[Reevaluating the shelf life of sterilized packaged items via a risk-analysis study]. / Réévaluation de la durée de péremption des dispositifs médicaux restérilisables via une analyse de risques.

In the hospital, all the reprocessed reusable medical devices (RMD) are conditioned with a sterile barrier system and a protection package and they expire after three months. The objective of this study is to reevaluate this shelf life via a risk-analysis study focusing on the steps whose malfunction can fail RMD sterility. The first step is analysing current conditions of packaging, transportation and storage of RMD. The risk-analysis study has been built on French National Authority for Health template. Risks are prioritized in three categories: non critical risks, risks that need to be kept track of and risks to manage as a priority. Storage conditions have been evaluated in 52 wards in ten different structures. All of the wards respect the paper side of the pouches. They were stored in a dedicated storage unit in 85 % of the units. They were closed at the moment of the observation in 58 % of the cases. RMD were stacked in 81 % of the units and 36 % of them had at leat one expired RMD in their storage unit. The risk-analysis study identified two risks to manage as a priority. Some RMD were damaged during transportation to a subcontractor hospital. This step is barely manageable due to the human factor but the transport rules have been reminded in order to lower the risks on the materials. The operating rooms common storage include shelves that alter pouches and wraps, but a replacement of equipments is under discussion. Thanks to a better understanding of RMD circuit current conditions, allowing a better control of sensitive steps, their shelf life is reevaluated up to 6 months for containers and 4 months for other pouches.

[Comparison between implantation costs of peripherally inserted central catheter and implanted subcutaneous ports]. / Comparaison entre le coût d'une pose de cathéter veineux central d'insertion périphérique et d'une chambre implantable.

INTRODUCTION: Peripherally Inserted Central Catheter or PICC Line and implanted subcutaneous ports are two types of central catheters allowing drug administration and blood samplings. These two devices are very controversial (because of infectious and thrombotic complications), it seemed interesting to estimate their cost of implantation and to correlate them with the reimbursement by the Health Insurance. MATERIALS AND METHODS: Direct (material and drugs) and indirect (use of the room and staff) costs were prospectively evaluated for PICC Lines and implanted subcutaneous ports. RESULTS: The global costs of the implantation of a PICC Line and of an implanted subcutaneous port in the interventional radiology room and in the operating room were respectively evaluated at 220.2 €, 286.6 € and 666.3 €. DISCUSSION-CONCLUSION: Only a PICC Line in outpatients can be reimbursed by the health insurance; which amounts to 110.4 €. The establishment therefore loses money with every implantation. However, PICC Lines offer to the patients a fast access to a central venous way and thus an optimal therapeutic care, fulfilling one of the main missions of the public health institutions. Implanted subcutaneous ports are economically worth being implanted only in ambulatory inpatients. Its implantation in radiology seemed more profitable because the indirect costs were much more moderate.

Haemoglobin sickle d punjab: - a case report.

Haemoglobin S D-Punjab is a rare compound heterozygous haemoglobinopathy characterised by the presence of two ß globin gene variants: Β6(GAG→GTG) and Β121(GAA→CAA). These patients' clinical and haematological features mimic haemoglobin S disease. We describe the first case of doubly heterozygous HbSD-Punjab from Malaysia managed with regular blood transfusion at the age of one. This case highlights the propensity for occurrence of rare phenotypes within our multi-ethnic population and emphasises the importance of accurate genotyping to avoid erroneous counselling, and to plan an effective patient management strategy before complication evolves.

[Proposal of a costing method for the provision of sterilization in a public hospital]. / Proposition d'une méthode de facturation de la prestation de stérilisation dans un centre hospitalier public.

INTRODUCTION: To refine the billing to institutions whose operations of sterilization are outsourced, a sterilization cost approach was developed. The aim of the study is to determine the value of a sterilization unit (one point "S") evolving according to investments, quantities processed, types of instrumentation or packaging. MATERIALS AND METHODS: The time of preparation has been selected from all sub-processes of sterilization to determine the value of one point S. The time of preparation of sterilized large and small containers and pouches were raised. The reference time corresponds to one bag (equal to one point S). Simultaneously, the annual operating cost of sterilization was defined and divided into several areas of expenditure: employees, equipments and building depreciation, supplies, and maintenance. RESULTS: A total of 136 crossing times of containers were measured. Time to prepare a pouch has been estimated at one minute (one S). A small container represents four S and a large container represents 10S. By dividing the operating cost of sterilization by the total number of points of sterilization over a given period, the cost of one S can be determined. DISCUSSION/CONCLUSION: This method differs from traditional costing method in sterilizing services, considering each item of expenditure. This point S will be the base for billing of subcontracts to other institutions.

