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  • 1
    Electronic Resource
    Electronic Resource
    Microglia-specific expression of microsomal prostaglandin E2 synthase-1 contributes to lipopolysaccharide-induced prostaglandin E2 production (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 94 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Microsomal prostaglandin E2 synthase (mPGES)-1 is an inducible protein recently shown to be an important enzyme in inflammatory prostaglandin E2 (PGE2) production in some peripheral inflammatory lesions. However, in inflammatory sites in the brain, the induction of mPGES-1 is poorly understood. In this study, we demonstrated the expression of mPGES-1 in the brain parenchyma in a lipopolysaccharide (LPS)-induced inflammation model. A local injection of LPS into the rat substantia nigra led to the induction of mPGES-1 in activated microglia. In neuron-glial mixed cultures, mPGES-1 was co-induced with cyclooxygenase-2 (COX-2) specifically in microglia, but not in astrocytes, oligodendrocytes or neurons. In microglia-enriched cultures, the induction of mPGES-1, the activity of PGES and the production of PGE2 were preceded by the induction of mPGES-1 mRNA and almost completely inhibited by the synthetic glucocorticoid dexamethasone. The induction of mPGES-1 and production of PGE2 were also either attenuated or absent in microglia treated with mPGES-1 antisense oligonucleotide or microglia from mPGES-1 knockout (KO) mice, respectively, suggesting the necessity of mPGES-1 for microglial PGE2 production. These results suggest that the activation of microglia contributes to PGE2 production through the concerted de novo synthesis of mPGES-1 and COX-2 at sites of inflammation of the brain parenchyma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2005.03302.x
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  • 2
    Electronic Resource
    Electronic Resource
    Estrogens inhibit l-glutamate uptake activity of astrocytes via membrane estrogen receptor α (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 86 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We investigated the effects of estrogen-related compounds including xenoestrogens [17β-estradiol (E2), 17α-ethynylestradiol (EE), diethylstilbestrol (DES), p-nonylphenol (PNP), bisphenol A (BPA) and 17α-estradiol (17α)] on l-glu uptake by cultured astrocytes via glutamate-aspartate transporter (GLAST). After 24 h treatment, E2 inhibited the l-glu uptake at 1 µm and higher concentrations. EE and DES also inhibited the l-glu uptake at 1 nm and higher concentrations. The other four compounds had no effect. The effects of E2, EE and DES were completely blocked by 10 nm of ICI182 780 (ICI). β-Estradiol 17-hemisuccinate : bovine serum albumin (E2-BSA), a membrane-impermeable conjugate of E2, also elicited the inhibition of l-glu uptake at 1 nm and higher concentrations, and the effect was blocked by ICI. 16α-Iodo-17β-estradiol (16αIE2), an estrogen receptor α (ERα) selective ligand, revealed an inhibitory effect at 10 nm, while genistein, an ERβ selective ligand, failed to reveal such an effect at this concentration. Western blot analysis showed that the predominant ER of cultured astrocytes was ERα. The colocalization of ERα with GLAST on plasma membranes was immunohistochemically detected in these cells. From these results, we concluded that estrogens down-regulate l-glu uptake activity of astrocytes via membrane ERα.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.01953.x
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  • 3
    Electronic Resource
    Electronic Resource
    Hippocampal long-term depression as an index of spatial working memory (2002)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 16 (2002), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Long-term potentiation (LTP), a form of synaptic plasticity in the hippocampus, is a cellular model for the neural basis of learning and memory, but few studies have investigated the contribution of long-term depression (LTD), a counterpart of LTP. To address the possible relationship between hippocampal LTD and spatial performance, the spatial cognitive ability of a rat was assessed in a spontaneous alternation test and, thereafter, LTD in response to low-frequency burst stimulation (LFBS) was monitored in the dentate gyrus of the same rat under anaesthesia. To enhance a divergence in the ability for spatial performance, some of the animals received fimbria–fornix (FF) transection 14 days before the experiments. LTD was reliably induced by application of LFBS to the medial perforant path of intact rats, while no apparent LTD was elicited in rats with FF lesions. The behavioural parameters of spatial memory showed a significant correlation with the magnitude of LTD. We found no evidence that the cognitive ability correlated with other electrophysiological parameters, e.g. basal synaptic responses, stimulus intensity to produce half-maximal responses, paired-pulse facilitation or paired-pulse depression. These results suggest that the magnitude of LTD in the dentate gyrus serves as a reliable index of spatial cognitive ability, providing insights into the functional significance of hippocampal LTD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2002.02159.x
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  • 4
    Electronic Resource
    Electronic Resource
    BDNF attenuates hippocampal LTD via activation of phospholipase C: implications for a vertical shift in the frequency–response curve of synaptic plasticity (2002)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 16 (2002), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Recent evidence shows that neurotrophins are not only involved in neuronal survival and differentiation during development but also in modulating synaptic strength in the mature brain. To understand how neurotrophins alter this synaptic modification, we have investigated the effect of brain-derived neurotrophic factor (BDNF) on long-term depression (LTD) at Schaffer collateral–CA1 synapses in rat hippocampal slices. The slices treated with BDNF for 5 min showed significantly less LTD in response to a 1-Hz tetanus compared with controls but displayed normal LTD when the afferents were tetanized at 10 Hz. Because BDNF enhanced long-term potentiation (LTP) induced by a 30-Hz tetanus, the synaptic modification threshold (θm) as defined in the ‘BCM’ theory of Bienenstock Cooper & Monroe [Bienenstock et al. (1982), J. Neurosci., 2, 32–48] was not shifted. BNDF is likely to alter the capability of the plastic changes in synaptic efficacy, i.e. to produce an upward shift in the BCM curve. The suppressive effect of BDNF on LTD was prevented by either the tyrosine kinase (Trk) receptor inhibitor K252a or the phospholipase C inhibitor U73122. Thus, TrkB activation may attenuate LTD through phospholipase C signalling pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2002.02051.x
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  • 5
    Electronic Resource
    Electronic Resource
    Phospholipase A2 mediates ischemic injury in the hippocampus: a regional difference of neuronal vulnerability (2001)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 13 (2001), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Although it is well known that the hippocampal CA1 subfield is highly vulnerable to ischemic injury, cellular mechanisms leading to this neuronal degeneration are not fully understood. Using organotypic cultures of rat hippocampal slices, we determined whether phospholipase A2 (PLA2) is activated in response to ischemic conditions (OGD; oxygen and glucose deprivation). The PLA2 activity in the pyramidal cell layer increased immediately following a 35-min exposure to OGD, which was likely to be mediated by selective activation of cytosolic Ca2+-dependent PLA2 subtype (cPLA2). This enhancement lasted for at least 24 h. Interestingly, no apparent increase was detected in the dentate gyrus. Twenty-four hours after the OGD exposure, neuronal death was detected mainly in the CA1 region of hippocampal slices. To examine whether the PLA2 activation is causally or protectively involved in the ischemic injury, we investigated the effect of pharmacological blockade of PLA2 on the OGD-induced neuronal death. The PLA2 inhibitor bromophenacyl bromide efficiently prevented the cell death in a concentration-dependent manner. Similar results were obtained for the selective cPLA2 inhibitor AACOCF3. However, the Ca2+-independent PLA2 inhibitor bromoenol lactone and the secretory PLA2 inhibitor LY311727 were virtually ineffective. These results suggest that cPLA2 plays a causative role in the neuronal death following OGD exposure. Thus, the present study may provide novel therapeutic targets for the development of neuroprotective agents.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0953-816x.2001.01623.x
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  • 6
    Electronic Resource
    Electronic Resource
    Rapid regrowth of hippocampal mossy fibres and preceding maturation of NMDA receptor-mediated neurotransmission (2002)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 15 (2002), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Early in postnatal development, glutamatergic synapses contain primarily NMDA receptors and progressively acquire AMPA receptor function. To determine whether this transformation occurs in a process of regenerative synaptogenesis following axotomy, we investigated the recovery of AMPA and NMDA receptor-mediated neurotransmission after the transection of mossy fibres (MF) in organotypic hippocampal cultures. An NMDA component could already be elicited 1 day after the lesion and reached a saturated level after 3 days. Thereafter, an AMPA component appeared and slowly matured after 10 days. The preceding establishment of NMDA receptor function implies that immature MF synapses are functionally silent at least for the first several days of recovery. The appearance of AMPA receptor-mediated neurotransmission was unchanged in the presence of an NMDA-receptor antagonist or tetrodotoxin, which suggests that the AMPA receptor maturation is virtually independent of neuronal activity. Thus, the conversion of silent to functional synapses is not unique to synaptic plasticity or developmental processes but also occurs in recovery after brain damage, but its mechanism is likely to differ from NMDA receptor-dependent recruitment of AMPA receptors in synaptic plasticity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2002.02035.x
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  • 7
    Electronic Resource
    Electronic Resource
    5-Hydroxytryptamine is emetogenic in the house musk shrew, Suncus murinus (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 344 (1991), S. 564-567 
    Details
    ISSN: 1432-1912
    Keywords: Vomiting ; 5-HT ; 2-Me-5-HT ; 5-HT3 Receptor antagonism ; Cancer Chemotherapy ; House musk shrew (Suncus murinus)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The emetic effects of 5-hydroxytryptamine (5-HT) and 5-HT3 receptor agonists were investigated in the house musk shrew, Suncus murinus. 5-Hydroxytryptamine (5-HT; i.p., i.v., s.c.) and 2-methyl-5-HT (2-Me-5HT; i.p.) but not 5-hydroxyindoleacetic acid (i.p.) or 5-ethoxytryptamine (i.p.) induced emesis with very short latency. Tropisetron (ICS 205-930, a 5-HT3 receptor antagonist, s.c.) blocked the emesis induced by 5-HT (10 mg/kg, i.p.) and 2-Me-5-HT (5 mg/kg, i.p.) with respective ID50 values of 7.8 and 70.9 μg/kg. Pindolol (5-HT1 receptor antagonist) and ketanserin (5-HT2 receptor antagonist) were about 100 times less potent than tropisetron. The emesis induced by 5-HT was prevented by surgical vagotomy but not by pretreatment with a combination of atropine (0.1 mg/kg, s.c.) and hexamethonium (10 mg/kg, s.c.). These results clearly indicate that 5-HT is emetogenic probably through a stimulation of peripheral 5-HT3 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170653
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  • 8
    Electronic Resource
    Electronic Resource
    Effects of calcitonin gene-related peptide (CGRP) on Ca2+-channel current of isolated smooth muscle cells from rat vas deferens (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 346 (1992), S. 515-522 
    Details
    ISSN: 1432-1912
    Keywords: Calcitonin gene-related peptide ; Smooth muscle cells ; Vas deferens - Membrane currents ; Ca2+ channel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of calcitonin gene-related peptide (CGRP), a putative non-adrenergic non-cholinergic neutrotransmitter on the electrical properties of the cell membrane, were investigated in enzymically dispersed smooth muscle cells from rat vas deferens. Under current clamp conditions, CGRP (up to 10−7 M) did not induce significant changes in membrane potentials or input resistance in the resting state. The configurations of action potentials elicited by depolarizing current pulses were also unaffected, except that a prolongation of the duration of the action potentials by a high dose (10−7 M) of CGRP was observed in some of the cells. Under whole cell voltage clamp conditions, the transient and sustained K+ currents, activated by depolarizing voltage-steps, were apparently decreased in the presence of 10−9 to 10−7 M CGRP. The peptide increased the voltage-gated Ca2+ current in cells loaded with 145 mM Cs+ solution in order to block the K+ currents. The voltage-dependency of the peak Ca2+ current was not changed by CGRP. Ba2+ (10.8 mM) was used as a charge carrier for the Ca2+-channel current to clarify further the effects of CGRP on the properties of the current. CGRP (10−8 M) delayed the inactivation time course of the Ca2+-channel current and slowed the recovery from inactivation. The peptide did not affect the steady-state inactivation measured by changing the holding potential. The Ca2+-channel current in the presence of CGRP was suppressed by nicardipine (10−6 M) to the same extent as the current under control conditions. The results suggest that CGRP modifies the L-type Ca2+ channel in smooth muscle cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169006
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  • 9
    Electronic Resource
    Electronic Resource
    Contractile response and electrophysiological properties in enzymatically dispersed smooth muscle cells of rat vas deferens (1987)
    Springer
    Pflügers Archiv 408 (1987), S. 112-119 
    Details
