TY  - JOUR
A1  - Wippert, Pia-Maria
A1  - Wiebking, C.
T1  - Adaptation to physical activity and mental stress in the context of pain. Psychobiological aspects
JF  - Der Schmerz : Organ der Deutschen Gesellschaft zum Studium des Schmerzes, der Österreichischen Schmerzgesellschaft und der Deutschen Interdisziplinären Vereinigung für Schmerztherapie
N2  - The genesis of chronic pain is predominantly explained by a multidimensional pain model approach that is based on the dysfunctional influence of biological, psychological and social variables as key risk factors inducing aberrant long-term changes. Biological facets comprise adaptation processes on the neuronal, musculoskeletal and (psycho) biological level that can be influenced by physical training or psychosocial factors, such as stress. These factors can play a causative role in developing dysfunctional adaptation mechanisms, which in turn prepare the biological ground to facilitate negative long-term changes in the peripheral and central nervous systems. Hence, these processes can be assumed to be fundamentally involved in the transition from acute to chronic and persistent pain. The aim of this review article is to discuss hypotheses for the genesis of chronic pain and possible treatment strategies. Selected research results about maladaptive processes in chronic pain due to psychological stress and physical activity are presented in order to inspire discussions about the ideal dose-response relationship of physical activity and the combination of different therapeutic concepts.
KW  - Chronic pain
KW  - Neuronal plasticity
KW  - Pain management
KW  - Central nervous system
KW  - Peripheral nervous system
Y1  - 2016
U6  - https://doi.org/10.1007/s00482-016-0147-0
SN  - 0932-433X
SN  - 1432-2129
VL  - 30
SP  - 429
EP  - 436
PB  - Springer
CY  - New York
ER  - 
TY  - JOUR
A1  - Blankenburg, Stefanie
A1  - Balfanz, Sabine
A1  - Hayashi, Y.
A1  - Shigenobu, S.
A1  - Miura, T.
A1  - Baumann, Otto
A1  - Baumann, Arnd
A1  - Blenau, Wolfgang
T1  - Cockroach GABA(B) receptor subtypes: Molecular characterization, pharmacological properties and tissue distribution
JF  - Neuropharmacology
N2  - gamma-aminobutyric acid (GABA) is the predominant inhibitory neurotransmitter in the central nervous system (CNS). Its effects are mediated by either ionotropic GABA(A) receptors or metabotropic GABA(B) receptors. GABA(B) receptors regulate, via Gi/o, G-proteins, ion channels, and adenylyl cyclases. In humans, GABA(B) receptor subtypes are involved in the etiology of neurologic and psychiatric disorders. In arthropods, however, these members of the G-protein-coupled receptor family are only inadequately characterized. Interestingly, physiological data have revealed important functions of GABA(B) receptors in the American cockroach, Periplaneta americana. We have cloned cDNAs coding for putative GABA(B) receptor subtypes 1 and 2 of P. americana (PeaGB1 and PeaGB2). When both receptor proteins are co-expressed in mammalian cells, activation of the receptor heteromer with GABA leads to a dose-dependent decrease in cAMP production. The pharmacological profile differs from that of mammalian and Drosophila GABA(B) receptors. Western blot analyses with polyclonal antibodies have revealed the expression of PeaGB1 and PeaGB2 in the CNS of the American cockroach. In addition to the widespread distribution in the brain, PeaGB1 is expressed in salivary glands and male accessory glands. Notably, PeaGB1-like immunoreactivity has been detected in the GABAergic salivary neuron 2, suggesting that GABA(B) receptors act as autoreceptors in this neuron.
KW  - GABA(B) receptor
KW  - G-protein-coupled receptor
KW  - Periplaneta americana
KW  - Central nervous system
KW  - Adenylyl cyclase
KW  - Salivary gland
Y1  - 2015
U6  - https://doi.org/10.1016/j.neuropharm.2014.08.022
SN  - 0028-3908
SN  - 1873-7064
VL  - 88
SP  - 134
EP  - 144
PB  - Elsevier
CY  - Oxford
ER  -