| 6351. |
- Bjursten, Lars Magnus, et al.
(författare)
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Behavioural repertory of cats without cerebral cortex from infancy
- 1976
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Ingår i: Experimental Brain Research. - 0014-4819. ; 25:2, s. 115-130
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Tidskriftsartikel (refereegranskat)abstract
- Bilateral removal of the cerebral cortex was made in cats neonatally. Spontaneous and imposed behaviour was studied while they were growing up and after they had become adult. Special emphasis was put on the utilization of visual cues and on learning. The cats ate, drank and groomed themselves adequately. Adequate maternal and female sexual behaviour was observed. They utilized the visual and haptic senses with respect to external space. Two cats were trained to perform visual discrimination if a T-maze. The adequacy of the behaviour of these cats is compared to that of animals with similar lesions made at maturity.
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| 6352. |
- Bjurstrom, M. F., et al.
(författare)
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Cerebrospinal Fluid Cytokines and Neurotrophic Factors in Human Chronic Pain Populations : A Comprehensive Review
- 2016
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Ingår i: Pain Pract. ; 16:2, s. 183-203
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Tidskriftsartikel (refereegranskat)abstract
- Chronic pain is a prevalent and debilitating condition, conveying immense human burden. Suffering is caused not only by painful symptoms, but also through psychopathological and detrimental physical consequences, generating enormous societal costs. The current treatment armamentarium often fails to achieve satisfying pain relief; thus, research directed toward elucidating the complex pathophysiological mechanisms underlying chronic pain syndromes is imperative. Central neuroimmune activation and neuroinflammation have emerged as driving forces in the transition from acute to chronic pain, leading to central sensitization and decreased opioid efficacy, through processes in which glia have been highlighted as key contributors. Under normal conditions, glia exert a protective role, but in different pathological states, a deleterious role is evident--directly and indirectly modulating and enhancing pain transmission properties of neurons, and shaping synaptic plasticity in a dysfunctional manner. Cytokines and neurotrophic factors have been identified as pivotal mediators involved in neuroimmune activation pathways and cascades in various preclinical chronic pain models. Research confirming these findings in humans has so far been scarce, but this comprehensive review provides coherent data supporting the clear association of a mechanistic role of altered central cytokines and neurotrophic factors in a number of chronic pain states despite varying etiologies. Given the importance of these factors in neuropathic and inflammatory chronic pain states, prospective therapeutic strategies, and directions for future research in this emerging field, are outlined.
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| 6353. |
- Bjurstrom, M. F., et al.
(författare)
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Quantitative validation of sensory mapping in persistent postherniorrhaphy inguinal pain patients undergoing triple neurectomy
- 2017
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Ingår i: Hernia. ; 21:2, s. 207-214
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Neurectomy of the inguinal nerves may be considered for selected refractory cases of chronic postherniorrhaphy inguinal pain (CPIP). There is to date a paucity of easily applicable clinical tools to identify neuropathic pain and examine the neurosensory effects of remedial surgery. The present quantitative sensory testing (QST) pilot study evaluates a sensory mapping technique. METHODS: Longitudinal (preoperative, immediate postoperative, and late postoperative) dermatomal sensory mapping and a comprehensive QST protocol were conducted in CPIP patients with unilateral, predominantly neuropathic inguinodynia presenting for triple neurectomy (n = 13). QST was conducted in four areas on the affected, painful side and in one contralateral comparison site. QST variables were compared according to sensory mapping outcomes: (o)/normal sensation, (+)/pain, and (-)/numbness. Diagnostic ability of the sensory mapping outcomes to detect QST-assessed allodynia or hypoesthesia was estimated through calculation of specificity and sensitivity values. RESULTS: Preoperatively, patients exhibited mechanical hypoesthesia and allodynia and pressure allodynia and hyperalgesia in painful areas mapped (+) (p < .05); sensory mapping outcome (+) demonstrated high ability to detect mechanical allodynia [sensitivity 0.74 (95% CI 0.61-0.86), specificity 0.94 (0.84-1.00)] and pressure allodynia [sensitivity 0.96 (0.89-1.00), specificity 1.00 (1.00-1.00)], but not thermal allodynia. Postoperatively, mapped areas of numbness (-) were associated with mechanical and thermal hypoesthesia (p < .05); (-) showed high sensitivity and specificity to detect mechanical and cold hypoesthesia. CONCLUSIONS: Sensory mapping provides an accurate clinical neuropathic assessment with strong correlation to QST findings of preoperative mechanical and pressure allodynia, and postoperative mechanical and thermal hypoesthesia in CPIP patients undergoing neurectomy.
