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Article ; Online: Using the exposome to understand environmental contributors to psychiatric disorders.

Burkett, James P / Miller, Gary W

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2020 Volume 46, Issue 1, Page(s) 263–264

MeSH term(s)	Exposome ; Humans ; Mental Disorders/etiology
Language	English
Publishing date	2020-09-08
Publishing country	England
Document type	News ; Research Support, N.I.H., Extramural
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-020-00851-0
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Article ; Online: Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity.

Bucher, Meghan L / Dunn, Amy R / Bradner, Joshua M / Egerton, Kristen Stout / Burkett, James P / Johnson, Michelle A / Miller, Gary W

The European journal of neuroscience

2024

Abstract: Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high-energy demand, and broad unmyelinated axonal arborisations. Impairments in the storage of dopamine compound this ...

Abstract	Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high-energy demand, and broad unmyelinated axonal arborisations. Impairments in the storage of dopamine compound this stress because of cytosolic reactions that transform the vital neurotransmitter into an endogenous neurotoxicant, and this toxicity is thought to contribute to the dopamine neuron degeneration that occurs Parkinson's disease. We have previously identified synaptic vesicle glycoprotein 2C (SV2C) as a modifier of vesicular dopamine function, demonstrating that genetic ablation of SV2C in mice results in decreased dopamine content and evoked dopamine release in the striatum. Here, we adapted a previously published in vitro assay utilising false fluorescent neurotransmitter 206 (FFN206) to visualise how SV2C regulates vesicular dopamine dynamics and determined that SV2C promotes the uptake and retention of FFN206 within vesicles. In addition, we present data indicating that SV2C enhances the retention of dopamine in the vesicular compartment with radiolabelled dopamine in vesicles isolated from immortalised cells and from mouse brain. Further, we demonstrate that SV2C enhances the ability of vesicles to store the neurotoxicant 1-methyl-4-phenylpyridinium (MPP
Language	English
Publishing date	2024-03-26
Publishing country	France
Document type	Journal Article
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.16311
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Article: Developmental pyrethroid exposure disrupts folate metabolism in mouse brain.

Curtis, Melissa A / Saferin, Nilanjana / Nguyen, Jennifer H / Imami, Ali S / Ryan, William G / Neifer, Kari L / Miller, Gary W / Burkett, James P

bioRxiv : the preprint server for biology

2024

Abstract: Environmental and genetic risk factors, and their interactions, contribute significantly to the etiology of neurodevelopmental disorders (NDDs). Recent epidemiology studies have implicated pyrethroid pesticides as an environmental risk factor for autism ... ...

Abstract	Environmental and genetic risk factors, and their interactions, contribute significantly to the etiology of neurodevelopmental disorders (NDDs). Recent epidemiology studies have implicated pyrethroid pesticides as an environmental risk factor for autism and developmental delay. Our previous research showed that low-dose developmental exposure to the pyrethroid pesticide deltamethrin in mice caused male-biased changes in the brain and in NDD-relevant behaviors in adulthood. Here, we used a metabolomics approach to determine the broadest possible set of metabolic changes in the adult male mouse brain caused by low-dose pyrethroid exposure during development. Using a litter-based design, we exposed mouse dams during pregnancy and lactation to deltamethrin (3 mg/kg or vehicle every 3 days) at a concentration well below the EPA-determined benchmark dose used for regulatory guidance. We raised male offspring to adulthood and collected whole brain samples for untargeted high-resolution metabolomics analysis. Developmentally exposed mice had disruptions in 116 metabolites which clustered into pathways for folate biosynthesis, retinol metabolism, and tryptophan metabolism. As a cross-validation, we integrated metabolomics and transcriptomics data from the same samples, which confirmed previous findings of altered dopamine signaling. These results suggest that pyrethroid exposure during development leads to disruptions in folate metabolism in the adult brain, which may inform both prevention and therapeutic strategies.
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.13.562226
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Article ; Online: Neurobehavioral and inflammatory responses following traumatic brain injury in male and female mice.

Bahader, Ghaith A / Naghavi, Farzaneh / Alotaibi, Ahmed / Dehghan, Amir / Swain, Caroline C / Burkett, James P / Shah, Zahoor A

Behavioural brain research

2023 Volume 456, Page(s) 114711

Abstract: Traumatic brain injury (TBI) is a leading cause of mortality and is associated with a high rate of functional comorbidities, including motor, cognitive, anxiety, depression, and emotional disorders. TBI pathophysiology and recovery are complicated and ... ...

