X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
Type of Material
Type of Publication
Consortium
Language
back to result list
  • 1
    Online Resource
    Online Resource
    Activation of glial glutamate transporter via MAPK p38 prevents enhanced and long-lasting non-evoked resting pain after surgical incision in rats (23)
    Details
    UID:
    (DE-627)1667932063
    Format: 11
    ISSN: 1873-7064
    Content: Pain after surgery has recently become a major issue not only due to lack of treatment success in the acute phase; even more alarming is the large number of patients developing prolonged pain after surgery. Because spinal glutamate as well as spinal glia plays a major role in acute incisional pain, we investigated the role of the spinal glial glutamate transporters (GT), GLAST, GLT-1, for acute and prolonged pain and hyperalgesia caused by an incision. Spinal administration of the GT-inhibitor DL-TBOA increased non-evoked pain but not evoked pain behavior (hyperalgesia) up to 2 weeks after incision. In accordance, spinal GLAST (and to a lesser degree GLT-1) were upregulated after incision for several days. Long-term incision induced GT upregulation was prevented by long-lasting p38-inhibitor administration but not by long-lasting ERK1/2-inhibition after incision. In accordance, daily treatment with the p38-inhibitor (but not the ERK1/2 inhibitor) prolonged non-evoked but not evoked pain behavior after incision. In electrophysiological experiments, spontaneous activity of high threshold (HT) (but not wide dynamic range (WDR)) neurons known to transmit incision induced non-evoked pain was increased after prolonged treatment with the p38-inhibitor. In conclusion, our findings indicate a new spinal pathway by which non-evoked pain behavior after incision is modulated. The pathway is modality (non-evoked pain) and neuron (HT) specific and disturbance contributes to prolonged long-term pain after surgical incision. This may have therapeutic implications for the treatment of acute and - even more relevant - for prevention of chronic pain after surgery in patients.
    Note: Gesehen am 25.06.2019
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 105(2016), Seite 607-617, 1873-7064
    In: volume:105
    In: year:2016
    In: pages:607-617
    In: extent:11
    Language: English
    DOI: 10.1016/j.neuropharm.2016.02.024
    URL: Volltext
    URL: Volltext
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
  • 2
    Online Resource
    Online Resource
    Activation of group I metabotropic glutamate receptors induces long-term depression at sensory synapses in superficial spinal dorsal horn (13)
    Details
    UID:
    (DE-627)1756957819
    Format: 13
    ISSN: 1873-7064
    Content: Low-frequency stimulation of primary afferent Aδ-fibers can induce long-term depression of synaptic transmission in rat superficial spinal dorsal horn. Here, we have identified another form of long-term depression in superficial spinal dorsal horn neurons that is induced by specific group I but not group II metabotropic glutamate receptor (mGluR) agonists. Synaptic strength between Aδ-fibers and dorsal horn neurons was examined by intracellular recordings in a spinal cord-dorsal root slice preparation from young rat. In the presence of bicuculline and strychnine, bath application of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid ((1S,3R)-ACPD) or the specific group I mGluR agonist (S)-3,5-dihydroxyphenylglycine ((S)-3,5-DHPG) but not the specific group II mGluR agonist (2S,2′R,3′R)-2-(2′,3′-dicarboxycyclopropyl)glycine (DCG-IV) for 20 min produced an acute and a long-term depression of synaptic strength. Bath application of the N-methyl-d-aspartate receptor antagonist d-2-amino-5-phosphonovaleric acid did not affect these depressions by (1S,3R)-ACPD. After pre-incubation of slices with pertussis toxin, a G-protein inhibitor, (1S,3R)-ACPD still induced acute and long-term depressions. The phospholipase C inhibitor U73122 stereoselectively blocked the induction of long-term depression without affecting acute synaptic inhibition. This study demonstrates that, in the spinal cord, direct activation of group I mGluRs that are coupled to phospholipase C through pertussis toxin-insensitive G-proteins induces a long-term depression of synaptic strength. This may be relevant to the processing of sensory information in the spinal cord, including nociception.
