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Article ; Online: The promises and perils of psychedelic pharmacology for psychiatry.

McClure-Begley, Tristan D / Roth, Bryan L

2022 Volume 21, Issue 6, Page(s) 463–473

Abstract: Psychedelic drugs including psilocybin, N,N'-dimethyltryptamine (DMT) and lysergic acid diethylamide (LSD) are undergoing a renaissance as potentially useful drugs for various neuropsychiatric diseases, with a rapid onset of therapeutic activity. Notably, ...

Abstract	Psychedelic drugs including psilocybin, N,N'-dimethyltryptamine (DMT) and lysergic acid diethylamide (LSD) are undergoing a renaissance as potentially useful drugs for various neuropsychiatric diseases, with a rapid onset of therapeutic activity. Notably, phase II trials have shown that psilocybin can produce statistically significant clinical effects following one or two administrations in depression and anxiety. These findings have inspired a 'gold rush' of commercial interest, with nearly 60 companies already formed to explore opportunities for psychedelics in treating diverse diseases. Additionally, these remarkable phenomenological and clinical observations are informing hypotheses about potential molecular mechanisms of action that need elucidation to realize the full potential of this investigative space. In particular, despite compelling evidence that the 5-HT
MeSH term(s)	Hallucinogens/adverse effects ; Hallucinogens/pharmacology ; Hallucinogens/therapeutic use ; Humans ; Lysergic Acid Diethylamide/adverse effects ; Lysergic Acid Diethylamide/pharmacology ; Lysergic Acid Diethylamide/therapeutic use ; Mental Disorders/drug therapy ; Psilocybin/adverse effects ; Psilocybin/pharmacology ; Psilocybin/therapeutic use ; Psychiatry ; Receptor, Serotonin, 5-HT2A/metabolism
Chemical Substances	Hallucinogens ; Receptor, Serotonin, 5-HT2A ; Psilocybin (2RV7212BP0) ; Lysergic Acid Diethylamide (8NA5SWF92O)
Language	English
Publishing date	2022-03-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062954-0
ISSN	1474-1784 ; 1474-1776
ISSN (online)	1474-1784
ISSN	1474-1776
DOI	10.1038/s41573-022-00421-7
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Article: Nuclear roles for cilia-associated proteins.

McClure-Begley, Tristan D / Klymkowsky, Michael W

Cilia

2017 Volume 6, Page(s) 8

Abstract: Cilia appear to be derived, evolutionarily, from structures present in the ancestral (pre-ciliary) eukaryote, such as microtubule-based vesicle trafficking and chromosome segregation systems. Experimental observations suggest that the ciliary gate, the ... ...

Abstract	Cilia appear to be derived, evolutionarily, from structures present in the ancestral (pre-ciliary) eukaryote, such as microtubule-based vesicle trafficking and chromosome segregation systems. Experimental observations suggest that the ciliary gate, the molecular complex that mediates the selective molecular movement between cytoplasmic and ciliary compartments, shares features with nuclear pores. Our hypothesis is that this shared transport machinery is at least partially responsible for the observation that a number of ciliary and ciliogenesis-associated proteins are found within nuclei where they play roles in the regulation of gene expression, DNA repair, and nuclear import and export. Recognizing the potential for such nuclear roles is critical when considering the phenotypic effects that arise from the mutational modification of ciliary proteins.
Language	English
Publishing date	2017-05-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2689513-4
ISSN	2046-2530
ISSN	2046-2530
DOI	10.1186/s13630-017-0052-x
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Article ; Online: Differential effects of withdrawal from intermittent and continuous nicotine exposure on reward deficit and somatic aspects of nicotine withdrawal and expression of α4β2* nAChRs in Wistar male rats.

Semenova, Svetlana / Jin, Xinchun / McClure-Begley, Tristan D / Tadman, Matthew Philip / Marks, Michael J / Markou, Athina

Pharmacology, biochemistry, and behavior

2018 Volume 171, Page(s) 54–65

Abstract: Background: Chronic nicotine exposure produces neuroadaptations in brain reward systems and α4β2 nicotinic acetylcholine receptors (nAChRs) in the corticolimbic brain areas. We previously demonstrated opposite effects of nicotine exposure delivered by ... ...

