including the hippocampus, septum or locus coeruleus. These results demonstrate age-related reduction in social interaction, indicative of enhanced anxiety-related behaviour in aged rats. However, since the supposedly increased anxiety level was not accompanied by augmented Fos expression in any of the key brain areas of the fear/anxiety circuitry known to be activated by anxiogenic stimuli, it is suggested that reduced social interaction does not reflect enhanced anxiety in aged rats.     

Background noise does not modify song-induced genic activation in the bird brain

Specialised brain structures allow songbirds to process acoustic signals. One of these brain areas, the NCM (caudomedial neostriatum), shows an immediate-early gene ZENK response when a bird hears a conspecific song. Using a neuro-ethological approach, we investigate if high level of background noise added to conspecific song can modify this song-induced genic activation. We test the ZENK activation in the NCM of adult male Zebra finches Taeniopygya guttata (n = 17) by playing back conspecific signals mixed with different levels of noise, the successful discrimination being reflected by the birds' (n = 6) behavioural responses to these stimuli. From our results, it appears that a high genic activation of the NCM does not necessarily require the audition of an undegraded species-specific signal. Nevertheless, it requires that the signal still contains sufficient information to elicit a behavioural response. The genic activation of the NCM remains thus stable against very high levels of a wide-band background noise, as far as the signal recognition remains possible for the bird.     

Absence of cortical gray matter abnormalities in psychosis of epilepsy: a voxel-based MRI study in patients with temporal lobe epilepsy

The authors retrospectively explored cortical differences between 26 patients with temporal lobe epilepsy and psychosis of epilepsy (POE), 24 patients with temporal lobe epilepsy (TLE) alone, and 20 healthy comparison subjects. Using voxel-based morphometry based on statistical parametric mapping (SPM99), which is an unbiased and fully automated technique to test for morphometric differences, magnetic resonance imaging (MRI) 3D-datasets were acquired and analyzed. There were no significant cortical gray matter differences between the POE and the TLE group. Since cortical pathology is prominent in schizophrenia, POE may be a clinical entity separate from schizophrenia.     

Identification of a novel brain-specific and Reelin-regulated gene that encodes a protein colocalized with synapsin

We carried out a screening of genes that are differentially expressed in normal mice and reeler mutants and are characterized by abnormal neuronal migration and neurite deployment due to defective Reelin signalling. A novel gene, provisionally named C61, was overexpressed in Reelin-deficient embryonic mouse brain RNA. C61 encodes a 3.7 kb mRNA that is brain specific and developmentally regulated, with predominant expression in differentiating neurons. The predicted protein is 664 amino acids long, and contains LAG1 and Ezrin/Radixin/Moesin-Myosin-Filament motifs, suggesting that it may function as an intracellular adaptor. From E14.5 to birth, C61 was highly expressed in all neuronal differentiation fields, with the highest signal in the telencephalic cortical plate and mitral cells in the olfactory bulb. When expressed as a GFP fusion protein in transfected non-neuronal cells and primary neurons, this protein localizes, respectively, to the nuclear membrane or axonal outgrowths, indicating a function in axonal traffic or signalling.     

Effects of skull thickness, anisotropy, and inhomogeneity on forward EEG/ERP computations using a spherical three-dimensional resistor mesh model

Bone thickness, anisotropy, and inhomogeneity have been reported to induce important variations in electroencephalogram (EEG) scalp potentials. To study this effect, we used an original three-dimensional (3-D) resistor mesh model described in spherical coordinates, consisting of 67,464 elements and 22,105 nodes arranged in 36 different concentric layers. After validation of the model by comparison with the analytic solution, potential variations induced by geometric and electrical skull modifications were investigated at the surface in the dipole plane and along the dipole axis, for several eccentricities and bone thicknesses. The resistor mesh permits one to obtain various configurations, as local modifications are introduced very easily. This has allowed several head models to be designed to study the effects of skull properties (thickness, anisotropy, and heterogeneity) on scalp surface potentials. Results show a decrease of potentials in bone, depending on bone thickness, and a very small decrease through the scalp layer. Nevertheless, similar scalp potentials can be obtained using either a thick scalp layer and a thin skull layer, and vice versa. It is thus important to take into account skull and scalp thicknesses, because the drop of potential in bone depends on both. The use of three different layers for skull instead of one leads to small differences in potential values and patterns. In contrast, the introduction of a hole in the skull highly increases the maximum potential value (by a factor of 11.5 in our case), because of the absence of potential drop in the corresponding volume. The inverse solution without any a priori knowledge indicates that the model with the hole gives the largest errors in both position and dipolar moment. Our results indicate that the resistor mesh model can be used as a robust and user-friendly simulation tool in EEG or event-related potentials. It makes it possible to build up real head models directly from anatomic magnetic resonance imaging without tessellation, and is able to take into account head heterogeneities very simply by changing volume elements conductivity. Hum. Brain Mapping 21:84-95, 2004.     