    Note: Gesehen am 03.05.2021
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 39(2000), 12, Seite 2231-2243, 1873-7064
    In: volume:39
    In: year:2000
    In: number:12
    In: pages:2231-2243
    In: extent:13
    Language: English
    DOI: 10.1016/S0028-3908(00)00084-8
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
  • 3
    Online Resource
    Online Resource
    Alcohol and sweet reward are encoded by distinct meta-ensembles (11)
    Details
    UID:
    (DE-627)1776252896
    Format: 13
    ISSN: 1873-7064
    Content: Cue-reward associations form distinct memories that can drive appetitive behaviors and cravings for both drugs and natural rewards. It is still unclear how such memories are encoded in the brain's reward system. We trained rats to concurrently self-administer either alcohol or a sweet saccharin solution as drug or natural rewards, respectively. Memory recall due to cue exposure reactivated reward-associated functional ensembles in reward-related brain regions, marked by a neural cFos response. While the local ensembles activated by cue presentation for either reward consisted of similar numbers of neurons, using advanced statistical network theory, we found robust reward-specific co-activation patterns across brain regions. Interestingly, the resulting meta-ensemble networks differed by the most influential regions, which in case of saccharin comprised the prefrontal cortex, while for alcohol seeking control shifted to insular cortex with strong involvement of the amygdala. Our results support the view of memory representation as a differential co-activation of local neuronal ensembles. This article is part of the special issue on ‘Neurocircuitry Modulating Drug and Alcohol Abuse’.
    Note: Gesehen am 05.11.2021
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 195(2021) vom: 1. Sept., Artikel-ID 108496, Seite 1-13, 1873-7064
    In: volume:195
    In: year:2021
    In: day:1
    In: month:09
    In: elocationid:108496
    In: pages:1-13
    In: extent:13
    Language: English
    DOI: 10.1016/j.neuropharm.2021.108496
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
  • 4
    Online Resource
    Online Resource
    Approved cannabinoids for medical purposes : comparative systematic review and meta-analysis for sleep and appetite (15)
    Details
    UID:
    (DE-627)1832805565
    Format: 11
    ISSN: 1873-7064
    Content: Background - Cannabinoids are used for numerous disease indications. However, cannabinoids can also produce adverse effects; for example, they can disturb physiological functions such as sleep and appetite. The medical use of cannabinoids refers to a wide variety of preparations and products. Approved cannabinoid products include dronabinol ((−)-trans-Δ9-tetrahydrocannabinol (THC), nabilone (a THC analogue), and cannabidiol (CBD) that differ in their pharmacology and may thus have different adverse effects on sleep and appetite. - Objectives - Here we ask if (i) cannabinoids decrease sleep and appetite in somatic patients or patients that suffer from mental illness and if (ii) there is a difference between THC products (nabilone, dronabinol), vs. CBD in disturbing these physiological functions. - Methods - In order to answer these two questions, we performed a comparative systematic review (SR) for nabilone, dronabinol, and CBD. For the comparative SR we searched PubMed, Medline, Embase, and PsycINFO for randomized controlled trials (RCTs) and extracted information for adverse side effects or outcomes reporting a negative impact on sleep and appetite. RCT evidence was calculated as odds ratios (ORs) via fixed effects meta-analyses. Evidence quality was assessed by the Cochrane Risk of Bias and GRADE tools. This study is registered at PROSPERO (CRD42021229932). - Findings - A total of 17 RCTs (n = 1479) and 15 RCTs (n = 1974) were included for sleep and appetite, respectively. Pharmaceutical THC (nabilone, dronabinol) does not affect sleep or appetite. In contrast, there is moderate evidence that CBD decreases appetite (OR = 2.46 [1.74:4.01] but has also no effect on sleep. - Interpretations - Our comparative systematic study shows that approved cannabinoids can decrease appetite as a negative side effect - an effect that seems to be driven by CBD. Approved cannabinoid products do not negatively affect sleep in somatic and psychiatric patients. This article is part of the special Issue on “Cannabinoids”.
