Animal Models of Neurological Conditions : A Reference Guide for Neuroscience Researchers and Trainees.

Format:

Book

Author/Creator:

Raber, Jacob.

Language:

English

Subjects (All):

Animal models in research.

Neurosciences.

Physical Description:

1 online resource (613 pages)

Edition:

1st ed.

Place of Publication:

Chantilly : Elsevier Science & Technology, 2025.

Summary:

Animal Models of Neurological Conditions informs about novel animal models and their unique strengths and limitations in the research of neurological conditions.It demonstrates the importance of animal models' abilities to replicate only aspects of a given neurological condition and highlights the value of these animal models in increasing human.

Contents:

Front Cover

Animal Models of Neurological Conditions

Copyright Page

Contents

List of contributors

Preface

Acknowledgment

1 Animal models of alcohol and drugs of abuse

1 Mouse behavioral models of alcohol and drug hedonic effects

1.1 Introduction

1.2 Alcohol and drug intake

1.2.1 Two-bottle choice

1.2.2 Operant self-administration

1.2.3 Studies of genetic and cellular mechanisms

1.3 Drug reward and aversion

1.3.1 Conditioned reward

1.3.2 Conditioned aversion

1.3.3 Studies of genetic and cellular mechanisms

1.4 Concluding remarks

Acknowledgments and Funding

References

2 Nonhuman primate models of fetal alcohol spectrum disorders

2.1 Introduction

2.2 Considerations for designing preclinical studies of FASD with emphasis on factors unique to NHPs

2.3 Findings related to FASD pathophysiology

2.3.1 Fetal ethanol-exposed NHP offspring exhibit similarities to humans with FASD

2.3.1.1 Behavioral studies

2.3.1.2 Physical development

2.4 Effects of fetal ethanol exposure on brain development

2.4.1 Vulnerability of specific brain cell types to fetal ethanol exposure

2.5 Toward the use of NHPs in the development of therapeutic intervention strategies to address FASD

2.6 Conclusion

Acknowledgments

2 Posttraumatic stress disorder animal models

3 Rodent models of posttraumatic stress disorder

3.1 Introduction

3.2 Conceptual framework of animal models of posttraumatic stress disorder

3.3 Neurobiological correlates identified in rodent models of posttraumatic stress disorder

3.4 Stress-based rodent models of posttraumatic stress disorder

3.4.1 Single prolonged stress model

3.5 Predator stress and predator scent exposure models

3.6 Social defeat stress model

3.7 Social isolation model.

3.8 Chronic unpredictable mild stress model

3.9 Underwater trauma model

3.10 Witnessing trauma model

3.11 Early life stress models (maternal separation)

3.12 Immobilization/restraint stress model

3.13 Inescapable foot shock / learned helplessness model

3.14 Pavlovian conditioned defeat model

3.15 Blast-induced traumatic brain injury model

3.16 Limitations and future directions

Disclosure

3 Animal models of traumatic brain injury

4 Mouse models of traumatic brain injury

4.1 Introduction

4.2 Mouse models of traumatic brain injury

4.2.1 Closed head injury models

4.2.1.1 Closed head model with a mechanical impact

4.2.1.2 Controlled cortical impact

4.2.1.3 Fluid percussion injury

4.2.2 Blast models

4.2.3 Penetrating models

4.2.4 In vitro and organoid models

4.3 General limitations of traumatic brain injury mouse models

4.3.1 Challenges imposed by the heterogeneity of traumatic brain injury

4.4 Advances in traumatic brain injury research with mouse models

4.5 Conclusions

4 Animal models of ischemic and vascular conditions

5 Sheep model of hypoxia to the developing brain

5.1 Introduction

5.1.1 Overview of the clinical problems to be addressed in preterm fetal sheep

5.1.2 Advantages and disadvantages of the fetal sheep to model white matter injury

5.2 Fetal ovine models of white matter injury in preterm neonates

5.2.1 White matter injury in human preterm neonates

5.2.2 Hypoxia-ischemia in fetal sheep generates pathological features of white matter injury

5.2.3 Pathophysiological mechanisms of white matter injury in preterm ovine models of global cerebral ischemia

5.2.4 Role of vascular endzones in cerebral white matter injury.

5.2.5 Relative contributions of hypoxia-ischemia and oligodendrocyte lineage immaturity to acute white matter injury

5.2.6 High field MRI to define pathological features of white matter injury

5.3 Fetal ovine hypoxemia models of neonatal gray matter dysmaturation

5.3.1 Preterm neonates are at risk for hypoxemia-related neurodevelopmental disabilities

5.3.2 Roles for hypoxemia in neuronal dysmaturation

5.4 Final conclusions

Further reading

6 Animal models of ischemic and hemorrhagic stroke

6.1 Introduction

6.2 Animal models of ischemic stroke

6.2.1 Focal cerebral ischemia - middle cerebral artery occlusion

6.2.2 Distal middle cerebral artery occlusion