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| 6354. |
- Bjurstrom, M. F., et al.
(författare)
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Reciprocal Relationship Between Sleep Macrostructure and Evening and Morning Cellular Inflammation in Rheumatoid Arthritis
- 2017
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Ingår i: Psychosom Med. ; 79:1, s. 24-33
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: This study examined the reciprocal associations between sleep macrostructure and levels of cellular inflammation in rheumatoid arthritis (RA) patients and controls. METHODS: RA patients (n = 24) and matched controls (n = 48) underwent all-night polysomnography, along with assessment of spontaneous- and Toll-like receptor-4-stimulated monocytic production of tumor necrosis factor alpha (TNF) and interleukin (IL)-6 at 11:00 PM and 8:00 AM. RESULTS: As compared with controls, RA patients showed lower levels of sleep efficiency (mean [standard deviation], 88.1 [6.1] versus 83.8 [7.0]), a higher percentage stage 3 sleep (9.3 [6.4] versus 13.1 [6.9]), and higher levels of percentage of monocytes either spontaneously expressing TNF at 11:00 PM (log transformed, 1.07 [0.28] versus 1.22 [0.17]), and higher Toll-like receptor-4-stimulated production of IL6 at 8:00 AM (log transformed, 3.45 [0.80] versus 3.83 [0.39]). Higher levels of stimulated production of TNF at 11:00 PM were associated with higher sleep efficiency (0.74). In turn, sleep efficiency had a countervailing relationship on TNF production at 8:00 AM (-0.64). Higher levels of spontaneous and stimulated production of IL6 at 11:00 PM were associated with more stage 3 (0.39), stage 4 (0.43), and slow-wave sleep (0.49), with evidence that stage 4 had a countervailing relationship on IL6 production at 8:00 AM (-0.60). CONCLUSIONS: RA patients show evidence of sleep fragmentation, greater sleep depth, and higher levels of cellular inflammation. Sleep maintenance and sleep depth show countervailing relationships with evening and morning levels of monocytic production of TNF and IL-6, respectively, which support the hypothesis of a feedback loop between sleep maintenance, slow-wave sleep, and cellular inflammation that is cytokine specific.
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| 6355. |
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| 6356. |
- Björefeldt, Andreas, 1982, et al.
(författare)
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Efficient opto- and chemogenetic control in a single molecule driven by FRET-modified bioluminescence
- 2024
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Ingår i: NEUROPHOTONICS. - 2329-423X .- 2329-4248. ; 11:2
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Tidskriftsartikel (refereegranskat)abstract
- Significance Bioluminescent optogenetics (BL-OG) offers a unique and powerful approach to manipulate neural activity both opto- and chemogenetically using a single actuator molecule (a LuMinOpsin, LMO). Aim To further enhance the utility of BL-OG by improving the efficacy of chemogenetic (bioluminescence-driven) LMO activation. Approach We developed novel luciferases optimized for F & ouml;rster resonance energy transfer when fused to the fluorescent protein mNeonGreen, generating bright bioluminescent (BL) emitters spectrally tuned to Volvox Channelrhodopsin 1 (VChR1). Results A new LMO generated from this approach (LMO7) showed significantly stronger BL-driven opsin activation compared to previous and other new variants. We extensively benchmarked LMO7 against LMO3 (current standard) and found significantly stronger neuronal activity modulation ex vivo and in vivo, and efficient modulation of behavior. Conclusions We report a robust new option for achieving multiple modes of control in a single actuator and a promising engineering strategy for continued improvement of BL-OG.
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| 6357. |
- Björefeldt, Andreas, 1982, et al.
(författare)
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Human cerebrospinal fluid increases the excitability of pyramidal neurons in the in vitro brain slice.