Abstract	Background: Chronic nicotine exposure produces neuroadaptations in brain reward systems and α4β2 nicotinic acetylcholine receptors (nAChRs) in the corticolimbic brain areas. We previously demonstrated opposite effects of nicotine exposure delivered by self-administration or pumps on brain reward thresholds that can be attributed to the different temporal pattern and contingency of nicotine exposure. We investigated the effects of these two factors on reward thresholds and somatic signs during nicotine withdrawal, and on nAChRs binding in corticolimbic brain areas. Methods: The intracranial self-stimulation procedure was used to assess reward thresholds in rats prepared with pumps delivering various doses of nicotine continuously or intermittently. Separate group of rats were randomly exposed to nicotine via pumps (non-contingent) or nicotine self-administration (contingent) to determine [ Results: Withdrawal from continuous non-contingent nicotine exposure led to significant elevations in thresholds and increases in somatic signs in rats, while there was no significant effect of withdrawal from intermittent non-contingent nicotine exposure at the same doses. nAChRs were upregulated during withdrawal from continuous non-contingent nicotine exposure. α4β2* nAChRs were upregulated in the ventral tegmental area and prelimbic cortex during withdrawal from non-contingent intermittent exposure and in the nucleus accumbens during withdrawal from contingent intermittent nicotine exposure to the same dose. Conclusions: During non-contingent nicotine exposure, the temporal pattern of nicotine delivery differentially affected thresholds and somatic signs of withdrawal. Upregulation of α4β2* nAChRs was brain site-specific and depended on both temporal pattern and contingency of nicotine exposure.
MeSH term(s)	Animals ; Autoantigens ; Bridged Bicyclo Compounds, Heterocyclic/metabolism ; Drug Administration Schedule ; Infusion Pumps, Implantable ; Iodine Radioisotopes/metabolism ; Limbic Lobe/metabolism ; Male ; Nicotine/administration & dosage ; Nicotine/adverse effects ; Nucleus Accumbens/metabolism ; Pyridines/metabolism ; Radioligand Assay ; Rats ; Rats, Wistar ; Receptors, Nicotinic/metabolism ; Reward ; Substance Withdrawal Syndrome/diagnosis ; Substance Withdrawal Syndrome/metabolism ; Up-Regulation ; Ventral Tegmental Area/metabolism
Chemical Substances	Autoantigens ; Bridged Bicyclo Compounds, Heterocyclic ; Iodine Radioisotopes ; Pyridines ; Receptors, Nicotinic ; nicotinic receptor alpha4beta2 ; Nicotine (6M3C89ZY6R) ; epibatidine (M6K314F1XX)
Language	English
Publishing date	2018-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2018.06.002
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Article ; Online: Presynaptic GABAB autoreceptor regulation of nicotinic acetylcholine receptor mediated [(3)H]-GABA release from mouse synaptosomes.

McClure-Begley, Tristan D / Grady, Sharon R / Marks, Michael J / Collins, Allan C / Stitzel, Jerry A

Biochemical pharmacology

2014 Volume 91, Issue 1, Page(s) 87–96

Abstract: Activation of nicotinic acetylcholine receptors (nAChRs) can elicit neurotransmitter release from presynaptic nerve terminals. Mechanisms contributing to cell-and-terminal specific regulation of nAChR-mediated neurotransmitter exocytosis are not fully ... ...

