Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Jon Sinclair is active.

Publication


Featured researches published by Jon Sinclair.


Neurochemistry International | 2000

Astroglia and glutamate in physiology and pathology: aspects on glutamate transport, glutamate-induced cell swelling and gap-junction communication

Elisabeth Hansson; Håkan Muyderman; Julia Leonova; Louise Allansson; Jon Sinclair; Fredrik Blomstrand; Thorleif Thorlin; Michael Nilsson; Lars Rönnbäck

Astroglia have the capacity to monitor extracellular glutamate (Glu) and maintain it at low levels, metabolize Glu, or release it back into the extracellular space. Glu can induce an increase in astroglial cell volume with a resulting decrease of the extracellular space, and thereby alter the concentration of extracellular substances. Many lines of evidence show that K(+) can be buffered within the astroglial gap-junction-coupled network, and recent results show that gap junctions are permeable for Glu. All these events occur dynamically: the astroglial network has the capacity to interfere actively with neurotransmission, thereby contributing to a high signal-to-noise ratio for the Glu transmission. High-quality neuronal messages during normal physiology can then be maintained. With the same mechanisms, astroglia might exert a neuroprotective function in situations of moderately increased extracellular Glu concentrations, i.e., corresponding to conditions of pathological hyper-excitability, or corresponding to early stages of an acute brain injury. If the astroglial functions are failing, neuronal dysfunction can be reinforced.


Neurochemistry International | 2001

Activation of β-adrenoceptors opens calcium-activated potassium channels in astroglial cells

Håkan Muyderman; Jon Sinclair; Kent E. Jardemark; Elisabeth Hansson; Michael Nilsson

In the present study, effects of the alpha(2)- and beta-adrenoceptor agonists clonidine and isoproterenol on astrocytes in astroglial/neuronal cocultures from rat cerebral cortex were evaluated. The calcium- and potassium-sensitive dyes fura-2 and potassium-binding benzofuran isophtalate (PBFI) were used to study alterations in intracellular concentrations of calcium ([Ca(2+)](i)) and potassium ([K(+)](i)), respectively, while the perforated patch clamp technique was used to analyze transmembrane currents. Exposure to isoproterenol or clonidine elicited an immediate increase in [Ca(2+)](i) that was totally abolished in calcium-free extracellular media. Isoproterenol also decreased [K(+)](i), but clonidine did not. The reduction in [K(+)](i) was inhibited in Ca(2+)-free media. As evaluated with the perforated patch technique, isoproterenol (10(-6)-10(-4) M) induced a slowly developing and long lasting outward current that also was totally abolished in calcium-free buffer. This current was blocked by external tetraethylammonium (TEA, 10 mM) and charybdotoxin (ChTX, 10 nM), but was not affected by apamin (50 nM). The current-to-voltage (I-V) relationships for the isoproterenol-induced currents showed a markedly negative reversal potential, -96 mV+/-7, (mean+/-S.D., n=5). These results suggest that the stimulation of astroglial beta-adrenoceptors by isoproterenol opens calcium-activated potassium channels (K((Ca))). Preincubation with forskolin significantly increased the isoproterenol-induced currents compared with controls, indicating that the opening of astroglial K((Ca)) channels after beta-adrenergic stimulation not only depends on [Ca(2+)](i) but also synergistically involves the cAMP transduction system to which beta-adrenoceptors are known to be positively coupled.


PLOS ONE | 2016

The Role of Reactive Oxygen Species in β-Adrenergic Signaling in Cardiomyocytes from Mice with the Metabolic Syndrome

Monica Llano-Diez; Jon Sinclair; Takashi Yamada; Mei Zong; Jérémy Fauconnier; Shi-Jin Zhang; Abram Katz; Kent Jardemark; Håkan Westerblad; Daniel C. Andersson; Johanna T. Lanner

The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice). We hypothesized that cardiomyocytes of mice with the metabolic syndrome would experience excessive ROS levels that trigger cellular dysfunctions. Fluorescent dyes and confocal microscopy were used to assess mitochondrial ROS production, cellular Ca2+ handling and contractile function in freshly isolated adult cardiomyocytes. Immunofluorescence, western blot and enzyme assay were used to study protein biochemistry. Unexpectedly, our results point towards decreased cardiac ROS signaling in a stable, chronic phase of the metabolic syndrome because: β-adrenergic-induced increases in the amplitude of intracellular Ca2+ signals were insensitive to antioxidant treatment; mitochondrial ROS production showed decreased basal rate and smaller response to β-adrenergic stimulation. Moreover, control hearts and hearts with the metabolic syndrome showed similar basal levels of ROS-mediated protein modification, but only control hearts showed increases after β-adrenergic stimulation. In conclusion, in contrast to the situation in control hearts, the cardiomyocyte response to acute β-adrenergic stimulation does not involve increased mitochondrial ROS production in a stable, chronic phase of the metabolic syndrome. This can be seen as a beneficial adaptation to prevent excessive ROS levels.


Analytical Chemistry | 2005

Microfluidic gradient-generating device for pharmacological profiling

Johan Pihl; Jon Sinclair; Eskil Sahlin; Mattias Karlsson; Fredrik Petterson; Jessica Olofsson; Owe Orwar


Archive | 2003

Systems and methods for rapidly changing the solution environment around sensors

Owe Orwar; Daniel Chiu; Johan Pihl; Jon Sinclair; Jessica Olofsson; Matthias Karlsson; Kent Jardemark


Analytical Chemistry | 2002

A Cell-Based Bar Code Reader for High-Throughput Screening of Ion Channel−Ligand Interactions

Jon Sinclair; Johan Pihl; Jessica Olofsson; Mattias Karlsson; Kent Jardemark; Daniel T. Chiu; Owe Orwar


Journal of the American Chemical Society | 2003

Nanotube-vesicle networks with functionalized membranes and interiors

Max Davidson; Mattias Karlsson; Jon Sinclair; Kristin Sott; Owe Orwar


Proceedings of the National Academy of Sciences of the United States of America | 2005

A chemical waveform synthesizer

Jessica Olofsson; Helen Bridle; Jon Sinclair; Daniel Granfeldt; Eskil Sahlin; Owe Orwar


Analytical Chemistry | 2004

A Microfluidics Approach to the Problem of Creating Separate Solution Environments Accessible from Macroscopic Volumes

Jessica Olofsson; Johan Pihl; Jon Sinclair; Eskil Sahlin; Mattias Karlsson; Owe Orwar


Archive | 2003

System and method for obtaining and maintaining high-resistance seals in patch clamp recordings

Mattias Karlsson; Owe Orwar; Daniel T. Chiu; Jon Sinclair; Kent Jardemark; Jessica Olofsson; Johan Pihl; Cecilia Farre

Collaboration


Dive into the Jon Sinclair's collaboration.

Top Co-Authors

Avatar

Owe Orwar

University of Gothenburg

View shared research outputs
Top Co-Authors

Avatar

Jessica Olofsson

Chalmers University of Technology

View shared research outputs
Top Co-Authors

Avatar

Kent Jardemark

University of Gothenburg

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Cecilia Farre

University of Gothenburg

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Eskil Sahlin

New Mexico State University

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Maria Millingen

Chalmers University of Technology

View shared research outputs
Researchain Logo
Decentralizing Knowledge