- 2015
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Ingår i: The Journal of physiology. - : Wiley. - 1469-7793 .- 0022-3751. ; 593:1, s. 231-43
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Tidskriftsartikel (refereegranskat)abstract
- The cerebrospinal fluid contains numerous neuromodulators at ambient levels but whether, and how, they affect the activity of central neurons is unknown. This study provides experimental evidence that human cerebrospinal fluid (hCSF) increases the excitability of hippocampal and neocortical pyramidal neurons. Hippocampal CA1 pyramidal neurons in hCSF displayed lowered firing thresholds, depolarized resting membrane potentials and reduced input resistance, mimicking properties of pyramidal neurons recorded in vivo. The excitability-increasing effect of hCSF on CA1 pyramidal neurons was entirely occluded by intracellular application of GTPγS, suggesting that neuromodulatory effects were mediated by G-protein coupled receptors. These results indicate that the CSF promotes spontaneous excitatory neuronal activity, and may help to explain observed differences in the activity of pyramidal neurons recorded in vivo and in vitro.
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| 6358. |
- Björefeldt, Andreas, 1982, et al.
(författare)
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Neuromodulation of fast-spiking and non-fast-spiking hippocampal CA1 interneurons by human cerebrospinal fluid.
- 2016
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Ingår i: The Journal of physiology. - 1469-7793. ; 594:4, s. 937-52
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Tidskriftsartikel (refereegranskat)abstract
- GABAergic interneurons intricately regulate the activity of hippocampal and neocortical networks. Their function in vivo is likely to be tuned by neuromodulatory substances in brain extracellular fluid. However, in vitro investigations of GABAergic interneuron function do not account for such effects, as neurons are kept in artificial extracellular fluid. To examine the neuromodulatory influence of brain extracellular fluid on GABAergic activity, we recorded from fast-spiking and non-fast-spiking CA1 interneurons, as well as from pyramidal cells, in the presence of human cerebrospinal fluid (hCSF), using a matched artificial cerebrospinal (aCSF) fluid as control. We found that hCSF increased the frequency of spontaneous firing more than twofold in the two groups of interneurons, and more than fourfold in CA1 pyramidal cells. hCSF did not affect the resting membrane potential of CA1 interneurons but caused depolarization in pyramidal cells. The increased excitability of interneurons and pyramidal cells was accompanied by reductions in afterhyperpolarization amplitudes and a left-shift in the frequency-current relationships. Our results suggest that ambient concentrations of neuromodulators in the brain extracellular fluid powerfully influence the excitability of neuronal networks. This article is protected by copyright. All rights reserved.
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| 6359. |
- Björefeldt, Andreas, 1982, et al.
(författare)
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Neuromodulation via the Cerebrospinal Fluid: Insights from Recent in Vitro Studies.
- 2018
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Ingår i: Frontiers in neural circuits. - : Frontiers Media SA. - 1662-5110. ; 12
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Tidskriftsartikel (refereegranskat)abstract
- The cerebrospinal fluid (CSF) occupies the brain's ventricles and subarachnoid space and, together with the interstitial fluid (ISF), forms a continuous fluidic network that bathes all cells of the central nervous system (CNS). As such, the CSF is well positioned to actively distribute neuromodulators to neural circuitsin vivovia volume transmission. Recentin vitroexperimental work in brain slices and neuronal cultures has shown that human CSF indeed contains neuromodulators that strongly influence neuronal activity. Here we briefly summarize these new findings and discuss their potential relevance to neural circuits in health and disease.
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| 6360. |
- Björk, Karl, et al.
(författare)
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Ethanol-induced activation of AKT and DARPP-32 in the mouse striatum mediated by opioid receptors
- 2010
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Ingår i: Addiction Biology. - : Wiley-Blackwell. - 1355-6215 .- 1369-1600. ; 15:3, s. 299-303
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Tidskriftsartikel (refereegranskat)abstract
- The reinforcing properties of ethanol are in part attributed to interactions between opioid and dopaminergic signaling pathways, but intracellular mediators of such interactions are poorly understood. Here we report that an acute ethanol challenge induces a robust phosphorylation of two key signal transduction kinases, AKT and DARPP-32, in the striatum of mice. Ethanol-induced AKT phosphorylation was blocked by the opioid receptor antagonist naltrexone but unaffected by blockade of dopamine D2 receptors via sulpiride. In contrast, DARPP-32 phosphorylation was abolished by both antagonists. These data suggest that ethanol acts via two distinct but potentially synergistic striatal signaling cascades. One of these is D2-dependent, while the other is not. These findings illustrate that pharmacology of ethanol reward is likely more complex than that for other addictive drugs.
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