Abstract	Activation of nicotinic acetylcholine receptors (nAChRs) can elicit neurotransmitter release from presynaptic nerve terminals. Mechanisms contributing to cell-and-terminal specific regulation of nAChR-mediated neurotransmitter exocytosis are not fully understood. The experiments discussed here examine how activation of GABAB auto- and hetero-receptors suppress nAChR-mediated release of [(3)H]-GABA and [(3)H]-dopamine ((3)H-DA) from mouse striatal synaptosomes. Activation of presynaptic GABAB receptors with (R)-baclofen decreased both [(3)H]-GABA and [(3)H]-DA release evoked by potassium depolarization. However, when nAChRs were activated with ACh to evoke neurotransmitter release, (R)-baclofen had no effect on [(3)H]-DA release, but potently inhibited ACh-evoked [(3)H]-GABA release. Inhibition of nAChR-evoked [(3)H]-GABA release by (R)-baclofen was time sensitive and the effect was lost after prolonged exposure to the GABAB agonist. The early inhibitory effect of GABAB activation on ACh-evoked [(3)H]-GABA release was partially attenuated by antagonists of the phosphatase, calcineurin. Furthermore, antagonists of protein kinase C (PKC) prevented the time-dependent loss of the inhibitory (R)-baclofen effect on [(3)H]-GABA release. These results suggest that α4β2-nAChRs present on GABAergic nerve terminals in the striatum are subject to functional regulation by GABAB autoreceptors that is apparently cell-type specific, since it is absent from DAergic striatal nerve terminals. In addition, the functional modulation of α4β2-type nAChRs on striatal GABAergic nerve terminals by GABAB autoreceptor activation is time-sensitive and appears to involve opposing actions of calcineurin and PKC.
MeSH term(s)	Animals ; Autoreceptors/metabolism ; Baclofen/pharmacology ; Calcineurin Inhibitors ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Dopamine/metabolism ; Female ; GABA-B Receptor Agonists/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Potassium Chloride/pharmacology ; Presynaptic Terminals/drug effects ; Presynaptic Terminals/metabolism ; Protein Kinase C/metabolism ; Pyrethrins/pharmacology ; Receptors, GABA-B/metabolism ; Receptors, Nicotinic/metabolism ; Synaptosomes/drug effects ; Synaptosomes/metabolism ; Time Factors ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Autoreceptors ; Calcineurin Inhibitors ; GABA-B Receptor Agonists ; Pyrethrins ; Receptors, GABA-B ; Receptors, Nicotinic ; cypermethrin (1TR49121NP) ; gamma-Aminobutyric Acid (56-12-2) ; Potassium Chloride (660YQ98I10) ; Protein Kinase C (EC 2.7.11.13) ; Baclofen (H789N3FKE8) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2014-06-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2014.06.010
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Article ; Online: Exploring the nicotinic acetylcholine receptor-associated proteome with iTRAQ and transgenic mice.

McClure-Begley, Tristan D / Stone, Kathy L / Marks, Michael J / Grady, Sharon R / Colangelo, Christopher M / Lindstrom, Jon M / Picciotto, Marina R

Genomics, proteomics & bioinformatics

2013 Volume 11, Issue 4, Page(s) 207–218

Abstract: Neuronal nicotinic acetylcholine receptors (nAChRs) containing α4 and β2 subunits are the principal receptors in the mammalian central nervous system that bind nicotine with high affinity. These nAChRs are involved in nicotine dependence, mood disorders, ...

Abstract	Neuronal nicotinic acetylcholine receptors (nAChRs) containing α4 and β2 subunits are the principal receptors in the mammalian central nervous system that bind nicotine with high affinity. These nAChRs are involved in nicotine dependence, mood disorders, neurodegeneration and neuroprotection. However, our understanding of the interactions between α4β2-containing (α4β2(∗)) nAChRs and other proteins remains limited. In this study, we identified proteins that interact with α4β2(∗) nAChRs in a genedose dependent pattern by immunopurifying β2(∗) nAChRs from mice that differ in α4 and β2 subunit expression and performing proteomic analysis using isobaric tags for relative and absolute quantitation (iTRAQ). Reduced expression of either the α4 or the β2 subunit results in a correlated decline in the expression of a number of putative interacting proteins. We identified 208 proteins co-immunoprecipitated with these nAChRs. Furthermore, stratified linear regression analysis indicated that levels of 17 proteins was correlated significantly with expression of α4β2 nAChRs, including proteins involved in cytoskeletal rearrangement and calcium signaling. These findings represent the first application of quantitative proteomics to produce a β2(∗) nAChR interactome and describe a novel technique used to discover potential targets for pharmacological manipulation of α4β2 nAChRs and their downstream signaling mechanisms.
MeSH term(s)	Animals ; Brain/metabolism ; Chromatography, Liquid ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nicotine/pharmacology ; Protein Binding ; Proteome/analysis ; Proteome/metabolism ; Proteomics/methods ; Receptors, Nicotinic/genetics ; Receptors, Nicotinic/metabolism ; Tandem Mass Spectrometry
Chemical Substances	Proteome ; Receptors, Nicotinic ; nicotinic receptor alpha4beta2 ; Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2013-07-25
Publishing country	China
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2240213-5
ISSN	2210-3244 ; 1672-0229
ISSN (online)	2210-3244
ISSN	1672-0229
DOI	10.1016/j.gpb.2013.05.005
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Article ; Online: Evaluation of the Nicotinic Acetylcholine Receptor-Associated Proteome at Baseline and Following Nicotine Exposure in Human and Mouse Cortex.

