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1. Orexins/hypocretins control bistability of hippocampal long-term synaptic plasticity through co-activation of multiple kinases

Author

N. Doreulee, Helmut L. Haas, Oliver Selbach, Olga A. Sergeeva, C. Bohla, Krister S. Eriksson, and A. Barbara

Subjects
Male, Aging, Physiology, Long-Term Potentiation, Hippocampus, Neurotransmission, Biology, Synaptic Transmission, Mice, Slice preparation, Ca2+/calmodulin-dependent protein kinase, Animals, Long-term depression, Neurotransmitter Agents, Orexins, Neuronal Plasticity, Long-Term Synaptic Depression, Neuropeptides, Phosphotransferases, Intracellular Signaling Peptides and Proteins, Brain, Long-term potentiation, Synaptic Potentials, Enzyme Activation, Mice, Inbred C57BL, nervous system, Trk receptor, Synapses, Synaptic plasticity, Neuroscience
Abstract

Aim: Orexins/hypocretins (OX/Hcrt) are hypothalamic neuropeptides linking sleep-wakefulness, appetite and neuroendocrine control. Their role and mechanisms of action on higher brain functions, such as learning and memory, are not clear. Methods: We used field recordings of excitatory post-synaptic potentials (fEPSP) in acute mouse brain slice preparations to study the effects of orexins and pharmacological inhibitors of multiple kinases on long-term synaptic plasticity in the hippocampus. Results: Orexin-A (OX-A) but not orexin-B (OX-B) induces a state-dependent long-term potentiation of synaptic transmission (LTP OX ) at Schaffer collateral-CA1 synapses in hippocampal slices from adult (8- to 12-week-old) mice. In contrast, OX-A applied to slices from juvenile (3- to 4-week-old) animals causes a long-term depression (LTD OX ) in the same pathway. LTP OX is blocked by pharmacological inhibition of orexin receptor-1 (OX1R) and plasticity-related kinases, including serine/threonine- (CaMKII, PKC, PKA, MAPK), lipid- (PI3K), and receptor tyrosine kinases (Trk). Inhibition of OX1R, CaMKII, PKC, PKA and Trk unmasks LTD OX in adult animals. Conclusion: Orexins control not only the bistability of arousal states and threshold for appetitive behaviours but, in an age- and kinase-dependent manner, also bidirectional long-term synaptic plasticity in the hippocampus, providing a possible link between behavioural state and memory functions.

Published
2010
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2. Orexins/hypocretins cause sharp wave- and theta-related synaptic plasticity in the hippocampus via glutamatergic, gabaergic, noradrenergic, and cholinergic signaling

Author

Olga A. Sergeeva, Oliver Selbach, Krister S. Eriksson, Helmut L. Haas, Ritchie E. Brown, W. Poelchen, N. Doreulee, and C. Bohla

Subjects
Male, Receptors, Neuropeptide, Long-Term Potentiation, Presynaptic Terminals, Hippocampus, Action Potentials, Glutamic Acid, Neurotransmission, In Vitro Techniques, Synaptic Transmission, Receptors, G-Protein-Coupled, Glutamatergic, Mice, Norepinephrine, Orexin Receptors, Metaplasticity, Neural Pathways, medicine, Animals, Theta Rhythm, Long-term depression, gamma-Aminobutyric Acid, Neurotransmitter Agents, Orexins, Neuronal Plasticity, Chemistry, General Neuroscience, Neuropeptides, Intracellular Signaling Peptides and Proteins, Long-term potentiation, Acetylcholine, Receptors, Neurotransmitter, Mice, Inbred C57BL, medicine.anatomical_structure, nervous system, Schaffer collateral, Synaptic plasticity, Carrier Proteins, Neuroscience
Abstract

Orexins (OX), also called hypocretins, are bioactive peptides secreted from glucose-sensitive neurons in the lateral hypothalamus linking appetite, arousal and neuroendocrine-autonomic control. Here, OX-A was found to cause a slow-onset long-term potentiation of synaptic transmission (LTPOX) in the hippocampus of young adult mice. LTPOX was induced at Schaffer collateral-CA1 but not mossy fiber-CA3 synapses, and required transient sharp wave-concurrent population field-burst activity generated by the autoassociative CA3 network. Exogenous long θ-frequency stimulation of Schaffer collateral axons erased LTPOX in intact hippocampal slices but not mini slices devoid of the CA3 region. Pharmacological analysis revealed that LTPOX requires co-activation of ionotropic and metabotropic glutamatergic, GABAergic, as well as noradrenergic and cholinergic receptors. Together these data indicate that OX-A induces a state-dependent metaplasticity in the CA1 region associated with sharp-wave and θ rhythm activity as well as glutamatergic, GABAergic, aminergic, and cholinergic transmission. Thus, orexins not only regulate arousal threshold and body weight but also threshold and weight of synaptic connectivity, providing a molecular prerequisite for homeostatic and behavioral state-dependent control of neuronal plasticity and presumably memory functions.

Published
2003

3. Orexins/hypocretins control bistability of hippocampal long-term synaptic plasticity through co-activation of multiple kinases.

Author

Selbach O, Bohla C, Barbara A, Doreulee N, Eriksson KS, Sergeeva OA, and Haas HL

Subjects
Aging physiology, Animals, Brain drug effects, Brain physiology, Enzyme Activation physiology, Intracellular Signaling Peptides and Proteins pharmacology, Long-Term Potentiation, Long-Term Synaptic Depression, Male, Mice, Mice, Inbred C57BL, Neuronal Plasticity drug effects, Neuropeptides pharmacology, Orexins, Synaptic Potentials drug effects, Synaptic Transmission drug effects, Hippocampus physiology, Intracellular Signaling Peptides and Proteins metabolism, Neuronal Plasticity physiology, Neuropeptides metabolism, Neurotransmitter Agents metabolism, Phosphotransferases metabolism, Synapses physiology
Abstract

Aim: Orexins/hypocretins (OX/Hcrt) are hypothalamic neuropeptides linking sleep-wakefulness, appetite and neuroendocrine control. Their role and mechanisms of action on higher brain functions, such as learning and memory, are not clear., Methods: We used field recordings of excitatory post-synaptic potentials (fEPSP) in acute mouse brain slice preparations to study the effects of orexins and pharmacological inhibitors of multiple kinases on long-term synaptic plasticity in the hippocampus., Results: Orexin-A (OX-A) but not orexin-B (OX-B) induces a state-dependent long-term potentiation of synaptic transmission (LTP(OX)) at Schaffer collateral-CA1 synapses in hippocampal slices from adult (8- to 12-week-old) mice. In contrast, OX-A applied to slices from juvenile (3- to 4-week-old) animals causes a long-term depression (LTD(OX)) in the same pathway. LTP(OX) is blocked by pharmacological inhibition of orexin receptor-1 (OX1R) and plasticity-related kinases, including serine/threonine- (CaMKII, PKC, PKA, MAPK), lipid- (PI3K), and receptor tyrosine kinases (Trk). Inhibition of OX1R, CaMKII, PKC, PKA and Trk unmasks LTD(OX) in adult animals., Conclusion: Orexins control not only the bistability of arousal states and threshold for appetitive behaviours but, in an age- and kinase-dependent manner, also bidirectional long-term synaptic plasticity in the hippocampus, providing a possible link between behavioural state and memory functions.

Published
2010
Full Text
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4. Orexins/hypocretins cause sharp wave- and theta-related synaptic plasticity in the hippocampus via glutamatergic, gabaergic, noradrenergic, and cholinergic signaling.

Author

Selbach O, Doreulee N, Bohla C, Eriksson KS, Sergeeva OA, Poelchen W, Brown RE, and Haas HL

Subjects
Acetylcholine metabolism, Action Potentials drug effects, Action Potentials physiology, Animals, Carrier Proteins pharmacology, Glutamic Acid metabolism, Hippocampus cytology, In Vitro Techniques, Long-Term Potentiation drug effects, Long-Term Potentiation physiology, Male, Mice, Mice, Inbred C57BL, Neural Pathways cytology, Neural Pathways drug effects, Neural Pathways metabolism, Neuronal Plasticity drug effects, Neuropeptides pharmacology, Norepinephrine metabolism, Orexin Receptors, Orexins, Presynaptic Terminals drug effects, Presynaptic Terminals metabolism, Receptors, G-Protein-Coupled, Receptors, Neuropeptide, Receptors, Neurotransmitter drug effects, Receptors, Neurotransmitter metabolism, Synaptic Transmission drug effects, gamma-Aminobutyric Acid metabolism, Carrier Proteins metabolism, Hippocampus metabolism, Intracellular Signaling Peptides and Proteins, Neuronal Plasticity physiology, Neuropeptides metabolism, Neurotransmitter Agents metabolism, Synaptic Transmission physiology, Theta Rhythm drug effects
Abstract

Orexins (OX), also called hypocretins, are bioactive peptides secreted from glucose-sensitive neurons in the lateral hypothalamus linking appetite, arousal and neuroendocrine-autonomic control. Here, OX-A was found to cause a slow-onset long-term potentiation of synaptic transmission (LTPOX) in the hippocampus of young adult mice. LTPOX was induced at Schaffer collateral-CA1 but not mossy fiber-CA3 synapses, and required transient sharp wave-concurrent population field-burst activity generated by the autoassociative CA3 network. Exogenous long theta-frequency stimulation of Schaffer collateral axons erased LTPOX in intact hippocampal slices but not mini slices devoid of the CA3 region. Pharmacological analysis revealed that LTPOX requires co-activation of ionotropic and metabotropic glutamatergic, GABAergic, as well as noradrenergic and cholinergic receptors. Together these data indicate that OX-A induces a state-dependent metaplasticity in the CA1 region associated with sharp-wave and theta rhythm activity as well as glutamatergic, GABAergic, aminergic, and cholinergic transmission. Thus, orexins not only regulate arousal threshold and body weight but also threshold and weight of synaptic connectivity, providing a molecular prerequisite for homeostatic and behavioral state-dependent control of neuronal plasticity and presumably memory functions.

Published
2004
Full Text
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