    ISSN: 1432-2013
    Keywords: Rat vas deferens ; Single smooth muscle cells ; Sensitivity to norepinephrine ; Voltage clamp ; Action potentials ; Membrane currents ; Ca current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Electrophysiological studies were performed on single smooth muscle cells isolated from the vas deferens of the rat. The tissue was preincubated in Ca-free modified Tyrode's solution for 1 h and then transferred to a high-K solution for 1 h. It was next minced and treated with the enzyme solution composed of 600–800 unit/ml collagenase and 40 unit/ml elastase. The procedure yielded about 50% spindle shaped Ca-tolerant cells (100–250 μm in length and about 10 μm in diameter). These cells could contract during the superfusion with the solutions containing 10−8 to 10−3M norepinephrine (NE) or adenosine triphosphate (ATP). The cells isolated from the epididymal portion were more sensitive to norepinephrine than were those from the prostatic part. Their basic electrical properties were studied using tight-seal suction electrode technique. The cells had resting potentials around −40 mV and their input resistance was about 0.8 GΩ. Action potentials could be evoked by application of depolarizing current. During whole cell voltage clamp, an inward current followed by an outward current was recorded when 800 ms pulses from a holding potential of −60 mV to test potentials positive than −40 mV were applied. The transient outward current generally recorded in other smooth muscle cells was not seen in these cells. The amplitude of the inward current was Ca dependent and sensitive to a Ca antagonist, nicardipine, indicating that Ca ion is the main carrier of this component of the current. When the pipette was filled with Cs-containing solution, the outward current was abolished. In this condition, the reversal potential of Ca current was +53.4 mV, and the time course of inactivation was composed of more than one exponential component. The results suggest that these isolated cells retain many characteristics of analogous multicellular preparation and that they are a useful model of the postsynaptic properties in smooth muscle especially when studied electro-physiologically.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581338
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  • 10
    Electronic Resource
    Electronic Resource
    Fast and slowly inactivating components of Ca-channel current and their sensitivities to nicardipine in isolated smooth muscle cells from rat vas deferens (1988)
    Springer
    Pflügers Archiv 411 (1988), S. 289-295 
    Details
    ISSN: 1432-2013
    Keywords: Vas deferens ; Isolated smooth muscle cells ; Whole cell recording ; Ca-channel current ; Inactivation ; Sensitivity to nicardipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract (1) Fast and slowly inactivating components of Ca-channel current were compared to clarify whether more than one type of Ca-channel exists in smooth muscle cells from rat vas deferens using the whole cell variant of the patch clamp technique. The pipette was filled with 150 mM Cs solution to eliminate outward current and Ba was used as the charge carrier for Ca-channel current. (2) When activated by a 5 s test pulse to 0 mV from a holding potential of −60 mV, the inactivation process of Ba-current was well fitted by the sum of two exponentials. The time constant of the faster inactivating component was 100–300 ms and that of the slower inactivating component was 1.5–3 s. Steadystate inactivation curves of the fast- and slow-components were very similar. (3) The inward current activated at 0 mV from −80 mV was inactivated faster than that from −30 mV. The voltage-dependencies of the peak current from holding potentials of −30 mV and −80 mV were similar. Both had voltage threshold at −30 mV and were maximal at +10 mV. (4) Low concentrations of nicardipine (10−9 to 10−7 M) preferentially inhibited the slow component while higher concentration (10−6 to 10−5 M) were required to block the fast component. The current activated from a holding potential of −30 mV was almost fully suppressed by 10−7 M nicardipine whereas that from −80 mV was blocked only slightly. The voltage dependencies of the peak currents before and during the superfusion with nicardipine (10−7 M) were similar although the peak amplitude was suppressed in the presence of the drug. (5) These results suggest that the existence of either (a) two populations of Ca channels that differ in the time course of inactivation and the sensitivity to nicardipine, but have nearly identical dependence on membrane potential or (b) one population of Ca channel having two different states of inactivation and the sensitivity of nicardipine, in rat vas deferens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585117
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