McClure-Begley, Tristan D / Esterlis, Irina / Stone, Kathryn L / Lam, TuKiet T / Grady, Sharon R / Colangelo, Christopher M / Lindstrom, Jon M / Marks, Michael J / Picciotto, Marina R

eNeuro

2016 Volume 3, Issue 4

Abstract: Nicotinic acetylcholine receptors (nAChRs) support the initiation and maintenance of smoking, but the long-term changes occurring in the protein complex as a result of smoking and the nicotine in tobacco are not known. Human studies and animal models ... ...

Abstract	Nicotinic acetylcholine receptors (nAChRs) support the initiation and maintenance of smoking, but the long-term changes occurring in the protein complex as a result of smoking and the nicotine in tobacco are not known. Human studies and animal models have also demonstrated that increasing cholinergic tone increases behaviors related to depression, suggesting that the nAChR-associated proteome could be altered in individuals with mood disorders. We therefore immunopurified nAChRs and associated proteins for quantitative proteomic assessment of changes in protein-protein interactions of high-affinity nAChRs containing the β2 subunit (β2-nAChRs) from either cortex of mice treated with saline or nicotine, or postmortem human temporal cortex tissue from tobacco-exposed and nonexposed individuals, with a further comparison of diagnosed mood disorder to control subjects. We observed significant effects of nicotine exposure on the β2-nAChR-associated proteome in human and mouse cortex, particularly in the abundance of the nAChR subunits themselves, as well as putative interacting proteins that make up core components of neuronal excitability (Na/K ATPase subunits), presynaptic neurotransmitter release (syntaxins, SNAP25, synaptotagmin), and a member of a known nAChR protein chaperone family (14-3-3ζ). These findings identify candidate-signaling proteins that could mediate changes in cholinergic signaling via nicotine or tobacco use. Further analysis of identified proteins will determine whether these interactions are essential for primary function of nAChRs at presynaptic terminals. The identification of differences in the nAChR-associated proteome and downstream signaling in subjects with various mood disorders may also identify novel etiological mechanisms and reveal new treatment targets.
MeSH term(s)	Animals ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Cotinine/metabolism ; Female ; Humans ; Mental Disorders/metabolism ; Mental Disorders/pathology ; Mice, Transgenic ; Nicotine/pharmacology ; Nicotinic Agonists/pharmacology ; Proteome/drug effects ; Receptors, Nicotinic/genetics ; Receptors, Nicotinic/metabolism ; Smoking/metabolism ; Smoking/pathology ; Tobacco Use Disorder/metabolism ; Tobacco Use Disorder/pathology
Chemical Substances	Nicotinic Agonists ; Proteome ; Receptors, Nicotinic ; Nicotine (6M3C89ZY6R) ; Cotinine (K5161X06LL)
Language	English
Publishing date	2016-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0166-16.2016
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Article ; Online: Morphine dependence and withdrawal induced changes in cholinergic signaling.