    Note: Gesehen am 31.01.2023
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 196(2021) vom: Sept., Artikel-ID 108680, Seite 1-11, 1873-7064
    In: volume:196
    In: year:2021
    In: month:09
    In: elocationid:108680
    In: pages:1-11
    In: extent:11
    Language: English
    DOI: 10.1016/j.neuropharm.2021.108680
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
  • 5
    Online Resource
    Online Resource
    Atomoxetine improves attentional orienting in a predictive context (2019)
    Details
    UID:
    (DE-627)1741519330
    ISSN: 1873-7064
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 150(2019), Seite 595-69, 1873-7064
    In: volume:150
    In: year:2019
    In: pages:595-69
    Language: English
    DOI: 10.1016/j.neuropharm.2019.03.012
    URL: kostenfrei
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    BSZ
  • 6
    Online Resource
    Online Resource
    The ATP required for potentiation of skeletal muscle contraction is released via pannexin hemichannels (11)
    Details
    UID:
    (DE-627)1786036142
    Format: 10
    ISSN: 1873-7064
    Content: During repetitive stimulation of skeletal muscle, extracellular ATP levels raise, activating purinergic receptors, increasing Ca2+ influx, and enhancing contractile force, a response called potentiation. We found that ATP appears to be released through pannexin1 hemichannels (Panx1 HCs). Immunocytochemical analyses and function were consistent with pannexin1 localization to T-tubules intercalated with dihydropyridine and ryanodine receptors in slow (soleus) and fast (extensor digitorum longus, EDL) muscles. Isolated myofibers took up ethidium (Etd+) and released small molecules (as ATP) during electrical stimulation. Consistent with two glucose uptake pathways, induced uptake of 2-NBDG, a fluorescent glucose derivative, was decreased by inhibition of HCs or glucose transporter (GLUT4), and blocked by dual blockade. Adult skeletal muscles apparently do not express connexins, making it unlikely that connexin hemichannels contribute to the uptake and release of small molecules. ATP release, Etd+ uptake, and potentiation induced by repetitive electrical stimulation were blocked by HC blockers and did not occur in muscles of pannexin1 knockout mice. MRS2179, a P2Y1R blocker, prevented potentiation in EDL, but not soleus muscles, suggesting that in fast muscles ATP activates P2Y1 but not P2X receptors. Phosphorylation on Ser and Thr residues of pannexin1 was increased during potentiation, possibly mediating HC opening. Opening of Panx1 HCs during repetitive activation allows efflux of ATP, influx of glucose and possibly Ca2+ too, which are required for potentiation of contraction. This article is part of the Special Issue Section entitled ‘Current Pharmacology of Gap Junction Channels and Hemichannels’.
    Note: Gesehen am 14.01.2022
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 75(2013) vom: Dez., Seite 594-603, 1873-7064
    In: volume:75
    In: year:2013
    In: month:12
    In: pages:594-603
    In: extent:10
    Language: English
    DOI: 10.1016/j.neuropharm.2013.03.022
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
  • 7
    Online Resource
    Online Resource
    Could tuning of the inhibitory tone involve graded changes in neuronal chloride transport? (3)
    Details
    UID:
    (DE-627)1703266501
    Format: 11
    ISSN: 1873-7064
    Content: Hyperpolarizing synaptic inhibition through GABAA and glycine receptors depends on the presence of the neuronal cation-chloride-cotransporter protein, KCC2. Several transcriptional and post-transcriptional mechanisms have been shown to regulate KCC2 and thereby influence the polarity and efficacy of inhibitory synaptic transmission. It is unclear however whether regulation of KCC2 enables the transporter to attain different levels of activity thus allowing a neuron to modulate the strength of inhibitory synaptic transmission to its changing requirements. We therefore investigated whether phosphorylation can allow KCC2 to achieve distinct levels of [Cl−]i in neurons. We generated a variety of KCC2 alanine dephosphorylation mimics and used NH4+-induced pHi shifts in cultured hippocampal neurons to quantify the rate of KCC2 transport activity exhibited by these mutants. To explore the relationship between KCC2 transport and GABAA receptor-mediated current amplitudes we performed gramicidine perforated-patch recordings. The correlation between EGABA and NH4+-induced pHi shifts enabled an estimate of the range of chloride extrusion possible by kinase/phosphatase regulation of KCC2. Our results demonstrate that KCC2 transport can vary considerably in magnitude depending on the combination of alanine mutations present on the protein. Transport can be enhanced to sufficiently high levels that hyperpolarizing GABAA responses may be obtained even in neurons with an extremely negative resting membrane potential and at high extracellular K+ concentrations. Our findings highlight the significant potential for regulating the inhibitory tone by KCC2-mediated chloride extrusion and suggest that cellular signaling pathways may act combinatorially to alter KCC2 phosphorylation/dephosphorylation and thereby tune the strength of synaptic inhibition.