Abstract	Traumatic brain injury (TBI) is a leading cause of mortality and is associated with a high rate of functional comorbidities, including motor, cognitive, anxiety, depression, and emotional disorders. TBI pathophysiology and recovery are complicated and involve several mechanistic pathways that control neurobehavioral outcomes. In this study, male and female C57Bl/6 J mice were subjected to a controlled cortical impact model of TBI or sham injury and evaluated for different neurobehavioral and inflammatory outcomes over a month. We demonstrate that TBI mice have increased motor dysfunction at early and late time points following the injury as compared to the sham group. Anxiety-like symptoms were time- and task-dependent, with both sexes having increased anxiety-like behavior 2 weeks post-injury. Cognitive functions measured by T-maze presented greater deficits in TBI mice, while there was no sex or injury-related difference in depressive-like behaviors. Notably, a significant effect of sex was found in empathy-like behavior, with females showing more allogrooming and freezing behavior in the consoling and fear observational tests, respectively. Evaluating the impact of the injury-induced brain damage demonstrated a greater injury volume and neuronal degeneration in males compared to females one month after TBI. Moreover, male mice showed higher peripheral inflammatory responses, as represented by elevated serum levels of peripheral leukocytes and inflammatory markers. These results will have significant implications for understanding TBI's long-term consequences on neurobehavioral and inflammatory responses, which are sex-specific and can be considered for individualized therapeutic strategies in treating TBI.
MeSH term(s)	Mice ; Male ; Female ; Animals ; Brain Injuries, Traumatic ; Brain Injuries/complications ; Anxiety/etiology ; Cognition ; Leukocytes/metabolism ; Mice, Inbred C57BL ; Disease Models, Animal
Language	English
Publishing date	2023-10-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2023.114711
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Article ; Online: Hereditary convulsions in an outbred prairie vole line.

Swain, Caroline C / Wischmeier, James N / Neifer, Asha E / Lloyd, Ethan A R / Neifer, Kari L / Kile, Kara B / Burkett, James P

Epilepsy research

2023 Volume 195, Page(s) 107202

Abstract: Patients with epilepsy are significantly burdened by the disease due to long-term health risks, the severe side effect profiles of anti-epileptic drugs, and the strong possibility of pharmacoresistant refractory seizures. New animal models of epilepsy ... ...

Abstract	Patients with epilepsy are significantly burdened by the disease due to long-term health risks, the severe side effect profiles of anti-epileptic drugs, and the strong possibility of pharmacoresistant refractory seizures. New animal models of epilepsy with unique characteristics promise to further research to address these ongoing problems. Here, we characterize a newly developed line of prairie voles (Microtus ochrogaster, UTol:HIC or "Toledo" line) that presents with a hereditary, adult-onset, handling-induced convulsion phenotype. Toledo voles were bred for four generations and tested to determine whether the observed phenotype was consistent with epileptic seizures. Toledo voles maintained a stable 22 % incidence of convulsions across generations, with an average age of onset of 12-16 weeks. Convulsions in Toledo voles were reliably evoked by rodent seizure screens and were phenotypically consistent with murine seizures. At the colony level, Toledo voles had a 7-fold increase in risk for sudden unexpected death from unknown causes, which parallels sudden unexpected death in epilepsy (SUDEP) in human patients. Finally, convulsions in Toledo voles were reduced or prevented by treatment with the anti-epileptic drug levetiracetam. Taken in combination, these results suggest that convulsions in Toledo voles may be epileptic seizures. The Toledo prairie vole strain may serve as a new rodent model of epilepsy in an undomesticated, outbred species.
MeSH term(s)	Humans ; Animals ; Mice ; Infant ; Grassland ; Seizures/drug therapy ; Seizures/genetics ; Epilepsy/drug therapy ; Epilepsy/genetics ; Levetiracetam ; Arvicolinae/physiology
Chemical Substances	Levetiracetam (44YRR34555)
Language	English
Publishing date	2023-08-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	632939-1
ISSN	1872-6844 ; 0920-1211
ISSN (online)	1872-6844
ISSN	0920-1211
DOI	10.1016/j.eplepsyres.2023.107202
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Article: Synaptic vesicle glycoprotein 2C enhances vesicular storage of dopamine and counters dopaminergic toxicity.

Bucher, Meghan L / Dunn, Amy R / Bradner, Joshua M / Egerton, Kristen Stout / Burkett, James P / Johnson, Michelle A / Miller, Gary W

bioRxiv : the preprint server for biology

2023

Abstract: Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high energy demand, and broad unmyelinated axonal arborizations. Impairments in the storage of dopamine compound this ...

Abstract	Dopaminergic neurons of the substantia nigra exist in a persistent state of vulnerability resulting from high baseline oxidative stress, high energy demand, and broad unmyelinated axonal arborizations. Impairments in the storage of dopamine compound this stress due to cytosolic reactions that transform the vital neurotransmitter into an endogenous neurotoxicant, and this toxicity is thought to contribute to the dopamine neuron degeneration that occurs Parkinson's disease. We have previously identified synaptic vesicle glycoprotein 2C (SV2C) as a modifier of vesicular dopamine function, demonstrating that genetic ablation of SV2C in mice results in decreased dopamine content and evoked dopamine release in the striatum. Here, we adapted a previously published
Language	English
Publishing date	2023-06-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.26.546143
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Article: Developmental pyrethroid exposure disrupts molecular pathways for MAP kinase and circadian rhythms in mouse brain.

Nguyen, Jennifer H / Curtis, Melissa A / Imami, Ali S / Ryan, William G / Alganem, Khaled / Neifer, Kari L / Saferin, Nilanjana / Nawor, Charlotte N / Kistler, Brian P / Miller, Gary W / Shukla, Rammohan / McCullumsmith, Robert E / Burkett, James P

bioRxiv : the preprint server for biology

2024

Abstract: Neurodevelopmental disorders (NDDs) are a category of pervasive disorders of the developing nervous system with few or no recognized biomarkers. A significant portion of the risk for NDDs, including attention deficit hyperactivity disorder (ADHD), is ... ...

Abstract	Neurodevelopmental disorders (NDDs) are a category of pervasive disorders of the developing nervous system with few or no recognized biomarkers. A significant portion of the risk for NDDs, including attention deficit hyperactivity disorder (ADHD), is contributed by the environment, and exposure to pyrethroid pesticides during pregnancy has been identified as a potential risk factor for NDD in the unborn child. We recently showed that low-dose developmental exposure to the pyrethroid pesticide deltamethrin in mice causes male-biased changes to ADHD- and NDD-relevant behaviors as well as the striatal dopamine system. Here, we used an integrated multiomics approach to determine the broadest possible set of biological changes in the mouse brain caused by developmental pyrethroid exposure (DPE). Using a litter-based, split-sample design, we exposed mouse dams during pregnancy and lactation to deltamethrin (3 mg/kg or vehicle every 3 days) at a concentration well below the EPA-determined benchmark dose used for regulatory guidance. We raised male offspring to adulthood, euthanized them, and pulverized and divided whole brain samples for split-sample transcriptomics, kinomics and multiomics integration. Transcriptome analysis revealed alterations to multiple canonical clock genes, and kinome analysis revealed changes in the activity of multiple kinases involved in synaptic plasticity, including the mitogen-activated protein (MAP) kinase ERK. Multiomics integration revealed a dysregulated protein-protein interaction network containing primary clusters for MAP kinase cascades, regulation of apoptosis, and synaptic function. These results demonstrate that DPE causes a multi-modal biophenotype in the brain relevant to ADHD and identifies new potential mechanisms of action.
Language	English
Publishing date	2024-03-11
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.08.28.555113
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Article ; Online: The evolution of centriole degradation in mouse sperm.

Khanal, Sushil / Jaiswal, Ankit / Chowdanayaka, Rajanikanth / Puente, Nahshon / Turner, Katerina / Assefa, Kebron Yeshitela / Nawras, Mohamad / Back, Ezekiel David / Royfman, Abigail / Burkett, James P / Cheong, Soon Hon / Fisher, Heidi S / Sindhwani, Puneet / Gray, John / Ramachandra, Nallur Basappa / Avidor-Reiss, Tomer

Nature communications

2024 Volume 15, Issue 1, Page(s) 117

Abstract: Centrioles are subcellular organelles found at the cilia base with an evolutionarily conserved structure and a shock absorber-like function. In sperm, centrioles are found at the flagellum base and are essential for embryo development in basal animals. ... ...

Abstract	Centrioles are subcellular organelles found at the cilia base with an evolutionarily conserved structure and a shock absorber-like function. In sperm, centrioles are found at the flagellum base and are essential for embryo development in basal animals. Yet, sperm centrioles have evolved diverse forms, sometimes acting like a transmission system, as in cattle, and sometimes becoming dispensable, as in house mice. How the essential sperm centriole evolved to become dispensable in some organisms is unclear. Here, we test the hypothesis that this transition occurred through a cascade of evolutionary changes to the proteins, structure, and function of sperm centrioles and was possibly driven by sperm competition. We found that the final steps in this cascade are associated with a change in the primary structure of the centriolar inner scaffold protein FAM161A in rodents. This information provides the first insight into the molecular mechanisms and adaptive evolution underlying a major evolutionary transition within the internal structure of the mammalian sperm neck.
MeSH term(s)	Male ; Animals ; Cattle ; Mice ; Centrioles/metabolism ; Semen ; Spermatozoa/metabolism ; Proteins/metabolism ; Cilia ; Mammals
Chemical Substances	Proteins
Language	English
Publishing date	2024-01-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44411-8
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Article ; Online: The behavioral, anatomical and pharmacological parallels between social attachment, love and addiction.