Neugebauer, Nichole M / Einstein, Emily B / Lopez, Maria B / McClure-Begley, Tristan D / Mineur, Yann S / Picciotto, Marina R

Pharmacology, biochemistry, and behavior

2013 Volume 109, Page(s) 77–83

Abstract: Cholinergic signaling is thought to be involved in morphine dependence and withdrawal, but the specific mechanisms involved remain unclear. The current study aimed to identify alterations in the cholinergic system that may contribute to the development ... ...

Abstract	Cholinergic signaling is thought to be involved in morphine dependence and withdrawal, but the specific mechanisms involved remain unclear. The current study aimed to identify alterations in the cholinergic system that may contribute to the development of morphine dependence and withdrawal. Acetylcholinesterase (AChE) activity and [³H]-epibatidine binding were evaluated in order to determine if morphine dependence and withdrawal induces alterations in cholinergic signaling or expression of high affinity nicotinic acetylcholine receptors (nAChRs) in the midbrain (MB), medial habenula (MHb) and interpeduncular nucleus (IPN). The effect of cholinergic signaling through nAChRs on morphine-withdrawal induced jumping behavior was then determined. Lastly, the contribution of β4-containing nAChRs receptors in the MHb to morphine-withdrawal induced jumping behavior and neuronal activity as indicated by c-fos expression was assessed. Chronic morphine administration decreased AChE activity in MB and MHb, an effect that was no longer present following precipitated withdrawal. Morphine dependent mice showed increased nicotinic acetylcholine receptor (nAChR) levels in MB. Further, nicotine (0.4 mg/kg) and lobeline (3 mg/kg) decreased jumping behavior while mecamylamine (1 mg/kg) had no effect. Knock-down of β4 subunit-containing nAChRs in the MHb attenuated c-fos activation, but did not decrease morphine withdrawal-induced jumping. Thus, morphine withdrawal induces cholinergic signaling in the MHb, but this does not appear to be responsible for the effects of cholinergic drugs on somatic signs of opiate withdrawal, as measured by jumping behavior.
MeSH term(s)	Acetylcholine/metabolism ; Animals ; Behavior, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Morphine/administration & dosage ; Morphine/adverse effects ; Morphine/metabolism ; Morphine Dependence/metabolism ; Naloxone/administration & dosage ; Narcotic Antagonists/administration & dosage ; Receptors, Nicotinic/metabolism ; Signal Transduction ; Substance Withdrawal Syndrome/metabolism
Chemical Substances	Narcotic Antagonists ; Receptors, Nicotinic ; Naloxone (36B82AMQ7N) ; Morphine (76I7G6D29C) ; Acetylcholine (N9YNS0M02X)
Language	English
Publishing date	2013-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2013.04.015
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Article: Exploring the Nicotinic Acetylcholine Receptor-associated Proteome with iTRAQ and Transgenic Mice

McClure-Begley, Tristan D / Stone, Kathy L / Marks, Michael J / Grady, Sharon R / Colangelo, Christopher M / Lindstrom, Jon M / Picciotto, Marina R

Genomics, proteomics & bioinformatics. 2013 Aug., v. 11, no. 4

2013

Abstract	Neuronal nicotinic acetylcholine receptors (nAChRs) containing α4 and β2 subunits are the principal receptors in the mammalian central nervous system that bind nicotine with high affinity. These nAChRs are involved in nicotine dependence, mood disorders, neurodegeneration and neuroprotection. However, our understanding of the interactions between α4β2-containing (α4β2∗) nAChRs and other proteins remains limited. In this study, we identified proteins that interact with α4β2∗ nAChRs in a genedose dependent pattern by immunopurifying β2∗ nAChRs from mice that differ in α4 and β2 subunit expression and performing proteomic analysis using isobaric tags for relative and absolute quantitation (iTRAQ). Reduced expression of either the α4 or the β2 subunit results in a correlated decline in the expression of a number of putative interacting proteins. We identified 208 proteins co-immunoprecipitated with these nAChRs. Furthermore, stratified linear regression analysis indicated that levels of 17 proteins was correlated significantly with expression of α4β2 nAChRs, including proteins involved in cytoskeletal rearrangement and calcium signaling. These findings represent the first application of quantitative proteomics to produce a β2∗ nAChR interactome and describe a novel technique used to discover potential targets for pharmacological manipulation of α4β2 nAChRs and their downstream signaling mechanisms.
Keywords	acetylcholine ; calcium signaling ; central nervous system ; cholinergic receptors ; cytoskeleton ; emotions ; genetically modified organisms ; linear models ; mice ; neuroprotective effect ; nicotine ; proteome ; proteomics ; regression analysis
Language	English
Dates of publication	2013-08
Size	p. 207-218.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2240213-5
ISSN	2210-3244 ; 1672-0229
ISSN (online)	2210-3244
ISSN	1672-0229
DOI	10.1016/j.gpb.2013.05.005
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Article ; Online: A novel α-conotoxin MII-sensitive nicotinic acetylcholine receptor modulates [(3) H]-GABA release in the superficial layers of the mouse superior colliculus.