Pregnancy as a risk factor for restless legs syndrome

Pregnant women have at least two or three times higher risk of experiencing restless legs syndrome (RLS) than the general population. These data come from few epidemiological studies finding an 11-27% prevalence of RLS during pregnancy. Women affected by pre-existing RLS often complain of worsening symptoms during pregnancy. This is usually a benign form of RLS, with the highest degree of severity in the third trimester and a tendency to disappear around delivery. The causes of the association between RLS and pregnancy are unknown. The most debated hypotheses are: metabolic alterations, with particular regard to iron and folate deficiency; hormonal influences related to the increase of prolactin, progesterone and estrogens during late pregnancy; and the changing motor habits and psychological state of pregnant women. The importance of folate and iron supplementation during pregnancy in preventing RLS is unclear. RLS in pregnant women is frequently unrecognized; they are often worried about the symptoms and do not receive an adequate explanation by doctors.     

Cerebral malaria -- a neurovascular pathology with many riddles still to be solved

Cerebral malaria (CM), one of the most common fatal complications of the heterogenous syndrome named severe malaria, is indubitably a post-infectious neurovascular pathology, as evidenced by histopathological analyses. This neurological syndrome is characterised not only by the cytoadherence of Plasmodium falciparum-infected erythrocytes, but also by morphological and functional alterations of brain microvascular endothelial cells subsequent to their interactions with circulating cells, such as platelets, monocytes, lymphocytes, and dendritic cells. During CM, host cells, in particular immune cells, are found recruited and activated at the site of sequestration, where they release various soluble molecules. Among these, cytokines play a major role in CM pathogenesis. Indeed, cerebral complications appear to be due to an imbalance between pro-inflammatory and anti-inflammatory mediators. Cytokines (notably interferon-gamma, tumour necrosis factor, lymphotoxin) and chemokine receptors (notably CCR5) are also responsible for blood-brain barrier alterations and biochemical changes leading to the brain parenchymal lesions that can be observed in CM. In return, glial cells can influence blood-borne elements, and thereby worsen the pathology. Numerous problems remain to be solved, especially the sequence of pathological events, namely the order in which the circulating cells sequester on the endothelial wall. A better understanding of the molecular mechanisms involved in CM pathogenesis is needed if we are capable of preventing cerebral complications and improving the quality of patient management.     

Effects of hyperglycemia and hypercapnia on lipid metabolism during complete brain ischemia

Ischemic damage is greatly enhanced by preischemic hyperglycemia or hypercapnia, which affects many intracellular responses including protein kinase C (PKC) translocation. We explored whether hyperglycemic or hypercapnic ischemia affects lipid metabolism, especially ischemia-induced release of free fatty acids (FFAs) and diacylglycerols (DAGs). A change in intraischemic level of acidosis was induced either by injecting glucose (hyperglycemic, HG) or by adding CO(2) (hypercapnic, HC). Complete cerebral ischemia was induced, and the brain was frozen in situ after 3, 5, and 10 min at 37 degrees C. Frontoparietal neocortex was dissected for FFA and DAG lipid analysis by thin-layer chromatography and gas-liquid chromatography. Significant differences were shown between normoglycemic and either hypercapnic or hyperglycemic values for individual and total FFAs. A significant delay in the release of FFA in ischemia with hyperglycemia or hypercapnia was observed. Significant differences were also shown in individual DAG-acyl groups and total DAGs. Hyperglycemic or hypercapnic ischemia resulted in a significant decrease of DAG at 10 min of ischemia. This was unexpected because a previous study showed that PKC translocation was significantly enhanced under similar condition at this time point. Upon cellular depolarization, massive influx of calcium and FFA accumulation may decrease the PKC dependence of DAG for translocation. In addition, PKC activation may lead to a negative feedback inhibition of phospholipase C.     

Somatostatin in the brain of the cave salamander, Hydromantes genei (Amphibia, Plethodontidae): immunohistochemical localization and biochemical characterization

The distribution of somatostatin-like immunoreactivity in the brain of the cave salamander Hydromantes genei (Amphibia, Plethodontidae) was investigated by using two distinct antisera raised against somatostatin-14. Most somatostatin-positive cells were detected in the ependymal cell layer surrounding the ventricles. These cells possessed the typical morphological characteristics of tanycytes or radial glial cells. Double-labeling with an antiserum against somatostatin and a monoclonal antibody against glial fibrillary acidic protein showed that somatostatin-immunoreactive cells lining the ventricles also exhibited GFAP-like immunoreactivity. Injection of the neurotracer biocytin into the lateral ventricle revealed that neurons lining the ventricles did not contain somatostatin-like immunoreactivity. In the telencephalon, somatostatin-like immunoreactivity was confined to radial glial cells. In the diencephalon, in addition to somatostatin-immunoreactive cells in the ependyma, positive cell bodies were also found in the periventricular preoptic nucleus, the infundibular nucleus, the epiphysis, and the subcommissural organ. In the metencephalon, positive cell bodies were found in the auricula cerebelli, whereas in the rhombencephalon numerous somatostatin-immunoreactive cells were seen lining the ventricular cavity. Immunoreactive nerve fibers were observed in the hypothalamus-median eminence complex. In the pituitary, a discrete group of somatostatin-positive cells was found in the pars distalis. High-performance liquid chromatography analysis of brain extracts revealed that the immunoreactive material coeluted with somatostatin-14. The present results show that the somatostatin peptidergic system in the brain of the cave salamander has a more simple organization than those described in the brain of frog and other vertebrates. This feature is probably related to the expression of high pedomorphic characters in plethodontids. The distribution of somatostatin-like immunoreactivity suggests that, in the cave salamander, somatostatin may act as a neurotransmitter and/or neuromodulator, a central regulator of fluid homeostasis, and a hypophysiotropic neurohormone.