Burkett, James P / Young, Larry J

Psychopharmacology

2012 Volume 224, Issue 1, Page(s) 1–26

Abstract: Rationale: Love has long been referred to as an addiction in literature and poetry. Scientists have often made comparisons between social attachment processes and drug addiction, and it has been suggested that the two may share a common neurobiological ... ...

Abstract	Rationale: Love has long been referred to as an addiction in literature and poetry. Scientists have often made comparisons between social attachment processes and drug addiction, and it has been suggested that the two may share a common neurobiological mechanism. Brain systems that evolved to govern attachments between parents and children and between monogamous partners may be the targets of drugs of abuse and serve as the basis for addiction processes. Objectives: Here, we review research on drug addiction in parallel with research on social attachments, including parent-offspring attachments and social bonds between mating partners. This review focuses on the brain regions and neurochemicals with the greatest overlap between addiction and attachment and, in particular, the mesolimbic dopamine (DA) pathway. Results: Significant overlap exists between these two behavioral processes. In addition to conceptual overlap in symptomatology, there is a strong commonality between the two domains regarding the roles and sites of action of DA, opioids, and corticotropin-releasing factor. The neuropeptides oxytocin and vasopressin are hypothesized to integrate social information into attachment processes that is not present in drug addiction. Conclusions: Social attachment may be understood as a behavioral addiction, whereby the subject becomes addicted to another individual and the cues that predict social reward. Understandings from both fields may enlighten future research on addiction and attachment processes.
MeSH term(s)	Animals ; Behavior, Addictive/physiopathology ; Behavior, Addictive/psychology ; Brain/physiology ; Dopamine/metabolism ; Humans ; Love ; Object Attachment ; Pair Bond ; Parent-Child Relations ; Reward ; Social Behavior ; Substance-Related Disorders/physiopathology ; Substance-Related Disorders/psychology
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2012-08-11
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-012-2794-x
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Ui I Zs.240: Show issues

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Article ; Online: Developmental pyrethroid exposure causes a neurodevelopmental disorder phenotype in mice.

Curtis, Melissa A / Dhamsania, Rohan K / Branco, Rachel C / Guo, Ji-Dong / Creeden, Justin / Neifer, Kari L / Black, Carlie A / Winokur, Emily J / Andari, Elissar / Dias, Brian G / Liu, Robert C / Gourley, Shannon L / Miller, Gary W / Burkett, James P

PNAS nexus

2023 Volume 2, Issue 4, Page(s) pgad085

Abstract: Neurodevelopmental disorders (NDDs) are a widespread and growing public health challenge, affecting as many as 17% of children in the United States. Recent epidemiological studies have implicated ambient exposure to pyrethroid pesticides during pregnancy ...

Abstract	Neurodevelopmental disorders (NDDs) are a widespread and growing public health challenge, affecting as many as 17% of children in the United States. Recent epidemiological studies have implicated ambient exposure to pyrethroid pesticides during pregnancy in the risk for NDDs in the unborn child. Using a litter-based, independent discovery-replication cohort design, we exposed mouse dams orally during pregnancy and lactation to the Environmental Protection Agency's reference pyrethroid, deltamethrin, at 3 mg/kg, a concentration well below the benchmark dose used for regulatory guidance. The resulting offspring were tested using behavioral and molecular methods targeting behavioral phenotypes relevant to autism and NDD, as well as changes to the striatal dopamine system. Low-dose developmental exposure to the pyrethroid deltamethrin (DPE) decreased pup vocalizations, increased repetitive behaviors, and impaired both fear conditioning and operant conditioning. Compared with control mice, DPE mice had greater total striatal dopamine, dopamine metabolites, and stimulated dopamine release, but no difference in vesicular dopamine capacity or protein markers of dopamine vesicles. Dopamine transporter protein levels were increased in DPE mice, but not temporal dopamine reuptake. Striatal medium spiny neurons showed changes in electrophysiological properties consistent with a compensatory decrease in neuronal excitability. Combined with previous findings, these results implicate DPE as a direct cause of an NDD-relevant behavioral phenotype and striatal dopamine dysfunction in mice and implicate the cytosolic compartment as the location of excess striatal dopamine.
Language	English
Publishing date	2023-04-25
Publishing country	England
Document type	Journal Article
ISSN	2752-6542
ISSN (online)	2752-6542
DOI	10.1093/pnasnexus/pgad085
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