McClure-Begley, Tristan D / Wageman, Charles R / Grady, Sharon R / Marks, Michael J / McIntosh, J Michael / Collins, Allan C / Whiteaker, Paul

Journal of neurochemistry

2012 Volume 122, Issue 1, Page(s) 48–57

Abstract: Mouse superficial superior colliculus (SuSC) contains dense GABAergic innervation and diverse nicotinic acetylcholine receptor subtypes. Pharmacological and genetic approaches were used to investigate the subunit compositions of nicotinic acetylcholine ... ...

Abstract	Mouse superficial superior colliculus (SuSC) contains dense GABAergic innervation and diverse nicotinic acetylcholine receptor subtypes. Pharmacological and genetic approaches were used to investigate the subunit compositions of nicotinic acetylcholine receptors (nAChR) expressed on mouse SuSC GABAergic terminals. [(125) I]-Epibatidine competition-binding studies revealed that the α3β2* and α6β2* nicotinic subtype-selective peptide α-conotoxin MII-blocked binding to 40 ± 5% of SuSC nAChRs. Acetylcholine-evoked [(3) H]-GABA release from SuSC crude synaptosomal preparations is calcium dependent, blocked by the voltage-sensitive calcium channel blocker, cadmium, and the nAChR antagonist mecamylamine, but is unaffected by muscarinic, glutamatergic, P2X and 5-HT3 receptor antagonists. Approximately 50% of nAChR-mediated SuSC [(3) H]-GABA release is inhibited by α-conotoxin MII. However, the highly α6β2-subtype-selective α-conotoxin PIA did not affect [(3) H]-GABA release. Nicotinic subunit-null mutant mouse experiments revealed that ACh-stimulated SuSC [(3) H]-GABA release is entirely β2 subunit-dependent. α4 subunit deletion decreased total function by >90%, and eliminated α-conotoxin MII-resistant release. ACh-stimulated SuSC [(3) H]-GABA release was unaffected by β3, α5 or α6 nicotinic subunit deletions. Together, these data suggest that a significant proportion of mouse SuSC nicotinic agonist-evoked GABA-release is mediated by a novel, α-conotoxin MII-sensitive α3α4β2 nAChR. The remaining α-conotoxin MII-resistant, nAChR agonist-evoked SuSC GABA release appears to be mediated via α4β2 subtype nAChRs.
MeSH term(s)	6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Acetylcholine/pharmacology ; Adenosine Triphosphate/analogs & derivatives ; Adenosine Triphosphate/pharmacology ; Animals ; Bridged Bicyclo Compounds, Heterocyclic/pharmacokinetics ; Bungarotoxins/pharmacology ; Conotoxins/pharmacology ; Dizocilpine Maleate/pharmacology ; Dose-Response Relationship, Drug ; Drug Interactions ; Excitatory Amino Acid Antagonists/pharmacology ; Female ; In Vitro Techniques ; Iodine Isotopes/pharmacokinetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nicotinic Agonists/pharmacokinetics ; Nicotinic Antagonists/pharmacology ; Protein Binding/drug effects ; Protein Subunits/genetics ; Protein Subunits/physiology ; Pyridines/pharmacokinetics ; Receptors, Nicotinic/deficiency ; Receptors, Nicotinic/physiology ; Serotonin Antagonists/pharmacology ; Superior Colliculi/cytology ; Superior Colliculi/drug effects ; Superior Colliculi/metabolism ; Synaptosomes/drug effects ; Synaptosomes/metabolism ; Tritium/metabolism ; Tropanes/pharmacology ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Bridged Bicyclo Compounds, Heterocyclic ; Bungarotoxins ; Conotoxins ; Excitatory Amino Acid Antagonists ; Iodine Isotopes ; Nicotinic Agonists ; Nicotinic Antagonists ; Protein Subunits ; Pyridines ; Receptors, Nicotinic ; Serotonin Antagonists ; Tropanes ; alpha-conotoxin MII ; Tritium (10028-17-8) ; gamma-Aminobutyric Acid (56-12-2) ; 2',3'-O-(2,4,6-trinitro-cyclohexadienylidine)adenosine 5'-triphosphate (61368-63-6) ; Dizocilpine Maleate (6LR8C1B66Q) ; 6-Cyano-7-nitroquinoxaline-2,3-dione (6OTE87SCCW) ; Adenosine Triphosphate (8L70Q75FXE) ; epibatidine (M6K314F1XX) ; Acetylcholine (N9YNS0M02X) ; bemesetron (O98T3677PA)
Language	English
Publishing date	2012-05-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2012.07759.x
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Article ; Online: Changes in the cholinergic system between bipolar depression and euthymia as measured with [123I]5IA single photon emission computed tomography.

