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Article ; Online: Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala.

Meis, Susanne / Endres, Thomas / Munsch, Thomas / Lessmann, Volkmar

International journal of molecular sciences

2019 Volume 20, Issue 17

Abstract: Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling ...

Abstract	Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABA
MeSH term(s)	Amygdala/metabolism ; Animals ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Female ; Long-Term Potentiation/genetics ; Long-Term Potentiation/physiology ; Mice ; Mice, Knockout ; Neuronal Plasticity/genetics ; Neuronal Plasticity/physiology ; Patch-Clamp Techniques ; Synaptic Transmission/genetics ; Synaptic Transmission/physiology ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Brain-Derived Neurotrophic Factor ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2019-09-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20174310
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Article ; Online: ProBDNF Dependence of LTD and Fear Extinction Learning in the Amygdala of Adult Mice.

Ma, Xiaoyun / Vuyyuru, Harish / Munsch, Thomas / Endres, Thomas / Lessmann, Volkmar / Meis, Susanne

Cerebral cortex (New York, N.Y. : 1991)

2021 Volume 32, Issue 7, Page(s) 1350–1364

Abstract: Neurotrophins are secreted proteins that control survival, differentiation, and synaptic plasticity. While mature neurotrophins regulate these functions via tyrosine kinase signaling (Trk), uncleaved pro-neurotrophins bind preferentially to the p75 ... ...

Abstract	Neurotrophins are secreted proteins that control survival, differentiation, and synaptic plasticity. While mature neurotrophins regulate these functions via tyrosine kinase signaling (Trk), uncleaved pro-neurotrophins bind preferentially to the p75 neurotrophin receptor (p75NTR) and often exert opposite effects to those of mature neurotrophins. In the amygdala, brain-derived neurotrophic factor (BDNF) enables long-term potentiation as well as fear and fear extinction learning. In the present study, we focused on the impact of mature BDNF and proBDNF signaling on long-term depression (LTD) in the lateral amygdala (LA). Hence, we conducted extracellular field potential recordings in an in vitro slice preparation and recorded LTD in cortical and thalamic afferents to the LA. LTD was unchanged by acute block of BDNF/TrkB signaling. In contrast, LTD was inhibited by blocking p75NTR signaling, by disinhibition of the proteolytic cleavage of proBDNF into mature BDNF, and by preincubation with a function-blocking anti-proBDNF antibody. Since LTD-like processes in the amygdala are supposed to be related to fear extinction learning, we locally inhibited p75NTR signaling in the amygdala during or after fear extinction training, resulting in impaired fear extinction memory. Overall, these results suggest that in the amygdala proBDNF/p75NTR signaling plays a pivotal role in LTD and fear extinction learning.
MeSH term(s)	Amygdala/metabolism ; Animals ; Extinction, Psychological/physiology ; Fear/physiology ; Learning/physiology ; Mice ; Neuronal Plasticity
Language	English
Publishing date	2021-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhab265
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Article ; Online: Periprosthetic hypoxia as consequence of TRPM7 mediated cobalt influx in osteoblasts.

Römmelt, Constantin / Munsch, Thomas / Drynda, Andreas / Lessmann, Volkmar / Lohmann, Christoph H / Bertrand, Jessica

Journal of biomedical materials research. Part B, Applied biomaterials

2018 Volume 107, Issue 6, Page(s) 1806–1813

Abstract: The reasons for the high number of loosened metal-on-metal (MoM) hip implants are still not fully understood. Hypoxia-inducible factor 1 (HIF-1) mediated signaling pathways, which normally modulate tissue metabolism under hypoxic circumstances, could be ... ...

Abstract	The reasons for the high number of loosened metal-on-metal (MoM) hip implants are still not fully understood. Hypoxia-inducible factor 1 (HIF-1) mediated signaling pathways, which normally modulate tissue metabolism under hypoxic circumstances, could be triggered by metallic wear debris and influence bone metabolism favoring osteolysis. This may lead to early loosening of the orthopedic implants. Immunhistochemical staining of periprosthetic tissues of failed artificial hip implants showed that the concentration of HIF-1α in the surrounding tissues of failed MoM hip implants was significantly higher in comparison to failed metal-on-polyethylene (MoP) hip implants and osteoarthritic tissues. Therefore, we examined the Co
MeSH term(s)	Cell Hypoxia ; Cell Line ; Cobalt/pharmacokinetics ; Gene Expression Regulation ; Hip Prosthesis ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis ; Metal-on-Metal Joint Prostheses ; Osteoblasts/metabolism ; Protein-Serine-Threonine Kinases/biosynthesis ; TRPM Cation Channels/biosynthesis
Chemical Substances	HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; TRPM Cation Channels ; Cobalt (3G0H8C9362) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; TRPM7 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2018-12-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2099992-6
ISSN	1552-4981 ; 1552-4973 ; 0021-9304
ISSN (online)	1552-4981
ISSN	1552-4973 ; 0021-9304
DOI	10.1002/jbm.b.34273
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Zs.A 6196: Show issues

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Article ; Online: Neuropeptide S-mediated facilitation of synaptic transmission enforces subthreshold theta oscillations within the lateral amygdala.

Meis, Susanne / Stork, Oliver / Munsch, Thomas

PloS one

2011 Volume 6, Issue 3, Page(s) e18020

Abstract: The neuropeptide S (NPS) receptor system modulates neuronal circuit activity in the amygdala in conjunction with fear, anxiety and the expression and extinction of previously acquired fear memories. Using in vitro brain slice preparations of transgenic ... ...

Abstract	The neuropeptide S (NPS) receptor system modulates neuronal circuit activity in the amygdala in conjunction with fear, anxiety and the expression and extinction of previously acquired fear memories. Using in vitro brain slice preparations of transgenic GAD67-GFP (Δneo) mice, we investigated the effects of NPS on neural activity in the lateral amygdala as a key region for the formation and extinction of fear memories. We are able to demonstrate that NPS augments excitatory glutamatergic synaptic input onto both projection neurons and interneurons of the lateral amygdala, resulting in enhanced spike activity of both types of cells. These effects were at least in part mediated by presynaptic mechanisms. In turn, inhibition of projection neurons by local interneurons was augmented by NPS, and subthreshold oscillations were strengthened, leading to their shift into the theta frequency range. These data suggest that the multifaceted effects of NPS on amygdaloid circuitry may shape behavior-related network activity patterns in the amygdala and reflect the peptide's potent activity in various forms of affective behavior and emotional memory.
MeSH term(s)	Action Potentials/drug effects ; Amygdala/drug effects ; Amygdala/physiology ; Animals ; Excitatory Postsynaptic Potentials/drug effects ; Glutamic Acid/metabolism ; In Vitro Techniques ; Interneurons/drug effects ; Interneurons/physiology ; Mice ; Neuropeptides/pharmacology ; Patch-Clamp Techniques ; Synaptic Transmission/drug effects
Chemical Substances	Neuropeptides ; Glutamic Acid (3KX376GY7L)
Language	English
Publishing date	2011-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0018020
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Article ; Online: Prominent Postsynaptic and Dendritic Exocytosis of Endogenous BDNF Vesicles in BDNF-GFP Knock-in Mice.

Leschik, Julia / Eckenstaler, Robert / Endres, Thomas / Munsch, Thomas / Edelmann, Elke / Richter, Karin / Kobler, Oliver / Fischer, Klaus-Dieter / Zuschratter, Werner / Brigadski, Tanja / Lutz, Beat / Lessmann, Volkmar

Molecular neurobiology

2019 Volume 56, Issue 10, Page(s) 6833–6855

Abstract: Brain-derived neurotrophic factor (BDNF) is a secreted messenger molecule that is crucial for neuronal function and induction of synaptic plasticity. Although altered availability of BDNF underlies many neurological deficits and neurodegenerative ... ...

Abstract	Brain-derived neurotrophic factor (BDNF) is a secreted messenger molecule that is crucial for neuronal function and induction of synaptic plasticity. Although altered availability of BDNF underlies many neurological deficits and neurodegenerative disorders, secretion dynamics of endogenous BDNF are unexplored. We generated a BDNF-GFP knock-in (KiBE) mouse, in which GFP-labeled BDNF is expressed under the control of the unaltered endogenous mouse BDNF gene regulatory elements. This KiBE mouse model enables for the first time live cell imaging analysis of endogenous BDNF dynamics. We show that BDNF-GFP release and biological activity in vivo are unaffected by the GFP tag, since homozygous KiBE mice, which lack wild-type BDNF, are healthy and have a normal life expectancy. STED superresolution microscopy shows that 70% of BDNF-GFP vesicles in KiBE mouse neurites are localized in dendrites, being typically 200 nm away from synaptic release sites. Live cell imaging in hippocampal slices also reveals prominent targeting of endogenous BDNF-GFP vesicles to dendrites. Fusion pore opening and cargo release of dendritic BDNF vesicles start within 30 s after a strong depolarizing stimulus and continue for > 100 s thereafter, revealing an astonishingly delayed and prolonged release of endogenous BDNF.
MeSH term(s)	Animals ; Axons/metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Chromosomes, Mammalian/genetics ; Dendrites/metabolism ; Exocytosis ; Gene Knock-In Techniques ; Gene Targeting ; Genome ; Green Fluorescent Proteins/metabolism ; Hippocampus/metabolism ; Mice ; Synaptic Vesicles/metabolism
Chemical Substances	Brain-Derived Neurotrophic Factor ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2019-03-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-019-1551-0
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Zs.A 2411: Show issues

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Article ; Online: Dorsal tegmental dopamine neurons gate associative learning of fear.

Groessl, Florian / Munsch, Thomas / Meis, Susanne / Griessner, Johannes / Kaczanowska, Joanna / Pliota, Pinelopi / Kargl, Dominic / Badurek, Sylvia / Kraitsy, Klaus / Rassoulpour, Arash / Zuber, Johannes / Lessmann, Volkmar / Haubensak, Wulf

Nature neuroscience

2018 Volume 21, Issue 7, Page(s) 952–962

Abstract: Functional neuroanatomy of Pavlovian fear has identified neuronal circuits and synapses associating conditioned stimuli with aversive events. Hebbian plasticity within these networks requires additional reinforcement to store particularly salient ... ...

Abstract	Functional neuroanatomy of Pavlovian fear has identified neuronal circuits and synapses associating conditioned stimuli with aversive events. Hebbian plasticity within these networks requires additional reinforcement to store particularly salient experiences into long-term memory. Here we have identified a circuit that reciprocally connects the ventral periaqueductal gray and dorsal raphe region with the central amygdala and that gates fear learning. We found that ventral periaqueductal gray and dorsal raphe dopaminergic (vPdRD) neurons encode a positive prediction error in response to unpredicted shocks and may reshape intra-amygdala connectivity via a dopamine-dependent form of long-term potentiation. Negative feedback from the central amygdala to vPdRD neurons might limit reinforcement to events that have not been predicted. These findings add a new module to the midbrain dopaminergic circuit architecture underlying associative reinforcement learning and identify vPdRD neurons as a critical component of Pavlovian fear conditioning. We propose that dysregulation of vPdRD neuronal activity may contribute to fear-related psychiatric disorders.
MeSH term(s)	Animals ; Association Learning/physiology ; Behavior, Animal/physiology ; Conditioning, Classical/physiology ; Dopaminergic Neurons/physiology ; Fear/physiology ; Long-Term Potentiation/physiology ; Male ; Mice ; Neural Pathways/physiology ; Periaqueductal Gray/cytology ; Periaqueductal Gray/physiology ; Tegmentum Mesencephali/cytology ; Tegmentum Mesencephali/physiology
Language	English
Publishing date	2018-06-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-018-0174-5
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

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Article ; Online: Hyperpolarization-activated cation current contributes to spontaneous network activity in developing neocortical cultures.

Klueva, Julia / Lima, Ana D de / Meis, Susanne / Voigt, Thomas / Munsch, Thomas

Neuro-Signals

2012 Volume 20, Issue 1, Page(s) 35–47

Abstract: The mechanisms underlying spontaneous burst activity (SBA), appearing in networks of embryonic cortical neurons at the end of the first week in vitro, remain elusive. Here we investigated the contribution of the hyperpolarization-activated cation current ...

Abstract	The mechanisms underlying spontaneous burst activity (SBA), appearing in networks of embryonic cortical neurons at the end of the first week in vitro, remain elusive. Here we investigated the contribution of the hyperpolarization-activated cation current (I(h)) to SBA in cortical cultures of GAD67-GFP mice. I(h) current could be detected in GFP-positive large GABAergic interneurons (L-INs) and glutamatergic principal neurons (PNs) as early as DIV 5. Under current-clamp conditions, blockers of I(h) current, ZD7288 and Cs⁺, abolished the voltage sag and rebound depolarization. ZD7288 induced a hyperpolarization concomitant with an increase in the membrane input resistance in L-INs and PNs. Voltage-clamp recordings revealed I(h) as slowly activating inward current with a reversal potential close to -50 mV and a mid-activation point around -90 mV. Both, ZD7288 (1-10 μM) and Cs⁺ (1-2 mM) reduced SBA, spontaneous activity-driven Ca²⁺ transients, and frequency as well as amplitude of miniature GABAergic postsynaptic currents. Immunocytochemistry and Western blot demonstrated that HCN1 and HCN2 were the prevalent isoforms of HCN channels expressed in L-INs and PNs. These results suggest an important contribution of HCN channels to the maintenance of SBA in embryonic cortical cultures.
MeSH term(s)	Action Potentials/physiology ; Animals ; Animals, Newborn ; Cells, Cultured ; Cyclic Nucleotide-Gated Cation Channels/physiology ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Ion Channels/physiology ; Membrane Potentials/physiology ; Mice ; Mice, Inbred C57BL ; Neocortex/cytology ; Neocortex/embryology ; Neocortex/growth & development ; Nerve Net/cytology ; Nerve Net/embryology ; Nerve Net/growth & development ; Neural Conduction/physiology ; Potassium Channels/physiology ; Protein Isoforms/physiology
Chemical Substances	Cyclic Nucleotide-Gated Cation Channels ; Hcn1 protein, mouse ; Hcn2 protein, mouse ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Ion Channels ; Potassium Channels ; Protein Isoforms
Language	English
Publishing date	2012
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074039-6
ISSN	1424-8638 ; 1424-862X
ISSN (online)	1424-8638
ISSN	1424-862X
DOI	10.1159/000330813
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Zs.A 3503: Show issues

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Book ; Thesis: Elektrophysiologische Untersuchungen zur Wirkung von 5-Hydroxytryptamin an Neuronen im Zentralnervensystem des medizinischen Blutegels

Munsch, Thomas

1991

Author's details	von Thomas Munsch
Language	German
Size	V, 85 [41] S, Ill., graph. Darst, 20,5 cm
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Düsseldorf, 1991
Database	Former special subject collection: coastal and deep sea fishing

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Book ; Thesis: Elektrophysiologische Untersuchungen zur Wirkung von 5-Hydroxytryptamin an Neuronen im Zentralnervensystem des medizinischen Blutegels

Munsch, Thomas

1991

Author's details	von Thomas Munsch
Language	German
Size	V, 85 [41] S, Ill., graph. Darst, 20,5 cm
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Düsseldorf, 1991
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article: BDNF-induced nitric oxide signals in cultured rat hippocampal neurons: time course, mechanism of generation, and effect on neurotrophin secretion.

Kolarow, Richard / Kuhlmann, Christoph R W / Munsch, Thomas / Zehendner, Christoph / Brigadski, Tanja / Luhmann, Heiko J / Lessmann, Volkmar

Frontiers in cellular neuroscience

2014 Volume 8, Page(s) 323

Abstract: BDNF and nitric oxide signaling both contribute to plasticity at glutamatergic synapses. However, the role of combined signaling of both pathways at the same synapse is largely unknown. Using NO imaging with diaminofluoresceine in cultured hippocampal ... ...

Abstract	BDNF and nitric oxide signaling both contribute to plasticity at glutamatergic synapses. However, the role of combined signaling of both pathways at the same synapse is largely unknown. Using NO imaging with diaminofluoresceine in cultured hippocampal neurons we analyzed the time course of neurotrophin-induced NO signals. Application of exogenous BDNF, NT-4, and NT-3 (but not NGF) induced NO signals in the soma and in proximal dendrites of hippocampal neurons that were sensitive to NO synthase activity, TrkB signaling, and intracellular calcium elevation. The effect of NO signaling on neurotrophin secretion was analyzed in BDNF-GFP, and NT-3-GFP transfected hippocampal neurons. Exogenous application of the NO donor sodium-nitroprusside markedly inhibited neurotrophin secretion. However, endogenously generated NO in response to depolarization and neurotrophin stimulation, both did not result in a negative feedback on neurotrophin secretion. These results suggest that a negative feedback of NO signaling on synaptic secretion of neurotrophins operates only at high intracellular levels of nitric oxide that are under physiological conditions not reached by depolarization or BDNF signaling.
Language	English
Publishing date	2014-11-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2014.00323
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