[Direct cost of cataract surgery in public hospital]. / Approche du coût direct de la chirurgie de la cataracte dans un établissement de santé public.

INTRODUCTION: With more than 500,000 operations per year, cataract surgery is the most performed act nowadays in France. Several techniques can be used but the phacoemulsification after micro-incision is the most common and the purpose is to put an intraocular lens into the eye. AIM: To approach the direct cost of the cataract surgery and to compare it to the amounts of reimbursements, and to get some epidemiological and statistical data about this surgery. MATERIAL AND METHODS: This study is prospective; many operations were followed up in the operating room and every following data were recorded: age of the patient, type of anaesthesia, type of intraocular lens, adverse events, name of surgeon, duration of the intervention, single use material and medications used during operation and their quantity for each operation. RESULTS: One hundred and twenty-five cataract surgeries were followed. Patients mean age was 74,1 years and the anaesthesia was topical in 87,2% of cases; only two patients had general anaesthesia. The mean duration was 42 minutes. The mean direct cost was 366 € but reached 630 € in case of capsular tear. The cost greatly varied depending on the surgeon. Two references of lens (foldable monofocal, that cost between 100 and 150 €) represented 80% of the implanted lenses. CONCLUSION: This type of study may lead to a standardisation of surgical techniques and evaluate the proportion of supply and medications in that type of surgery.

Environmental enrichment brings a beneficial effect on beam walking and enhances the migration of doublecortin-positive cells following striatal lesions in rats.

Rats raised in an enriched environment (enriched rats) have been reported to show less motor dysfunction following brain lesions, but the neuronal correlates of this improvement have not been well clarified. The present study aimed to elucidate the effect of chemical brain lesions and environmental enrichment on motor function and lesion-induced neurogenesis. Three week-old, recently weaned rats were divided into two groups: one group was raised in an enriched environment and the other group was raised in a standard cage for 5 weeks. Striatal damage was induced at an age of 8 weeks by injection of the neuro-toxins 6-hydroxydopamine (6-OHDA) or quinolinic acid (QA) into the striatum, or by injection of 6-OHDA into the substantia nigra (SN), which depleted nigrostriatal dopaminergic innervation. Enriched rats showed better performance on beam walking compared with those raised in standard conditions, but both groups showed similar forelimb use asymmetry in a cylinder test. The number of bromodeoxyuridine-labeled proliferating cells in the subventricular zone was increased by a severe striatal lesion induced by QA injection 1 week after the lesion, but decreased by injection of 6-OHDA into the SN. Following induction of lesions by striatal injection of 6-OHDA or QA, the number of cells positive for doublecortin (DCX) was strongly increased in the striatum; however, there was no change in the number of DCX-positive cells following 6-OHDA injection into the SN. Environmental enrichment enhanced the increase of DCX-positive cells with migrating morphology in the dorsal striatum. In enriched rats, DCX-positive cells traversed the striatal parenchyma far from the corpus callosum and lateral ventricle. DCX-positive cells co-expressed an immature neuronal marker, polysialylated neural cell adhesion molecule, but were negative for a glial marker. These data suggest that environmental enrichment improves motor performance on beam walking and enhances neuronal migration toward a lesion area in the striatum.

Regulation of mitogen-activated protein kinases by sphingolipid products in oligodendrocytes.

Sphingolipid products such as ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP) are implicated in the regulation of cell growth and apoptosis. We have recently shown that cer, sph, and SPP differentially modulate ionic events in cultured oligodendrocytes (OLGs). Cer but not sph or SPP inhibits the inward rectifier (I(Kir)) in OLGs. To further investigate the role of sphingolipid products in OLGs, we studied the effect of cer, sph, and SPP on OLG survival and on the regulation of mitogen-activated protein kinases (MAPKs). We found that cer, sph, and SPP differentially modulate OLG survival and activation of MAPK members. Cer causes OLG apoptosis, sph causes OLG lysis, and SPP does not affect OLG survival. Cer induces a preferential activation of p38alpha, whereas sph and SPP induce a preferential activation of extracellular signal-regulated kinase 2 (ERK2) in OLGs. In addition, the effect of cer on p38alpha activity is mimicked by the inhibition of I(Kir) with Ba(2+). In contrast, exposure to cer results in increased activity of ERK2 but not of p38alpha in astrocytes. Cer-induced OLG apoptosis is attenuated by a p38 inhibitor, SB203580, and by expression of a p38alpha dominant negative mutant. We conclude that p38alpha is the mediator in cer-induced OLG apoptosis and that cer-induced I(Kir) inhibition may contribute to the sustained activation of p38alpha in OLGs.