6.2.3 Permanent focal cerebral ischemia

6.2.4 Embolic middle cerebral artery occlusion

6.2.5 Thromboembolic middle cerebral artery occlusion

6.2.6 Photothrombotic middle cerebral artery occlusion

6.2.7 Neonatal stroke models

6.2.8 Other models of focal cerebral ischemia

6.2.9 Global cerebral ischemia models

6.2.10 Summary

6.3 Animal models of hemorrhagic stroke

6.3.1 Endovascular perforation model of subarachnoid hemorrhage

6.3.2 Blood injection models of subarachnoid hemorrhage

6.3.2.1 Infratentorial injection

6.3.2.2 Supratentorial injection model of subarachnoid hemorrhage

6.3.3 Aneurysm rupture models of subarachnoid hemorrhage

6.3.4 Intracerebral hemorrhage models

6.3.4.1 Collagenase/elastase injection models of intracerebral hemorrhage

6.3.4.2 Blood injection models of intracerebral hemorrhage

6.3.4.3 The microballoon model of intracerebral hemorrhage

6.3.5 Summary

6.4 Spontaneous and transgenic stroke models

6.5 Applications of animal models of stroke

6.6 Advances in neuroimaging in Stroke research

6.7 Limitations, challenges, and future directions.

6.8 Conclusion

7 Animal models of depression: a novel preclinical framework for post-myocardial infarction depression

7.1 Introduction

7.1.1 Animal models of depression

7.1.2 Genetic models

7.1.2.1 Serotonin transporter (5-HTT) knockout

7.1.2.2 Brain-derived neurotrophic factor knockout

7.1.2.3 Glucocorticoid recepto knockout

7.1.2.4 Monoamine oxidase A knockout

7.1.3 Environmental models

7.1.3.1 Chronic mild stress

7.1.3.2 Social defeat stress

7.1.3.3 Chronic social isolation

7.1.3.4 Restraint stress

7.1.3.5 Early life stress

7.1.3.6 Learned helplessness

7.1.3.7 Maternal separation

7.1.4 Pharmacological models

7.1.4.1 Reserpine-induced depression

7.1.4.2 NMDA antagonist-induced depression

7.1.4.3 Corticosterone-induced depression

7.1.4.4 Lipopolysaccharide-induced inflammation

7.1.4.5 P-chlorophenylalanine-induced serotonin depletion

7.1.5 Isoniazid and hydrazine-induced depression

7.1.5.1 Neonatal clomipramine

7.1.6 Surgical models

7.1.6.1 Bilateral olfactory bulbectomy

7.1.6.2 Targeted brain lesions

7.1.6.3 Myocardial infarction

7.2 Acute myocardial infarction and depression

7.3 A preclinical model for investigating depression following myocardial infarction

7.4 Behavioral characterization of the post-MI depression animal model

7.5 Biochemical characterization of the post-MI depression animal model

7.6 Treatment of post-MI depression

7.7 Conclusions

7.8 Limitations and future directions

5 Animal models of mild cognitive impairment

8 Nonhuman primate model of mild cognitive impairment

8.1 Introduction

8.2 The rhesus macaque model of human aging

8.3 Cognition and normative aging

8.4 Aging and dementia

8.5 Cognitive changes in rhesus with age

8.6 Cognitive changes with mild cognitive impairment.

8.7 MRI biomarkers of mild cognitive impairment

8.7.1 Clinical imaging changes

8.7.2 Imaging and effects of age on rhesus brain volume

8.8 Other biomarkers

8.9 Hormone therapy and Alzheimer disease

8.10 Conclusion

6 Parkinson's disease animal models

9 MPTP progressive model of Parkinson's disease: changes in basal ganglia circuitry and restorative treatment strategies

9.1 Introduction

9.2 MPTP progressive model

9.2.1 Intervention versus restoration/recovery

9.2.2 Striatum, motor cortex, and glutamate synapses: role in motor function in Parkinson's disease

9.2.3 7,8-Dihyroxyflavone (7,8-DHF) and traumatic brain injury: effects on motor cortex glutamate transporter biomarkers

9.3 Summary and conclusions

7 Alzheimer's disease mouse models

10 Mouse models of Alzheimer's disease pathology

10.1 Introduction

10.2 Mouse models of β-amyloid pathology

10.2.1 Overexpression models

10.2.2 Knock-in models

10.3 Mouse models of Tau pathology

10.4 Mouse models of both β-amyloid and Tau pathology

10.5 Conclusion

11 Mouse models elucidating the role of apolipoprotein E in neurological conditions

11.1 Introduction

11.2 ApoE knockout mouse models reveal important functions of apoE in neurological conditions

11.3 Transgenic model expressing human apoE isoforms in the brain on an apoE knockout background and crossed with human APP and other AD-related transgenic mice to study AD-related neurological conditions

11.3.1 NSE-apoE model

11.3.2 GFAP-apoE model

11.3.3 Crosses of the NSE-apoE and GFAP-apoE models with models transgenic expression of dominant AD genetic factors to study AD-related neurological conditions

11.4 Human apoE targeted replacement mice to study the role of apoE in neurological and psychiatric conditions.

11.5 Human apoE TR mice and animal models of posttraumatic stress disorder.

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ISBN:

0-443-29091-1

9780443290916

OCLC:

1561171836