    Note: Gesehen am 02.07.2020
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 95(2015), Seite 321-331, 1873-7064
    In: volume:95
    In: year:2015
    In: pages:321-331
    In: extent:11
    Language: English
    DOI: 10.1016/j.neuropharm.2015.03.026
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
  • 8
    Online Resource
    Online Resource
    The effect of ketamine on optical and electrical characteristics of spreading depolarizations in gyrencephalic swine cortex (2014)
    Details
    UID:
    (DE-627)1527060306
    Format: 10
    ISSN: 1873-7064
    Note: Gesehen am 04.03.2016
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 84(2014), Seite 52-61, 1873-7064
    In: volume:84
    In: year:2014
    In: pages:52-61
    In: extent:10
    Language: English
    DOI: 10.1016/j.neuropharm.2014.04.018
    URL: Volltext
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
  • 9
    Online Resource
    Online Resource
    Eighteen-hour inhibitory effect of s-ketamine on potassium- and ischemia-induced spreading depolarizations in the gyrencephalic swine brain (5)
    Details
    UID:
    (DE-627)1821596137
    Format: 14
    ISSN: 1873-7064
    Content: Spreading depolarizations (SDs) are characterized by near-complete breakdown of the transmembrane ion gradients, cytotoxic edema, and glutamate release. SDs are associated with poor neurological outcomes in cerebrovascular diseases and brain trauma. Ketamine, a N-methyl-d-aspartate receptor antagonist, has shown to inhibit SDs in animal models and in humans. However, little is known about its SD-inhibitory effect during long-term administration. Lissencephalic animal models have shown that ketamine loses its SD-blocking effect after some minutes to hours. Physio-anatomical differences between lissencephalic and the more evolved gyrencephalic animals may affect their SDs-blocking effect. Therefore, information from the last may have more translational potential. Therefore, the aim of this study was to investigate the 18 h-effect of s-ketamine as a basis for its possible long-term clinical use for neuroprotection. For this purpose, two gyrencephalic swine brain models were used. In one, SDs were elicited through topical application of KCl; in the other model, SDs were spontaneously induced after occlusion of the middle cerebral artery. S-ketamine was administered at therapeutic human doses, 2, 4 and 5 mg/kg BW/h for up to 18 h. Our findings indicate that s-ketamine significantly reduces SD incidence and expansion without clear evidence of loss of its efficacy. Pharmacological susceptibility of SDs to s-ketamine in both the ischemic gyrencephalic brain and well-perfused brain was observed. SDs were most potently inhibited by s-ketamine doses that are above the clinically recommended (4 mg/kg BW/h and 5 mg/kg BW/h). Nonetheless, such doses are given by neurointensivists in individual cases. Our results give momentum to further investigate the feasibility of a multicenter, neuromonitoring-guided, proof-of-concept clinical trial.
    Note: Gesehen am 10.11.2022
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 216(2022), Artikel-ID 109176, Seite 1-14, 1873-7064
    In: volume:216
    In: year:2022
    In: elocationid:109176
    In: pages:1-14
    In: extent:14
    Language: English
    DOI: 10.1016/j.neuropharm.2022.109176
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Online Access
    Open Access Request
    BSZ
    GBV
  • 10
    Online Resource
    Online Resource
    Enhanced anandamide signaling reduces flight behavior elicited by an approaching robo-beetle (7)
    Details
    UID:
    (DE-627)1572202718
    Format: 9
    ISSN: 1873-7064
    Content: Our current knowledge of the implications of endocannabinoids in fear and anxiety is largely based on fear conditioning paradigms and approach-avoidance conflicts. Here we establish the ethobehavioral beetle mania task (BMT), which confronts mice with an erratically moving robo-beetle. With the help of this task we demonstrate decreased tolerance yet increased avoidance responses to an approaching beetle in high-anxiety behavior (HAB) and BALBc mice compared to C57BL/6N, CD1 and normal-anxiety behavior (NAB) mice. Also DBA/2N mice showed decreased passive and increased active behavior, but followed the robo-beetle more often than HAB and BALBc mice. Treatment with diazepam (1 mg/kg) increased tolerance without affecting avoidance behavior in HAB mice. Treatment with the MAGL inhibitor JZL184 (8 mg/kg) increased flight behavior, but did not affect tolerance. The FAAH inhibitor URB597 (0.3 mg/kg), however, reduced flight behavior and enhanced tolerance to the robo-beetle. The latter effects were blocked by co-treatment with the CB1 receptor antagonist SR141716A (3 mg/kg), which failed to affect the behavior by itself. Taken together, we validate the BMT as a novel test for studying endocannabinoids beyond traditional paradigms and for assessing active fear responses in mice. Furthermore, we demonstrate panicolytic consequences of pharmacological enhancement of anandamide, but not 2-AG signaling.
    Note: Gesehen am 20.04.2018
    In: Neuropharmacology, Amsterdam [u.a.] : Elsevier Science, 1970, 126(2017), Seite 233-241, 1873-7064
    In: volume:126
    In: year:2017
    In: pages:233-241
    In: extent:9
    Language: English
    DOI: 10.1016/j.neuropharm.2017.09.010
    URL: Volltext  (kostenfrei registrierungspflichtig)
    URL: Volltext  (kostenfrei registrierungspflichtig)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Fulltext
    Fulltext
    BSZ
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages