LIVIVO - Search results -

Search results

Result 1 - 10 of total 35

Search options

Article ; Online: Dopamine across timescales and cell types: Relevance for phenotypes in Parkinson's disease progression.

Seiler, Jillian L / Zhuang, Xiaowen / Nelson, Alexandra B / Lerner, Talia N

2024 Volume 374, Page(s) 114693

Abstract: Dopamine neurons in the substantia nigra pars compacta (SNc) synthesize and release dopamine, a critical neurotransmitter for movement and learning. SNc dopamine neurons degenerate in Parkinson's Disease (PD), causing a host of motor and non-motor ... ...

Abstract	Dopamine neurons in the substantia nigra pars compacta (SNc) synthesize and release dopamine, a critical neurotransmitter for movement and learning. SNc dopamine neurons degenerate in Parkinson's Disease (PD), causing a host of motor and non-motor symptoms. Here, we review recent conceptual advances in our basic understanding of the dopamine system - including our rapidly advancing knowledge of dopamine neuron heterogeneity - with special attention to their importance for understanding PD. In PD patients, dopamine neuron degeneration progresses from lateral SNc to medial SNc, suggesting clinically relevant heterogeneity in dopamine neurons. With technical advances in dopamine system interrogation, we can understand the relevance of this heterogeneity for PD progression and harness it to develop new treatments.
MeSH term(s)	Humans ; Dopamine ; Parkinson Disease/genetics ; Substantia Nigra ; Dopaminergic Neurons ; Phenotype ; Disease Progression
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2024.114693
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 184: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Multiple stimulation parameters influence efficacy of deep brain stimulation in parkinsonian mice.

Schor, Jonathan S / Nelson, Alexandra B

The Journal of clinical investigation

2019 Volume 129, Issue 9, Page(s) 3833–3838

Abstract: Deep brain stimulation (DBS) is used to treat multiple neuropsychiatric disorders, including Parkinson's Disease (PD). Despite widespread clinical use, its therapeutic mechanisms are unknown. Here, we developed a mouse model of subthalamic nucleus (STN) ... ...

Abstract	Deep brain stimulation (DBS) is used to treat multiple neuropsychiatric disorders, including Parkinson's Disease (PD). Despite widespread clinical use, its therapeutic mechanisms are unknown. Here, we developed a mouse model of subthalamic nucleus (STN) DBS for PD, to permit investigation using cell type-specific tools available in mice. We found that electrical STN DBS relieved bradykinesia, as measured by movement velocity. In addition, our model recapitulated several hallmarks of human STN DBS, including rapid onset and offset, frequency dependence, dyskinesia at higher stimulation intensity, and associations between electrode location, therapeutic benefit, and side effects. We used this model to assess whether high frequency stimulation is necessary for effective STN DBS, or if low frequency stimulation can be effective when paired with compensatory adjustments in other parameters. We found that low frequency stimulation, paired with greater pulse width and amplitude, relieved bradykinesia. Moreover, a composite metric incorporating pulse width, amplitude, and frequency predicted therapeutic efficacy better than frequency alone. We found a similar relationship between this composite metric and movement speed in a retrospective analysis of human data, suggesting correlations observed in the mouse model may extend to human patients. Together, these data establish a mouse model for elucidating mechanisms of DBS.
MeSH term(s)	Animals ; Behavior, Animal ; Deep Brain Stimulation/methods ; Disease Models, Animal ; Electrodes ; Humans ; Hypokinesia/metabolism ; Hypokinesia/therapy ; Mice ; Mice, Inbred C57BL ; Oxidopamine ; Parkinson Disease/physiopathology ; Parkinson Disease/therapy ; Retrospective Studies ; Subthalamic Nucleus/physiology
Chemical Substances	Oxidopamine (8HW4YBZ748)
Language	English
Publishing date	2019-06-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI122390
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ua VI Zs.184: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Directly to the Point: Dopamine Persistently Enhances Excitability of Direct Pathway Striatal Neurons.

McGregor, Matthew M / Nelson, Alexandra B

Neuron

2020 Volume 106, Issue 2, Page(s) 201–203

Abstract: In this issue of Neuron, Lahiri and Bevan (2020) investigate the effects of dopamine release on striatal projection neurons. Using perforated patch recordings and optogenetics, they show that dopamine release persistently enhances the intrinsic ... ...