Argyrophilic dark neurons represent various states of neuronal damage in brain insults: some come to die and others survive.

Argyrophilic dark neurons (DNs) reflect the early histopathological state of neurons following various brain insults. We examined the fate of DNs, about to either die or recover, following two types (heavy and light damage) of brain insult. Wistar rats were injected ibotenic acid unilaterally into the hippocampal CA1 region (ibotenic acid [IA] injection) or were forced to swim (SWIM). Argyrophil III (DNs)-, activated caspase-3 immuno-, TUNEL- and hematoxylin-eosin (H-E)-staining and ultrastructural examinations were then performed. One to three hours after IA injection, typical DNs (argyrophilic both in somata and dendrites) with corkscrew-like dendrites were densely packed in the pyramidal cell layer of hippocampal CA1 around the injection site. After 12-24 h, DNs were argyrophilic only in the somata and proximal dendrites but absent in distal dendrites in the CA1 region. However, at this time typical DNs were found in remote areas. At 3 h, caspase-3 activation was detected at the injection site, which increased to a peak level after 12 h. Three to 7 days after injection, TUNEL positive cells were detected in the CA1 pyramidal cell layer. Immediately following SWIM, "brown" rather than "dark" neurons were detected in the various areas and most frequently in the CA1 pyramidal cell layer. No typical DNs were detected over the first 3 days. Some activation of caspase-3 was detected in a few CA3 pyramidal cells but no TUNEL-positive cells were detected. Ultrastructural examination revealed a diffuse distribution of aggregated silver particles in the dendrites and cytoplasm of pyramidal cells at the sites of IA injection. After SWIM, silver particles were detected mainly on mitochondria of affected cells. These data suggest that DNs provide a measure of neuronal damage: typically dark neurons with broad damage to the cytoskeleton of dendrites would die, while non-typical brown neurons, that may have a disturbance in mitochondria, predominantly survive.

3-Nitropropionic acid produces striatum selective lesions accompanied by iNOS expression.

Systemically administered 3-nitropropionic acid (3-NPA) that inhibits the mitochondrial oxidative phosphorylation induces selective lesions in the striatum. To investigate the nature of these selective lesions, we administered 3-NPA (20 mg/kg, s.c. daily for 2 or 3 days) to Wistar rats and investigated the behavioral disturbance, striatal lesions and their variations after modulating the activity of nitric oxide synthase (NOS). On the second or third day of 3-NPA administration, half the animals manifested behavioral disturbances (paddling, rolling, tremor, abnormal gait, and recumbence). A strong extravasation of immunoglobulin G (IgG) and a decrease in immunoreaction for glial fibrillary acidic protein (GFAP) were detected, and iNOS-like (iNOS-L) immunoreactive small cells appeared in the lateral and central striatum especially around the vessels. A week later, lesions lacking GFAP-immunoreaction were detected in the striatum in survived animals. Pretreatment with N-nitro-L-arginine methyl ester (L-NAME) along with each injection of 3-NPA did not improve the behavioral disturbances nor the survival rate, but attenuated the extravasation of IgG and iNOS-L immunoreaction. Pretreatment with aminoguanidine or FK506 improved the behavioral symptoms and survival rate. Extravasation of IgG and expression of iNOS-L immunoreactivity were attenuated, and the striatal lesion was reduced. Data indicate the involvement of NO in the high vulnerability of the striatum, and that iNOS, one of inflammatory markers, is induced following exposure to 3-NPA.

The striatum is the most vulnerable region in the brain to mitochondrial energy compromise: a hypothesis to explain its specific vulnerability.

The striatum, together with the hippocampus, is one of the most vulnerable regions in the brain. Recently, genetic abnormalities or mutations have been linked to various neurodegenerative diseases, that is, Huntington's disease, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), etc., but the processes from genetic abnormality to the final phenotypic expression are not well understood. Disturbances in energy metabolism especially in mitochondrial energy compromise could facilitate genetic abnormalities and enhance neuronal cell death. Here, we report that the striatum is the most vulnerable brain region to systemic intoxication with 3-nitropropionic acid (3-NPA), an inhibitor of succinate dehydrogenase inducing energy compromise. We hypothesize that the striatum-specific lesion by 3-NPA is due to cummulative insults characteristic to the striatum including glutamatergic excitotoxicity, dopaminergic toxicity, vulnerability of the lateral striatal artery and high activity in the glutamate-transporter. The former two are extravascular in origin while the latter two are intra-/perivascular. We also discuss the possibility that a high turnover rate in metabolism of nitric oxide (NO) might underlie the vulnerability of the lateral striatal artery. We posit that systemic intoxication with 3-NPA offers a good animal model to investigate the pathophysiology of neuronal/glial cell death, neurodegenerative disease, dysfunction of the blood-brain barrier (BBB), neuroimmune disorders, and stroke.

Early assessment of motor dysfunctions aids in successful occlusion of the middle cerebral artery.

Occlusion of the rodent middle cerebral artery by embolism, using an intraluminal filament, produces behavioral alterations which resemble many symptoms associated with stroke. This model has been used to examine treatment interventions for the disease, however, variable success rate in completely blocking the middle cerebral artery may present inconclusive interpretation of the data. To detect successful occlusion of the middle cerebral artery, we demonstrate here sensitive and reliable behavioral parameters including the elevated body swing test, the postural tail-hang test, the spontaneous rotational test, and the forelimb akinesia test. These assays provide a criterion for identifying animals with incomplete occlusion which could promote host-related spontaneous recovery and might confound true effects of experimental therapies on ischemia-induced dysfunctions. From a practical standpoint, the early reliable identification of partial cerebral ischemia aids in immediate and efficient adjustments of the surgical procedure to create a complete and stable ischemia stroke animal model.

Melatonin-secreting pineal gland: a novel tissue source for neural transplantation therapy in stroke.

Chronic systemic melatonin treatment attenuates abnormalities produced by occlusion of middle cerebral artery (MCA) in adult rats. Because the pineal gland secretes high levels of melatonin, we examined in the present study whether transplantation of pineal gland exerted similar protective effects in MCA-occluded adult rats. Animals underwent same-day MCA occlusion and either intrastriatal transplantation of pineal gland (harvested from 2-month-old rats) or vehicle infusion. Behavioral tests (from day of surgery to 3 days posttransplantation) revealed that transplanted stroke rats displayed significantly less motor asymmetrical behaviors than vehicle-infused stroke rats. Histological analysis at 3 days posttransplantation revealed that transplanted stroke rats had significantly smaller cerebral infarction than vehicle-infused rats. Additional experiments showed that pinealectomy affected transplantation outcome, in that transplantation of pineal gland only protected against stroke-induced deficits in stroke animals with intact pineal gland, but not in pinealectomized stroke rats. Interestingly, nonpinealectomized vehicle-infused stroke rats, as well as pinealectomized transplanted stroke rats, had significantly lower melatonin levels in the cerebrospinal fluid than nonpinealectomized transplanted stroke rats. We conclude that intracerebral transplantation of pineal gland, in the presence of host intact pineal gland, protected against stroke, possibly through secretion of melatonin.

Dopamine-denervation enhances the trophic activity in striatum: evaluation by morphological and electrophysiological development in PC12D cells.

To evaluate the possibility that dopamine (DA) denervation enhances the trophic activity in striatum, normal or DA-depleted striatal tissue extract (N- or L-extract, respectively) was obtained, and their trophic effects on PC12D cells were investigated from the viewpoints of differentiation using morphological and electrophysiological analyses. Treatment with N- or L-extract induced neurite outgrowth in a concentration-dependent manner, and induced the enlargement of cell size. These effects were stronger in L-extract than in N-extract. Cation currents were investigated in whole cell patch-clamp mode. Development of cation current started with delayed-rectifier type K+ current (IK) and transient type K+ current (IA), followed by Ca2+ current (ICa) and tetrodotoxin-sensitive Na+ current (INa). INa was expressed more frequently in L-extract treated cells than N-extract treated cells at D7-9. The larger IK amplitude in L-extract treatment at D7-9 seemed to be related to the expression of INa. Development of IA was similar at any stage for both treatments. ICa development started at D3-5 after treatments, and the amplitude and current density were similar in both treatments. ICa was strongly blocked by omega-conotoxin GVIA (3 microM), indicating that N-type channels were mainly expressed after treatments. The data suggests that L-extract has stronger effects to hasten the differentiation of PC12D cells than N-extract by promoting the neurite outgrowth, cell enlargement and expression of voltage-dependent cation channels, especially INa and IK.

Dopa-producing astrocytes generated by adenoviral transduction of human tyrosine hydroxylase gene: in vitro study and transplantation to hemiparkinsonian model rats.

Astrocytes secreting a large amount of 3,4-dihydroxyphenylalanine (dopa) were generated by adenoviral transduction of the human tyrosine hydroxylase (TH) gene. After characterizing in vitro, the effect of transplantation of these astrocytes to the striatum of hemiparkinsonian model rats was investigated. Subconfluent cortical astrocytes were infected by replication-defect adenovirus type 5 carrying the human TH-1 gene or the LacZ reporter gene under the promoter of the glial fibrillary acidic protein (AdexGFAP-HTH-1, AdexGFAP-NL-LacZ). Dopa secretion was not evident at 3 days after the transduction of the HTH-1 gene but it increased from 7 days up to at least 4 months. The secretion was substrate (tyrosine)-dependent, and was enhanced by loading tetrahydrobioputerin (BH4) concentration-dependently. One-third of the hemiparkinsonian model rats, that were transplanted the HTH-1 gene-transduced astrocytes or introduced the direct injection of the viral vector to the striatum, showed a reduction of methamphetamine-induced rotations for at least 6 weeks. Apomorphine-induced rotation was decreased to the 50% level of the control's, but the reduction was obtained equally by the transplantation of HTH-1 gene-transduced or LacZ reporter gene-transduced astrocytes, or by the introduction of HTH-1 or LacZ gene carrying adenovirus. Treatment with FK506 for 3 weeks improved the late-phase apomorphine-induced rotations following the introduction of the HTH-1 gene carrying adenovirus. Histological examination revealed that, in animals that showed a reduction of methamphetamine-rotation, the TH positive astrocytes-like cells were distributed widely in the host striatum for at least 4 weeks. The number of TH positive astrocytes-like cells and their immunoreactivity decreased after 6 weeks when OX-41 positive microglias/macrophages were infiltrated. Data indicate that the adenoviral transduction of the human TH gene to astrocytes and its introduction to the striatum is a promising approach for the treatment of Parkinson's disease. However, the further technical improvements are required to optimize the adenoviral gene delivery, such as the control of viral toxicity and the regulation of the immune response.

Acute 3-nitropropionic acid intoxication induces striatal astrocytic cell death and dysfunction of the blood-brain barrier: involvement of dopamine toxicity.

Mechanisms underlying the selective vulnerability of the lateral striatal area to the toxic effects of 3-nitropropionic acid (3-NPA) were investigated in rats. A single exposure to 3-NPA (20 mg/kg, s.c.) induced no deficits in behavior and histology, but subsequent injection produced motor symptoms, catalepsy, lip smacking, abnormal gait, paddling, rolling, opisthotonos, tremor, recombence, somnolence and so on, in 30% of the animals within a few hours. Diffusion-weighted magnetic resonance imaging of the brains revealed an area of high signal intensity in the bilateral striata. By this stage (within a few hours), striatal astrocytes had become swollen and disintegrated. Extravasation of immunoglobulin G was detected, indicating blood-brain barrier (BBB) dysfunction. Electron microscopy revealed edema and disorganization of structures inside the astrocytic end-feet around the branches of the lateral striatal artery. Neurons were less vulnerable than astrocytes to the 3-NPA injury. Treatment of the rats with D2 receptor agonist prior to exposure to 3-NPA attenuated the behavioral abnormalities and histological damage whereas pretreatment with D2 antagonist exacerbated these changes. The concentrations of extracellular dopamine (DA) and dihydroxyphenyl acetic acid (DOPAC) were both increased in rats exposed to 3-NPA. In vitro imaging of astrocytes revealed a progressive increase in [Ca2+]i after superfusion with 3-NPA, and the 'ceiling' level was maintained even after extensive washing. DA superfusion also increased the astrocytic [Ca2+]i and this increase was reversible. Data indicate that 3-NPA-induced striatal damage was associated with astrocytic cell death and dysfunction of the BBB. Intracellular edema and extreme Ca2+ overload induced by the toxin were further aggravated by an increase in the level of DA activity. These factors acting either singly or in combination may trigger astrocyte destruction.

GDNF is a major component of trophic activity in DA-depleted striatum for survival and neurite extension of DAergic neurons.

Extracts from dopamine (DA)-depleted striatal tissue (lesion extract) and from intact striatal tissue (intact extract) were prepared, and trophic activities in these extracts were evaluated using survival and neurite extension of DAergic neurons as indices. Levels of brain-derived neurotrophic factor (BDNF), basic fibroblast growth factor (bFGF), glial cell-line derived neurotrophic factor (GDNF) and neurotrophin-3 (NT-3) in extracts were measured using enzyme-linked immunosorbent assay (ELISA). The lesion extract exhibited a stronger trophic activity on survival and neurite extension of DAergic neurons than intact extract. In lesion extract, bFGF was slightly and GDNF was significantly increased, while BDNF and NT-3 were the same level in each extract. The peak increase of bFGF and GDNF was during 2 to 3 weeks after DA depletion. Trophic activity of extract was strongly attenuated after immunoprecipitation of GDNF and partly attenuated after immunoprecipitation of bFGF. In parallel immunohistological study, no significant variations were found for striatal microtubule-associated protein-2 (MAP-2)- nor OX-41-immunoreactive cells, while the number of strongly labeled glial fibrillary acidic protein (GFAP)-immunoreactive cells were increased in DA-depleted striatum, suggesting reactive gliosis. Data suggest that bFGF is a minor, while GDNF is a major component of trophic activity for DAergic neurons in DA-depleted striatum, and increased bFGF and GDNF levels may be mediated partly by reactive gliosis.

Argyrophilic dark neurons distribute with a different pattern in the brain after over hours treadmill running and swimming in the rat.

Argyrophil III staining is a useful method for the detection of dark neurons (DNs) that would reflect an early cytopathic feature. We examined the appearance of DNs following the stressful exercises (0.5-3 h swimming in a pool of 25-45 cm depth; 1-2 h running on a treadmill at the speed of 600-1200 cm/min) in the rat. After the swimming, DNs were detected in the hippocampus (CA1-2 pyramidal cell layer, oriens layer), somatosensory cortex, entorhinal cortex, hypothalamus, habenular nucleus, amygdaloid nucleus, striatum, accumbens and sometimes in lateral septal nucleus. After the running, DNs appeared in the visual cortex, deepest layer of area 17 and 18a, motor cortex, red nucleus, somatosensory cortex, entorhinal cortex, and hippocampus (dentate gyrus). Thus, the DNs appeared mainly in the limbic structure after the swimming, and in the limbic structure, motor-related regions and visual cortex after the running. Further, the number of the DNs and the extent of area where they distributed were dependent on the strength and the duration of the exercises. In hematoxylin-eosin (H-E) staining, we often detected pycnotic cells (dark stained soma) in CA1 hippocampus where argyrophil positive cells were most abundant. The picnotic cells were not so common in other areas. Data suggest that DNs are induced by stressful exercises. They might reflect an early cell injury following stress and overexcitation.

Tissue extract from dopamine-depleted striatum enhances differentiation of cultured striatal type-1 astrocytes.

The effects of tissue extract from dopamine (DA)-depleted striatum (lesion extract, L-ext) on morphological and electrophysiological natures of cultured striatal astrocytes were investigated. L-ext treatment suppressed the proliferation of type-1 astrocytes. They became fibrous in a concentration-dependent manner. These changes were not observed in type-2 astrocytes. By whole cell patch-clamp recording, two kinetically and pharmacologically distinct voltage-activated potassium currents, A current and delayed rectifier, were identified. L-ext treatment enhanced both currents in type-1 astrocytes, but only A current in type-2. Data suggest that in tissue extract from DA-depleted striatum, there are increased trophic activities that promote the differentiation of type-1 astrocytes.

Appearance of deteriorated neurons on regionally different time tables in rat brain thin slices maintained in physiological condition.

Brain slices are widely used for electrophysiological experiments. However, the time table of the chronological cell deterioration and its regional difference in slices are unknown. The argyrophil III staining method can demonstrate deteriorated ('collapsed') neurons specifically. Therefore we studied the appearance of the 'collapsed' neurons with time in coronal brain 'thin' slices maintained in vitro to evaluate possible regional differences in vulnerability. In the hippocampus, CA1 pyramidal, dentate gyrus granule, and non-pyramidal cells in any subfield became argyrophilic most easily, as did layer V-VI pyramidal neurons in the neocortex. These results suggest that some subclasses of neurons in brain slices degrade earlier than others even when maintained in physiological condition.