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PubMedDate not supplied

Tyrosinemia: computed tomography, magnetic resonance imaging, diffusion magnetic resonance imaging, and proton spectroscopy findings in the brain.

In a 5-month-old boy with tyrosinemia, computed tomography revealed diffuse hypodensity in the centrum semiovale. Magnetic resonance (MR) imaging revealed partial signal differences in the white matter and perirolandic regions, and the posterior limbs of the internal capsules revealed higher signal compared with the remainder of the white matter. There were high-signal changes (restricted water diffusion) in the corresponding regions on images of diffusion-weighted MR imaging (b = 1000 s/mm). This likely represented the presence of intramyelinic edema attributable to status spongiosus. Proton MR spectroscopy (repetition time = 1500 milliseconds, echo time = 40 milliseconds) from the lesion sites revealed 2 separate prominent peaks spread between 3.4 and 3.9 ppm. These peaks could represent the CH and CH2 aliphatic protons of the tyrosine molecule.

Brain↗
PubMedDate not supplied

A prion disease--possible Gerstmann-Straussler-Scheinker disease: a case report.

A 50-year-old patient with a 6-month history of progressive cognitive and motor disability is presented. There were no myoclonic jerks on examination and no periodic sharp waves by electroencephalography. Imaging showed high signal on T2-weighted scans in the basal ganglia and posterior limbs of the internal capsules, with no restricted diffusion and parenchymal volume loss. A brain biopsy was performed. Western blot analysis revealed a protease-resistant prion protein fragment (PrP7-8), the molecular hallmark of Gerstmann-Straussler-Scheinker disease.

Blotting, Western↗
PubMed2000

Thiocapsa litoralis sp. nov., a new purple sulfur bacterium from microbial mats from the White Sea.

A new phototrophic purple sulfur bacterium, isolated from benthic microbial mats from the White Sea littoral zone, is described. Individual cells were spherical, non-motile and lacked gas vesicles. In pure cultures cells appeared in regular platelet-like arrangements of four, eight or sixteen cells. Cell division occurred inside a common envelope, surrounded by a thick capsule. Internal photosynthetic membranes were of the vesicular type. The colour of cell suspensions was pink to rose-red. Bacteriochlorophyll a and carotenoids of the spirilloxanthin series were found as photosynthetic pigments. Under anoxic conditions in the light, photolithoautotrophic growth occurred with sulfide, thiosulfate, sulfite and elemental sulfur as electron donors. Sulfur globules were stored as an intermediary oxidation product and were visible microscopically inside the cells. In the presence of sulfide and bicarbonate, photomixotrophic growth occurred with a number of organic substrates. Sulfate could serve as sole assimilatory source of sulfur. Chemolithoautotrophic growth in the dark was possible with sulfide and thiosulfate as electron donors. Optimum growth occurred in the presence of 1% NaCl, at pH 6.5 and at 30 degrees C. The DNA base composition of the type strain, BM5T, was 64.0 mol% G+C. According to 16S rDNA sequence information and DNA-DNA hybridization, the new isolate clearly belongs to the genus Thiocapsa, but is sufficiently different from other recognized Thiocapsa species to be described as a new species of this genus for which the name Thiocapsa litoralis sp. nov. is proposed. The type strain is BM5T (= ATCC 700894).

Bacteriochlorophylls↗
PubMed2003

The legacy of the silver methods and the new anatomy of the basal forebrain: implications for neuropsychiatry and drug abuse.

The first part of the paper highlights the remarkable legacy of the silver methods, with special emphasis on the travails and opportunities offered by the various Nauta methods and their modifications. When the tracer methods based on axoplasmic flow were introduced in the early 1970s, they were exploited on a backdrop of a basic anatomical framework, which had already been established through the tracing of the major CNS pathways by the aid of the silver methods, especially the widely used Nauta-Gygax methods and their modifications. Some of the silver methods that were developed in the late 1960s for the staining of degenerating boutons (e.g. the Fink-Heimer method and de Olmos cupric silver method) provided the necessary technical improvements that eventually led to a new and more productive way to look at the basal forebrain functional/anatomical organization; if it was not for the silver methods, we would in all likelihood still be promoting the nebulous notion of the substantia innominata rather than the concepts of the ventral striatopallidal system and the extended amygdala. The discovery and elaboration of these two macroanatomical systems symbolize what might deservedly be called the "new anatomy" of the basal forebrain. Following a review of the critical experiments which led to the development of the new anatomy of the basal forebrain, its topography in the human is reviewed in drawings of an abbreviated series of coronal sections. The discovery of the ventral striatopallidal system and its thalamic projection to the mediodorsal thalamus rather than to the ventral anterior-ventral lateral thalamic complex ushered in the idea of parallel cortico-subcortical reentrant circuits, which to a large extent has replaced the limbic system as a theoretical framework for neuropsychiatric disorders. The extended amygdala, which appears as a large ring formation around the internal capsule, is still controversial in some quarters, although it is slowly but surely making its way into the general neuroscience literature, especially in the field of addictive disorders. The ventral striatopallidal system and the extended amygdala are interwoven in a complex fashion with the basal nucleus of Meynert within the basal forebrain. Together, these three systems represent important output channels for so-called "limbic" forebrain regions, especially orbitomedial prefrontal cortex and medial temporal lobe structures, which are increasingly implicated in major neuropsychiatric disorders.

Animals↗
PubMed1996

Region-specific DNA synthesis in brains of F344 rats following a six-day bromodeoxyuridine infusion.

Prolonged exposure to certain alkylating chemicals induces glial and meningeal tumours in rats, probably resulting from DNA damage to dividing neural cells. The present work evaluated DNA synthesis in the brains of untreated, young adult male F344 rats in order to define a BrdUrd infusion protocol to more adequately assess proliferation in slowly dividing neural cell populations. BrdUrd (2.5 to 160 mg/ml) was administered for 6 days via subcutaneous osmotic pumps. Clinical toxicity was not observed at any dose. The labelling index (LI; % of cells per brain area that incorporated BrdUrd) and unit length labelling index (ULLI; % of cells per meningeal length that incorporated BrdUrd) were calculated for selected regions by counting labelled neural cells in defined areas of the right hemisphere in coronal brain sections. Intensely stained cells were numerous in the cerebral subependymal layer (LI = 35.8%); scattered in cerebral white matter tracts (e.g. corpus callosum and internal capsule; LI = 6.2%) as well as cerebral (ULLI = 4.2%) and cerebellar (ULLI = 3.6%) meninges; and rare in the hippocampus (LI > 0.1%). Mildy stained cells were dispersed in the pons (LI = 2.1%), deep cerebral (LI = 1.8%) and cerebellar (LI = 1.0%) grey matter, and thalamus (LI = 0.3%). Phenotypically, BrdUrd-positive cells in neuropil were glial cell precursors and their progeny, while those associated with meninges were usually located in the superficial subarachnoid space and appeared to be fibrocytes. Using BrdUrd infusion, LI for glial precursors at these sites ranged from two- to 10-fold higher than those reported previously after a brief parenteral pulse dose. These data indicate that continuous BrdUrd infusion for 6 days by subcutaneous osmotic pump is an efficient means of labelling neural cells throughout the brain.

Animals↗
PubMed1994

Testosterone implants in specific neural sites activate female sexual behaviour.

Sexual behaviour in most female mammals is regulated by oestrogen, often acting synergistically with progesterone. Moreover, the most important neural site of action for oestradiol is the ventromedial nucleus. In the female musk shrew, Suncus murinus, testosterone (T) activates sexual behaviour. Virgin females first engage in copulatory behaviour many hours in advance of follicular development and ovulation, when plasma oestradiol levels are very low. Testosterone, produced by the ovaries and the adrenal glands, must be aromatized centrally to oestradiol to initiate sexual behaviour. To identify the neural sites of action for T, ovariectomized females received unilateral hormone implants containing testosterone propionate. Hormone pellets were placed in 1 of several brain sites including the medial preoptic area and the dorsalmedial hypothalamus (DMH). Implants in either of these 2 sites, but not in the lateral preoptic area, internal capsule, nor anterior hypothalamus stimulated the induction of sexual behaviour. Hormone implants in the ventrolateral hypothalamus resulted in partially receptive animals. Immunocytochemistry was employed to determine which steroid receptors were present in the 2 behaviourally active sites. The medial preoptic area (MPO) and the dorsal and ventromedial hypothalamus both contain many cells that express oestrogen receptor immunoreactivity. A smaller subset of neurons in these regions are immunoreactive for androgen receptors. In summary, testosterone can act specifically in either the MPO or the DMH to induce female sexual behaviour. Both sites contain cells that express oestrogen and androgen receptors. Thus, testosterone may work via one or both of these steroid receptors to regulate behaviour.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Renal (uremic) encephalopathy in a goat.

Renal encephalopathy was diagnosed in a 2-year-old male boar goat with a history of chronic weight loss and ataxia. Histopathological examination of the brain revealed a striking myelin vacuolation distributed mainly in two patterns: (i) along the junction of the neocortex and corona radiata, and (ii) in the bundles of the internal capsule as it dissects through the basal nuclei. The kidneys had diffuse severe tubular and glomerular necrosis and degeneration. The neural lesions are consistent with renal (uremic) encephalopathy. To the authors' knowledge, this is the first report of renal encephalopathy in a goat.

Animals↗
PubMed1977

An autopsy case of cycloserine poisoning.

Cycloserine was given to a 29-year-old girl with pulmonary tuberculosis for 500 days (total dose 250 g). Following this treatment, she began to show several psychiatric and neurologic symptoms and died. Histopathologically, deletion of the nerve cells in the cerebrum was diffusely observed, especially in the IIIrd layer of the frontal and temporal cortex and patchy demyelinations were found in the white matter of the parietal lobe. Characteristic findings were the change of small blood vessels and deletion of the nerve cell around the area of vessels in the hypothalamus, putamen and pallidum. The same changes of the blood vessels were found in the internal capsule. In the cerebellum, shrinkage of Purkinje cells and increase of Bergmann's glia were observed.

Adult↗
PubMed1994

An early-onset case of multiple sclerosis with thalamic lesions on MRI.

We present here an early-onset case of multiple sclerosis (MS) with thalamic lesions. The patient first experienced an episode of ataxic gait at 2 years 3 months of age, with spontaneous remission within 1 month. At 5 years 4 months, she was admitted because of cerebellar ataxia, oculomotor restriction and feeding difficulty. Magnetic resonance imaging (MRI) showed multiple well-defined lesions in the white matter of the cerebellum, mid-brain, periventricle and right frontal lobe. Cerebrospinal fluid (CSF) showed a mild elevation of both immunoglobulin G (IgG) and myelin basic protein (MBP). Serum anti-myelin antibody was also positive, although leukocytosis and elevation of C-reactive protein were not found. Methylprednisolone pulse therapy relieved symptoms within 2 weeks and the abnormal MRI and CSF findings gradually improved. At 6 years 6 months of age, she incurred a third episode of cerebellar ataxia and disturbance of consciousness. Magnetic resonance imaging revealed recurrence and extension of the previous lesions as well as new lesions in the thalamus and internal capsule. CSF IgG and MBP level showed a higher elevation than in the second episode. The combination of the cerebellar, brain-stem, cerebral and thalamic lesions with remission and exacerbation, supported by MRI and CSF findings, allowed the diagnosis of clinically definite MS to be made. This is one of the youngest cases of MS yet described, with the first attack occurring at 27 months of age. In addition, this case is unique for the involvement of the gray matter in the thalamus.

Age Factors↗
PubMed1990

Tracing of Neuronal Connections in the Human Brain by Magnetic Resonance Imaging in vivo.

Axon degeneration after disruption of fibre tracts in the mammalian nervous system is accompanied by myelin breakdown which leads to changes in its magnetic resonance properties. In two patients with pure motor strokes due to small ischaemic lesions restricted to the internal capsule, magnetic resonance imaging disclosed a narrow band of pathological signal increase descending band-like into the brain stem and ascending to the precentral gyrus, which corresponded to the well-known path of the pyramidal tract. The findings suggest that in man anterograde and possibly retrograde fibre degeneration can be traced in vivo by conventional magnetic resonance imaging techniques. Critical conditions are the presence of small, strategically located lesions, appropriate choice of imaging plane, and the interval between time of lesion and of imaging. This demonstration may open a new era for functional neuroanatomy of man.

Journal Article↗
PubMed1991

Differential Expression of the GABAA Receptor Complex in the Dorsal Thalamus and Reticular Nucleus: An Immunohistochemical Study in the Adult and Developing Rat.

The distribution of the GABAA receptor/benzodiazepine receptor/chloride channel complex was investigated in the thalamus of the rat by means of immunohistochemistry in adulthood, as well as during embryonic and postnatal development, using a monoclonal antibody. In adults, the immunoreactivity for the GABAA receptor complex was intensely expressed by neuronal processes throughout the dorsal thalamus. Neuronal perikaryal membranes were frequently outlined by punctate immunostaining; cell bodies, intrathalamic fibre bundles and the internal capsule did not display immunoreactivity for the GABAA receptor. Regional differences in the expression of the receptor were consistently observed: the immunostaining was much lighter in the thalamic reticular nucleus than in the dorsal thalamic nuclei and, among the latter, the anteroventral nucleus and the ventral nuclear complex displayed the most intense immunopositivity. Immunostaining for the GABAA receptor was already expressed in embryos at E14, and was homogeneously distributed throughout the neuropil of the dorsal and ventral thalamic primordia. During the first two postnatal weeks, a regional differentiation of the immunopositivity was appreciable in the thalamus, with a progressive reduction in the reticular nucleus and a parallel increase in the dorsal thalamic structures. Immunoreactive neuronal perikarya were not observed in the thalamus at any developmental stage. The expression of the GABAA receptor complex appeared to have reached a mature configuration by the end of the third postnatal week. These findings indicate that in adults the GABAA receptor is differentially expressed by thalamic nuclear structures, including the reticular nucleus. Furthermore, the maturation of the receptor in the thalamus undergoes a rearrangement during the first postnatal weeks that results in a considerable regression within the reticular nucleus.

Journal Article↗
PubMed1993

Cellular localization of interleukin 6 mRNA and interleukin 6 receptor mRNA in rat brain.

The distribution of interleukin 6 (IL-6) mRNA and IL-6 receptor (IL-6R) mRNA in the brain of adult male rats was studied at the light microscope level by in situ hybridization histochemistry using 35S-labelled oligonucleotides. The transcripts of both genes were localized in the pyramidal neurons and in the granular neurons of the hippocampus, in neurons of the habenular nucleus as well as in the dorsomedial and ventromedial hypothalamus, in the piriform cortex, in scattered neurons of the cortex and in granular cells of the cerebellum. The medial preoptic nucleus and the anterior tip of the lateral ventricle contained mRNA encoding IL-6 and its receptor. Moreover, white matter areas, such as the internal capsule, which consist of only fibres and glial cells, were found to have autoradiographic signals above background. The mRNAs for IL-6 and IL-6R in hippocampus and cerebellum are not different, as shown by Northern blot analyses of RNA isolated from these tissues. We postulate that the cytokine IL-6 is expressed constitutively in discrete regions of the CNS and that it is involved in the mechanisms coordinating metabolic, behavioural and neuroendocrine changes not only during illness but also under normal physiological conditions. Our results suggest that IL-6 mRNA and IL-6R mRNA are colocalized, thus supporting a role of the cytokine in autocrine and paracrine communication.

Animals↗
PubMed1993

The effects of periaqueductally injected transmitter antagonists on forebrain-elicited vocalization in the squirrel monkey.

In 15 squirrel monkeys, vocalization-eliciting electrodes were implanted into the following forebrain structures: anterior cingulate cortex, genu of the internal capsule, amygdala, bed nucleus of the stria terminalis, hypothalamus, midline thalamus, inferior thalamic peduncle and periventricular grey. Then, injections of 29 transmitter antagonists were made into the midbrain periaqueductal grey (PAG) and their effects tested on the elicitability of vocalization from the forebrain. Vocalization could be blocked completely with glutamate antagonists. NMDA receptor antagonists as well as kainate/quisqualate receptor antagonists were effective. Facilitatory effects, i.e. a decrease in threshold of forebrain-elicited vocalization, was obtained with GABA-A receptor, glycine and opioid antagonists. The facilitatory effect of the opioid antagonist naloxone was limited to vocalizations expressing aversive emotional states. GABA-A receptor antagonists not only facilitated forebrain-induced vocalization but also produced vocalization themselves, i.e. without concomitant forebrain stimulation. No effects were obtained with antagonists of muscarinic and nicotinic receptors, with the GABA-B receptor antagonist phaclofen and antagonists of the monoamines dopamine, noradrenaline, adrenaline, serotonin and histamine. It is concluded that the PAG represents a crucial relay station of the vocalization-controlling system. In this station, transmission of vocalization-relevant information depends upon the activation of glutamatergic synapses. Inhibitory control is exerted by GABA, glycine and endogenous opioids. Acetylcholine, dopamine, noradrenaline, adrenaline, serotonin and histamine may play a transient modulatory role; forebrain-induced vocalization, however, does not depend upon the cholinergic or monoaminergic activation of PAG neurons.

Animals↗
PubMed1996

The course and termination of corticothalamic fibres arising in the visual cortex of the rat.

Corticothalamic axons have been studied in adult Lister hooded rats with single or dual injections of tracers into the visual cortex. Labelled axons leave medial and lateral injection sites in separate or partially overlapping bundles along parallel trajectories in the subcortical white matter. In the internal capsule they converge and both bundles enter roughly the same sector of the thalamic reticular nucleus (TRN). Their reticular terminal fields, however, differ. Axons from a medial injection site innervate more lateral parts of the TRN than do the axons from lateral injection sites. The most medial third of the TRN is not innervated from area 17 but receives a topographically arranged input from peristriate cortex (Crabtree and Killackey, 1989, Eur. J. Neurosci., 1, 94-109; Coleman and Mitrofanis, 1996, Eur. J. Neurosci., 8, 388-404). The two groups of axons then separate in the dorsal thalamus, axons from medial parts of visual cortex turning caudally into lateral regions of the lateral geniculate nucleus, whereas fibres from more lateral cortex continue into medial parts of the nucleus. Connolly and van Essen (1984, J. Comp. Neurol., 226, 544-564) and Nelson and LeVay (1985, J. Comp. Neurol., 240, 322-330) have shown that in the geniculocortical pathway the two groups of fibres cross over in the subcortical white matter, probably in the region of the subplate. We show that the corticothalamic pathway also has a crossing, but it occurs in, or close to, the diencephalon itself, in the region of the perireticular nucleus. This result suggests that each of these pathways, the geniculocortical and the corticogeniculate, may undergo reorganization within distinct cerebral zones, one diencephalic for the corticothalamic axons and the other telencephalic for the thalamocortical axons.

Animals↗
PubMed1996

BDNF and NT-3, but not NGF, prevent axotomy-induced death of rat corticospinal neurons in vivo.

Brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) have been identified as survival factors for adult axotomized rat corticospinal neurons (CSN) in vivo. Axotomy of corticospinal neurons at the level of the internal capsule induced death of 46% of the CSN within the first week after axotomy. The surviving population of CSN displayed severe atrophy with mean cross-sectional area 49% of their unlesioned contralateral counterparts 7 days after axotomy. Using in situ hybridization to assess the expression of the receptors for the family of neurotrophins, we found trkB and trkC but not trkA mRNA expression in CSN. Intraparenchymal application of BDNF or NT-3 at doses of 12 microg/day for 7 days via an osmotic minipump fully prevented the axotomy-induced death of CSN. Interestingly, no neuronal atrophy was seen after BDNF application while NT-3 had only a partial effect on the size of the axotomized CSN. Nerve growth factor did not prevent death or cell atrophy, consistent with lack of trkA mRNA expression in these neurons. These findings show that BDNF and NT-3 are survival factors for adult rat CSN in vivo, and may contribute to the development of therapeutic strategies aiming at the prevention of CSN degeneration in human motor neuron diseases.

Animals↗
PubMed2004

The cortically evoked secondary depolarization affects the integrative properties of thalamic reticular neurons.

Corticothalamic terminals on thalamic reticular (RE) neurons account for most synapses from afferent pathways onto this nucleus and these inputs are more powerful than those from axon collaterals of thalamocortical neurons. Given the supremacy of cortical inputs, we analysed here the characteristics and possible mechanisms underlying a secondary component of the cortically elicited depolarization in RE neurons, recorded in cats under barbiturate anesthesia. Electrical stimulation of corticothalamic axons in the internal capsule evoked fixed and short-latency excitatory postsynaptic potentials (EPSPs) that, by increasing stimulation intensity and at hyperpolarized levels (< -70 mV), developed into low-threshold spikes and spindle oscillations. The threshold for spindle oscillations was 60% higher than that required for evoking minimal EPSPs. The evoked EPSPs included a secondary depolarizing component, which appeared approximately 5 ms after the peak of the initial component and was voltage dependent, i.e. most prominent between -70 mV and -85 mV, while being greatly reduced or absent at more hyperpolarized levels. The secondary depolarizing component was sensitive to QX-314 in the recording micropipette. We suggest that the secondary component of cortically evoked EPSPs in RE neurons is due to the dendritic activation of T-currents, with a probable contribution of the persistent Na+ current. This late component affected the integrative properties of RE neurons, including their spiking output and temporal summation of incoming cortical inputs.

Anesthetics, Local↗
PubMed2004

Myelination triggers local loss of axonal CNR/protocadherin alpha family protein expression.

The cadherin-related neuronal receptor (CNR)/protocadherin (Pcdh) alpha family is one of the diverse protocadherin families expressed in developing axons. We observed a strong axonal expression of these proteins at late embryonic and early postnatal stages corresponding to regions where fibers had not yet been myelinated. We therefore followed the postnatal localization of CNR/Pcdh alpha protein in major axonal tracts, such as the internal capsule, lateral olfactory tract, and optic nerve, and found that its axonal localization was dramatically lost in parallel with the increased expression of myelin markers. Moreover, the hypomyelinated optic nerve tracts of the myelin-deficient Shiverer mouse exhibited elevated levels of CNR/Pcdh alpha expression. These axonal expression patterns of CNR/Pcdh alpha in wild-type and Shiverer mice were similar to those of growth associated protein 43 (GAP-43) and L1, both of which are associated with axonal maturation. Thus, myelination may be a trigger for the local loss of axonal CNR/Pcdh alpha protein, and this process may be important in the maturation of neural circuits.

Age Factors↗
PubMed2006

Localization and function of pre- and postsynaptic kainate receptors in the rat globus pallidus.

Kainate receptors (KARs) are widely expressed the basal ganglia. In this study, we used electron microscopic immunocytochemistry and whole-cell recording techniques to examine the localization and function of KARs in the rat globus pallidus (GP). Dendrites were the most common immunoreactive elements, while terminals forming symmetric or asymmetric synapses and unmyelinated axons comprised most of the presynaptic labeling. To determine whether synaptically released glutamate activates KARs, we recorded excitatory postsynaptic currents (EPSCs) in the GP following single-pulse stimulation of the internal capsule. 4-(8-Methyl-9H-1,3-dioxolo[4,5 h]{2,3}benzodiazepine-5-yl)-benzenamine hydrochloride (GYKI 52466, 100 microm), an alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionic acid (AMPA) receptor antagonist, reduced but did not completely block evoked EPSCs. The remaining EPSC component was mediated through activation of KARs because it was abolished by 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX), an AMPA/KAR antagonist. The rise time (10-90%) and decay time constant (tau) for those EPSCs were longer than those of AMPA-mediated EPSCs recorded before GYKI 52466 application. KAR activation inhibited EPSCs. This inhibition was associated with a significant increase in paired-pulse facilitation ratio, suggesting a presynaptic action of KAR. KAR inhibition of EPSCs was blocked by the G-protein inhibitor, N-ethylmaleimide (NEM), or the protein kinase C (PKC) inhibitor calphostin C. Our results demonstrate that KAR activation has dual effects on glutamatergic transmission in the rat GP: (1) it mediates small-amplitude EPSCs; and (2) it reduces glutamatergic synaptic transmission through a presynaptic G-protein coupled, PKC-dependent, metabotropic mechanism. These findings provide evidence for the multifarious functions of KARs in regulating synaptic transmission, and open up the possibility for the development of pharmacotherapies to reduce the hyperactive subthalamofugal projection in Parkinson's disease.

Age Factors↗