Abstract	In this issue of Neuron, Lahiri and Bevan (2020) investigate the effects of dopamine release on striatal projection neurons. Using perforated patch recordings and optogenetics, they show that dopamine release persistently enhances the intrinsic excitability of direct pathway striatal neurons.
MeSH term(s)	Corpus Striatum ; Dopamine ; Neurons ; Receptors, Dopamine D1 ; Receptors, Dopamine D2
Chemical Substances	Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2020-05-12
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2020.04.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2496: 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 92: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Striatal Indirect Pathway Dysfunction Underlies Motor Deficits in a Mouse Model of Paroxysmal Dyskinesia.

Nelson, Alexandra B / Girasole, Allison E / Lee, Hsien-Yang / Ptáček, Louis J / Kreitzer, Anatol C

The Journal of neuroscience : the official journal of the Society for Neuroscience

2022 Volume 42, Issue 13, Page(s) 2835–2848

Abstract: Abnormal involuntary movements, or dyskinesias, are seen in many neurologic diseases, including disorders where the brain appears grossly normal. This observation suggests that alterations in neural activity or connectivity may underlie dyskinesias. One ... ...

Abstract	Abnormal involuntary movements, or dyskinesias, are seen in many neurologic diseases, including disorders where the brain appears grossly normal. This observation suggests that alterations in neural activity or connectivity may underlie dyskinesias. One influential model proposes that involuntary movements are driven by an imbalance in the activity of striatal direct and indirect pathway neurons (dMSNs and iMSNs, respectively). Indeed, in some animal models, there is evidence that dMSN hyperactivity contributes to dyskinesia. Given the many diseases associated with dyskinesia, it is unclear whether these findings generalize to all forms. Here, we used male and female mice in a mouse model of paroxysmal nonkinesigenic dyskinesia (PNKD) to assess whether involuntary movements are related to aberrant activity in the striatal direct and indirect pathways. In this model, as in the human disorder PNKD, animals experience dyskinetic attacks in response to caffeine or alcohol. Using optically identified striatal single-unit recordings in freely moving PNKD mice, we found a loss of iMSN firing during dyskinesia bouts. Further, chemogenetic inhibition of iMSNs triggered dyskinetic episodes in PNKD mice. Finally, we found that these decreases in iMSN firing are likely because of aberrant endocannabinoid-mediated suppression of glutamatergic inputs. These data show that striatal iMSN dysfunction contributes to the etiology of dyskinesia in PNKD, and suggest that indirect pathway hypoactivity may be a key mechanism for the generation of involuntary movements in other disorders.
MeSH term(s)	Animals ; Chorea/chemically induced ; Corpus Striatum ; Disease Models, Animal ; Dyskinesias/etiology ; Female ; Levodopa/adverse effects ; Male ; Mice ; Neurons
Chemical Substances	Levodopa (46627O600J)
Language	English
Publishing date	2022-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1614-20.2022
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1668: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Circuit Mechanisms of Parkinson's Disease.

McGregor, Matthew M / Nelson, Alexandra B

Neuron

2019 Volume 101, Issue 6, Page(s) 1042–1056

Abstract: Parkinson's disease (PD) is a complex, multi-system neurodegenerative disorder. The second most common neurodegenerative disorder after Alzheimer's disease, it affects approximately 1% of adults over age 60. Diagnosis follows the development of one or ... ...

Abstract	Parkinson's disease (PD) is a complex, multi-system neurodegenerative disorder. The second most common neurodegenerative disorder after Alzheimer's disease, it affects approximately 1% of adults over age 60. Diagnosis follows the development of one or more of the core motor features of the disease, including tremor, slowing of movement (bradykinesia), and rigidity. However, there are numerous other motor and nonmotor disease manifestations. Many PD symptoms result directly from neurodegeneration; others are driven by aberrant activity patterns in surviving neurons. This latter phenomenon, PD circuit dysfunction, is an area of intense study, as it likely underlies our ability to treat many disease symptoms in the face of (currently) irreversible neurodegeneration. This Review will discuss key clinical features of PD and their basis in neural circuit dysfunction. We will first review important disease symptoms and some of the responsible neuropathology. We will then describe the basal ganglia-thalamocortical circuit, the major locus of PD-related circuit dysfunction, and some of the models that have influenced its study. We will review PD-related changes in network activity, subdividing findings into those that touch on the rate, rhythm, or synchronization of neurons. Finally, we suggest some critical remaining questions for the field and areas for new developments.
MeSH term(s)	Basal Ganglia/physiopathology ; Brain/physiopathology ; Cerebral Cortex/physiopathology ; Humans ; Neural Pathways/physiopathology ; Parkinson Disease/physiopathology ; Thalamus/physiopathology
Language	English
Publishing date	2019-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2019.03.004
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2496: 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 92: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Altered Iron and Microstructure in Huntington's Disease Subcortical Nuclei: Insight From 7T MRI.

Yao, Jingwen / Morrison, Melanie A / Jakary, Angela / Avadiappan, Sivakami / Rowley, Paul / Glueck, Julia / Driscoll, Theresa / Geschwind, Michael D / Nelson, Alexandra B / Possin, Kathrine L / Xu, Duan / Hess, Christopher P / Lupo, Janine M

Journal of magnetic resonance imaging : JMRI

2024

Abstract: Background: Pathophysiological changes of Huntington's disease (HD) can precede symptom onset by decades. Robust imaging biomarkers are needed to monitor HD progression, especially before the clinical onset.: Purpose: To investigate iron ... ...

Abstract	Background: Pathophysiological changes of Huntington's disease (HD) can precede symptom onset by decades. Robust imaging biomarkers are needed to monitor HD progression, especially before the clinical onset. Purpose: To investigate iron dysregulation and microstructure alterations in subcortical regions as HD imaging biomarkers, and to associate such alterations with motor and cognitive impairments. Study type: Prospective. Population: Fourteen individuals with premanifest HD (38.0 ± 11.0 years, 9 females; far-from-onset N = 6, near-onset N = 8), 21 manifest HD patients (49.1 ± 12.1 years, 11 females), and 33 age-matched healthy controls (43.9 ± 12.2 years, 17 females). Field strength/sequence: 7 T, T Assessment: Volume, susceptibility, fractional anisotropy (FA), and mean diffusivity (MD) within subcortical brain structures were compared across groups, used to establish HD classification models, and correlated to clinical measures and cognitive assessments. Statistical tests: Generalized linear model, multivariate logistic regression, receiver operating characteristics with the area under the curve (AUC), and likelihood ratio test comparing a volumetric model to one that also includes susceptibility and diffusion metrics, Wilcoxon paired signed-rank test, and Pearson's correlation. A P-value <0.05 after Benjamini-Hochberg correction was considered statistically significant. Results: Significantly higher striatal susceptibility and FA were found in premanifest and manifest HD preceding atrophy, even in far-from-onset premanifest HD compared to controls (putamen susceptibility: 0.027 ± 0.022 vs. 0.018 ± 0.013 ppm; FA: 0.358 ± 0.048 vs. 0.313 ± 0.039). The model with additional susceptibility, FA, and MD features showed higher AUC compared to volume features alone when differentiating premanifest HD from HC (0.83 vs. 0.66), and manifest from premanifest HD (0.94 vs. 0.83). Higher striatal susceptibility significantly correlated with cognitive deterioration in HD (executive function: r = -0.600; socioemotional function: r = -0.486). Data conclusion: 7 T MRI revealed iron dysregulation and microstructure alterations with HD progression, which could precede volume loss, provide added value to HD differentiation, and might be associated with cognitive changes. Evidence level: 2 TECHNICAL EFFICACY: Stage 2.
Language	English
Publishing date	2024-01-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1146614-5
ISSN	1522-2586 ; 1053-1807
ISSN (online)	1522-2586
ISSN	1053-1807
DOI	10.1002/jmri.29195
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3648: 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.MO 236: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Frontostriatal Projections Regulate Innate Avoidance Behavior.

Loewke, Adrienne C / Minerva, Adelaide R / Nelson, Alexandra B / Kreitzer, Anatol C / Gunaydin, Lisa A

The Journal of neuroscience : the official journal of the Society for Neuroscience

2021 Volume 41, Issue 25, Page(s) 5487–5501

Abstract: The dorsomedial prefrontal cortex (dmPFC) has been linked to avoidance and decision-making under conflict, key neural computations altered in anxiety disorders. However, the heterogeneity of prefrontal projections has obscured identification of specific ... ...

Abstract	The dorsomedial prefrontal cortex (dmPFC) has been linked to avoidance and decision-making under conflict, key neural computations altered in anxiety disorders. However, the heterogeneity of prefrontal projections has obscured identification of specific top-down projections involved. While the dmPFC-amygdala circuit has long been implicated in controlling reflexive fear responses, recent work suggests that dmPFC-dorsomedial striatum (DMS) projections may be more important for regulating avoidance. Using fiber photometry recordings in both male and female mice during the elevated zero maze task, we show heightened neural activity in frontostriatal but not frontoamygdalar projection neurons during exploration of the anxiogenic open arms. Additionally, using optogenetics, we demonstrate that this frontostriatal projection preferentially excites postsynaptic D
MeSH term(s)	Animals ; Avoidance Learning/physiology ; Behavior, Animal/physiology ; Corpus Striatum/physiology ; Female ; Instinct ; Male ; Mice ; Mice, Inbred C57BL ; Neural Pathways/physiology ; Prefrontal Cortex/physiology
Language	English
Publishing date	2021-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.2581-20.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1668: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Aberrant Striatal Activity in Parkinsonism and Levodopa-Induced Dyskinesia.

Ryan, Michael B / Bair-Marshall, Chloe / Nelson, Alexandra B

Cell reports

2018 Volume 23, Issue 12, Page(s) 3438–3446.e5

Abstract: Action selection relies on the coordinated activity of striatal direct and indirect pathway medium spiny neurons (dMSNs and iMSNs, respectively). Loss of dopamine in Parkinson's disease is thought to disrupt this balance. While dopamine replacement with ... ...

Abstract	Action selection relies on the coordinated activity of striatal direct and indirect pathway medium spiny neurons (dMSNs and iMSNs, respectively). Loss of dopamine in Parkinson's disease is thought to disrupt this balance. While dopamine replacement with levodopa may restore normal function, the development of involuntary movements (levodopa-induced dyskinesia [LID]) limits therapy. How chronic dopamine loss and replacement with levodopa modulate the firing of identified MSNs in behaving animals is unknown. Using optogenetically labeled striatal single-unit recordings, we assess circuit dysfunction in parkinsonism and LID. Counter to current models, we found that following dopamine depletion, iMSN firing was elevated only during periods of immobility, while dMSN firing was dramatically and persistently reduced. Most notably, we identified a subpopulation of dMSNs with abnormally high levodopa-evoked firing rates, which correlated specifically with dyskinesia. These findings provide key insights into the circuit mechanisms underlying parkinsonism and LID, with implications for developing targeted therapies.
MeSH term(s)	Action Potentials ; Animals ; Behavior, Animal ; Corpus Striatum/pathology ; Corpus Striatum/physiopathology ; Dopamine/metabolism ; Dopamine Agonists/pharmacology ; Dyskinesia, Drug-Induced/pathology ; Dyskinesia, Drug-Induced/physiopathology ; Levodopa/adverse effects ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity/drug effects ; Neurons/pathology ; Optogenetics ; Parkinsonian Disorders/pathology ; Parkinsonian Disorders/physiopathology ; Receptors, Dopamine/metabolism
Chemical Substances	Dopamine Agonists ; Receptors, Dopamine ; Levodopa (46627O600J) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2018-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.05.059
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Bridging the Gap: Muscarinic M4 Receptors Promote Striatal Plasticity in Health and Disease.

Girasole, Allison E / Nelson, Alexandra B

Neuron

2015 Volume 88, Issue 4, Page(s) 621–623

Abstract: In this issue of Neuron, Shen et al. (2015) demonstrate that the M4 muscarinic receptor regulates striatal plasticity. The authors use an M4-positive allosteric modulator, which facilitates long-term depression in direct pathway neurons and reverses ... ...

Abstract	In this issue of Neuron, Shen et al. (2015) demonstrate that the M4 muscarinic receptor regulates striatal plasticity. The authors use an M4-positive allosteric modulator, which facilitates long-term depression in direct pathway neurons and reverses aberrant plasticity in levodopa-induced dyskinesia.
MeSH term(s)	Animals ; Dopamine Agents/toxicity ; Dyskinesia, Drug-Induced/metabolism ; Levodopa/toxicity ; Neostriatum/drug effects ; Neuronal Plasticity/drug effects ; Parkinsonian Disorders/drug therapy ; RGS Proteins/metabolism ; Receptor, Muscarinic M4/metabolism
Chemical Substances	Dopamine Agents ; RGS Proteins ; Receptor, Muscarinic M4 ; Levodopa (46627O600J)
Language	English
Publishing date	2015-11-18
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2015.11.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2496: 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 92: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Probing striatal microcircuitry to understand the functional role of cholinergic interneurons.

Girasole, Allison E / Nelson, Alexandra B

Movement disorders : official journal of the Movement Disorder Society

2015 Volume 30, Issue 10, Page(s) 1306–1318

MeSH term(s)	Animals ; Cholinergic Neurons/physiology ; Humans ; Interneurons/physiology ; Neostriatum/metabolism ; Neostriatum/physiology ; Neostriatum/physiopathology ; Signal Transduction/physiology
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.26340
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2555: 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.MO 238: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito