Synthesis and characterization ofα-Fe2O3nanoparticles showing potential applications for sensing quaternary ammonium vapor at room temperature.

P-type and n-type metal oxide semiconductors are widely used in the manufacture of gas sensing materials, due to their excellent electronic, electrical and electrocatalytic properties. Hematite (α-Fe2O3) compound has been reported as a promising material for sensing broad types of gases, due to its affordability, good stability and semiconducting properties. In the present work, the efficient and easy-to-implement sol-gel method has been used to synthesizeα-Fe2O3nanoparticles (NPs). The TGA-DSC characterizations of the precursor gel provided information about the phase transformation temperature and the mass percentage of the hematite NPs. X-ray diffraction, transmission electron microscopy and x-ray photoelectron spectroscopy data analyses indicated the formation of two iron oxide phases (hematite and magnetite) when the NPs are subjected to thermal treatment at 400 °C. Meanwhile, only the hematite phase was determined for thermal annealing above 500 °C up to 800 °C. Besides, the crystallite size shows an increasing trend with the thermal annealing and no defined morphology. A clear reduction of surface defects, associated with oxygen vacancies was also evidenced when the annealing temperature was increased, resulting in changes on the electrical properties of hematite NPs. Resistive gas-sensing tests were carried out using hematite NPs + glycerin paste, to detect quaternary ammonium compounds. Room-temperature high sensitivity values (Sr âˆ¼ 4) have been obtained during the detection of ∼1 mM quaternary ammonium compounds vapor. The dependence of the sensitivity on the particle size, the mass ratio of NPs with respect to the organic ligand, changes in the dielectric properties, and the electrical conduction mechanism of gas sensing was discussed.

Exercise and the brain: angiogenesis in the adult rat cerebellum after vigorous physical activity and motor skill learning.

This study compared the morphology of cerebellar cortex in adult female rats exposed for 1 month to repetitive exercise, motor learning, or an inactive condition. In the exercise conditions, rats that were run on a treadmill or housed with access to a running wheel had a shorter diffusion distance from blood vessels in the molecular layer of the paramedian lobule when compared to rats housed individually or rats that participated in a motor skill learning task. Rats taught complex motor skills substantially increased the volume of the molecular layer per Purkinje neuron and increased blood vessel number sufficiently to maintain the diffusion distance. These results dissociate angiogenesis associated with increased neuropil volume (as seen in the motor learning group) from angiogenesis associated with increased metabolic demands (as seen in the exercise groups). While the volume fraction of mitochondria did not differ among groups, the mitochondrial volume fraction per Purkinje cell was significantly increased in the motor skill rats. This appears to parallel the previously reported increase in synapses and associated neuropil volume change.

Developmental regulation of Fos and Fos-related antigens in cerebral cortex, striatum, hippocampus, and cerebellum of the rat.

Previous work has associated the proto-oncogene c-fos with such events as neuronal excitation and cell growth and differentiation. This study specifically examined the expression of the Fos protein as well as other Fos-related antigens (Fras) during postnatal development of rat brain. Ages P1 through P15 as well as adult animals (P60) were examined. Particular focus was placed on developing cerebral cortex, striatum, hippocampus, and cerebellum. We used both the Alu antiserum, which recognizes the Fos protein specifically, and the M5 antiserum, which recognizes both Fos and a family of Fos-related antigens. Fos and Fras were developmentally regulated in a region- and cell-specific manner. Differential nuclear and cytoplasmic labeling appeared age dependent. Transient Fos expression was generally followed by a more protracted time course of Fra expression. Fos and a delayed or an extended expression of Fras were observed in subplate neurons between P1 and P15, in striatal striosome and matrix neurons between P1 and P9, and in hippocampal pyramidal neurons between P1 and P9. Fras alone were expressed in cerebral cortex pyramidal neurons and other cortical neurons between ages P1 and P15. Fos and Fras were concomitantly expressed in piriform and entorhinal cortical neurons between P1 and P9 and in cerebellar Purkinje cells between ages P5 and P10. Constitutive levels of Fos and Fras remained detectable in adult animals in a subset of cerebral cortical neurons and cerebellar Purkinje neurons.

5B4-CAM expression parallels neurite outgrowth and synaptogenesis in the developing rat brain.

In order to study whether 5B4-CAM expression parallels neurite outgrowth and synaptogenesis, a monoclonal antibody, 5B4, was used, which recognizes both fetal (185-250 kD) and adult (140 kD, 180 kD) forms of the neural cell adhesion molecule (N-CAM), to identify and localize the antigen in rat tissue during developmental ages P1 through P31 and in adults between P60 and 2 years of age. A ubiquitous pattern of intense immunolabelling was detected during the earliest stages of development. 5B4-CAM expression paralleled process outgrowth and the early stages of synaptogenesis in the cerebral cortex, hippocampal formation, and cerebellum. In the adult, immunoreactivity was generally less intense, but the cerebral cortex and hippocampal and cerebellar molecular layers, all areas implicated in learning-associated plasticity, retained substantial immunoreactivity. The inner one-third of the dentate gyrus molecular layer, an area implicated in axonal sprouting and reactive synaptogenesis, was particularly intensely labelled. Evidence from this work suggests that 5B4-CAM expression may be useful in monitoring neurite outgrowth and the early stages of synapse formation during development and possibly axonal sprouting and reactive synaptogenesis in the adult.

Muscarinic m1 and m2 receptor proteins in local circuit and projection neurons of the primate striatum: anatomical evidence for cholinergic modulation of glutamatergic prefronto-striatal pathways.

The cellular and subcellular localization of muscarinic receptor proteins m1 and m2 was examined in the neostriatum of macaque monkeys by using light and electron microscopic immunocytochemical techniques. Double-labeling immunocytochemistry revealed m1 receptors in calbindin-D28k--positive medium spiny projection neurons. Muscarinic m1 labeling was dramatically more intense in the striatal matrix compartment in juvenile monkeys but more intense in striosomes in the adult caudate, suggesting that m1 expression undergoes a developmental age-dependent change. Ultrastructurally, m1 receptors were predominantly localized in asymmetric synapse-forming spines, indicating that these spines receive extrastriatal excitatory afferents. The association of m1-positive spines with lesion-induced degenerating prefronto-striatal axon terminals demonstrated that these afferents originate in part from the prefrontal cortex. The synaptic localization of m1 in these spines indicates a role of m1 in the modulation of excitatory neurotransmission. To a lesser extent, m1 was present in symmetric synapses, where it may also modulate inhibitory neurotransmission originating from local striatal neurons or the substantia nigra. Conversely, m2/choline acetyltransferase (ChAT) double labeling revealed that m2-positive neurons corresponded to large aspiny cholinergic interneurons and ultrastructurally, that the majority of m2 labeled axons formed symmetric synapses. The remarkable segregation of the m1 and m2 receptor proteins to projection and local circuit neurons suggests a functional segregation of m1 and m2 mediated cholinergic actions in the striatum: m1 receptors modulate extrinsic glutamatergic and monoaminergic afferents and intrinsic GABAergic afferents onto projection neurons, whereas m2 receptors regulate acetylcholine release from axons of cholinergic interneurons.

Cholinergic interneurons of the nucleus accumbens and dorsal striatum are activated by the self-administration of cocaine.

The nucleus accumbens, a major component of the ventral striatum, and the dorsal striatum are primary targets of the mesolimbic dopamine pathway, which is a pathway that plays a critical role in reward and addiction. The shell compartment of the nucleus accumbens and the ventromedial striatum, in particular, receive extensive afferent projections from the ventral tegmental area, which is the major afferent source of the mesolimbic pathway [Prog Brain Res 99 (1993) 209; J Neurosci 7 (1987) 3915]. The present study focused on striatal cholinergic interneurons as potential key neurons involved in the neural basis of drug reinforcement. The main finding of this study is that cholinergic interneurons located in the shell compartment of the nucleus accumbens and the ventromedial striatum were activated, as measured by Fos labeling, following a 1 h session of the self-administration of cocaine in rats. A direct correlation existed between the percent of cholinergic interneurons that were activated and the amount of cocaine that was self-administered. The greatest amount of administered cocaine (approximately 10 mg/kg) resulted in the activation of approximately 80% of the cholinergic neurons. No such correlation existed in the group of animals that self-administered saline. In addition, activation was not found in the core compartment of the nucleus accumbens or the dorsolateral striatum, which receive extensive innervation from the substantia nigra and thus are more closely tied to the motor effects of the drug. In conclusion, cocaine-driven neuronal activation was specific to the shell compartment of the nucleus accumbens (R(2)=0.9365) and the ventromedial striatum (R(2)=0.9059). These findings demonstrate that cholinergic interneurons are involved in the initial stage of cocaine intake and that these neurons are located in areas of the nucleus accumbens and dorsal striatum that are more closely tied to the rewarding and hedonic effects rather than the motor effects of cocaine intake.

Antibodies directed against microtubule proteins from Drosophila melanogaster cross react with similar proteins in the rat brain.

Monoclonal antibodies (Mabs) were used to delineate the localization of three proteins in rat cerebral cortex, hippocampus and cerebellum. The proteins were identified by Mabs directed against Drosophila melanogaster microtubule proteins (MTP). We have provisionally designated these proteins as Drosophila microtubule-associated proteins (DMAPs). The corresponding monoclonal antibodies are designated Mab DMAP-45, -55 and -66 indicating the molecular weights of each protein. All three Mabs cross-react with proteins of similar molecular weights in the rat brain. Correspondingly, these rat proteins are designated DMAPRs. DMAP-45 binds microtubules in an ATP-dependent manner. The molecular weight and subcellular localization of DMAP-45R differs significantly from previously described mammalian brain MAPs suggesting that it represents a novel MAP. Biochemical evidence suggests it may be an actin-related protein. DMAP-55R co-purifies stoichiometrically with rat brain microtubules and appears to be a previously undescribed isoform of tubulin. DMAP-66, which co-purifies stoichiometrically with Drosophila microtubules, does not do so in the rat brain. Immunohistochemistry performed with all three Mabs revealed a general pattern of staining of cell somata and dendrites in the cortex, hippocampus and cerebellum. Mab DMAP-55 also stained axons. In cerebral cortex all three Mabs preferentially, but not exclusively, stained layer V neuronal somata and dendrites. In hippocampus, Mabs DMAP-45 and -66 stained cell somata and dendrites in all hippocampal subfields, particularly the subiculum and CA3, whereas Mab DMAP-55 was most prevalent in mossy fibers. All three Mabs stain Purkinje cells in cerebellum with additional staining of cerebellar basket cells and Golgi cells observed with Mab DMAP-66.

Motor-skill learning: changes in synaptic organization of the rat cerebellar cortex.

Rats trained on motor-skill learning tasks for 30 days were previously found to have more synapses in the volume of tissue proportional to a Purkinje cell than rats that exercised or were inactive. In the motor learning tasks, hooded rats were required to traverse an obstacle course requiring balance and coordination. Rats in two exercise groups were required to walk rapidly or allowed to run in activity wheels. Controls were relatively inactive in standard housing and handled once daily. Synapses were classified to determine which synaptic types changed in number across levels of the molecular layer in the paramedian lobule. The motor learning group had significantly more parallel fiber synapses and climbing fiber synapses per unit Purkinje cell reference volume than all other groups. There were also more synapses and more parallel fiber synapses per reference volume in the outermost than in the innermost molecular layer. The plasticity reported here occurs in vivo under normal physiological conditions. Excitatory synapses account for at least 80% of the synapses in the molecular layer. The results support prior predictions that parallel fiber synapses are modifiable during conditions of learning.

Glial hypertrophy is associated with synaptogenesis following motor-skill learning, but not with angiogenesis following exercise.

Rats reared from weaning in a complex environment have an increase in 1) glial surface area, 2) capillary volume, and 3) the number of synapses, per neuron. In that paradigm it has not been possible to determine whether the glial increase more closely correlates with the increase in synaptic numbers or with angiogenesis. More recently we have found that rats that exercised had an increase in the density of capillaries without an increase in the synaptic numbers, whereas rats that learned new motor skills had a greater number of synapses per neuron without an increase in the density of capillaries. Those findings provided the opportunity to investigate whether changes in glial volume in the cerebellum correspond to changes in the number of synapses or in capillary volume. Glial area fraction estimates were obtained using point counts on electron micrographs from the previous studies. The skill learning group had a greater volume of molecular layer per Purkinje cell, and also a greater volume of glia per Purkinje cell, than rats in either an inactive group or rats in two exercise groups. No significant differences were found in glial volume per synapse and glial volume per capillary across groups, although there was a tendency for glial volume per capillary to be lower in the exercise groups. The data indicate that glial volume correlates with synaptic numbers and not with capillary density.

Learning causes synaptogenesis, whereas motor activity causes angiogenesis, in cerebellar cortex of adult rats.

The role of the cerebellar cortex in motor learning was investigated by comparing the paramedian lobule of adult rats given difficult acrobatic training to that of rats that had been given extensive physical exercise or had been inactive. The paramedian lobule is activated during limb movements used in both acrobatic training and physical exercise. Acrobatic animals had greater numbers of synapses per Purkinje cell than animals from the exercise or inactive groups. No significant difference in synapse number or size between the exercised and inactive groups was found. This indicates that motor learning required of the acrobatic animals, and not repetitive use of synapses during physical exercise, generates new synapses in cerebellar cortex. In contrast, exercise animals had a greater density of blood vessels in the molecular layer than did either the acrobatic or inactive animals, suggesting that increased synaptic activity elicited compensatory angiogenesis.