Hannestad, Jonas O / Cosgrove, Kelly P / DellaGioia, Nicole F / Perkins, Evgenia / Bois, Frederic / Bhagwagar, Zubin / Seibyl, John P / McClure-Begley, Tristan D / Picciotto, Marina R / Esterlis, Irina

Biological psychiatry

2013 Volume 74, Issue 10, Page(s) 768–776

Abstract: Background: The cholinergic system is substantially altered in individuals with major depression and is partially restored when depression remits. We quantified the availability of β2-subunit-containing nicotinic acetylcholine receptors (β2*-nAChR) in ... ...

Abstract	Background: The cholinergic system is substantially altered in individuals with major depression and is partially restored when depression remits. We quantified the availability of β2-subunit-containing nicotinic acetylcholine receptors (β2-nAChR) in subjects with bipolar disorder. Methods:* Twenty-five subjects with bipolar disorder (15 depressed, 10 euthymic) and 25 sex- and age-matched control subjects had a [(123)I]5IA-85380 single photon emission computed tomography scan to quantify β2-nAChR VT/fP (total volume of distribution, corrected for individual differences in metabolism and protein binding of the radiotracer). Average VT/fP was compared between groups and correlated with clinical characteristics. Postmortem analysis of β2-nAChRs was conducted using equilibrium binding with [(125)I]5IA in subjects with bipolar disorder and matched control subjects. Results: We showed significantly lower β2-nAChR availability (20%-38%) in subjects with bipolar depression compared with euthymic and control subjects across all brain regions assessed (frontal, parietal, temporal, and anterior cingulate cortex, hippocampus, amygdala, thalamus, striatum). The postmortem binding study in which endogenous acetylcholine was washed out did not show a statistically significant difference in β2-nAChR number in temporal cortex of the bipolar depressed and control groups (15% difference; p = .2). Conclusions: We show that the alteration in the cholinergic system observed during a depressive episode appears to resolve during euthymia. We suggest that lower VT/fP observed in vivo may be due to a combination of higher endogenous acetylcholine levels during depression, which could compete with radiotracer binding to the receptor in vivo, and lower receptor number in bipolar depression. Identification of differences in cholinergic signaling in subjects with bipolar depression may improve our understanding of its etiology and reveal new treatment targets.
MeSH term(s)	Adult ; Azetidines/administration & dosage ; Bipolar Disorder/metabolism ; Brain Chemistry ; Female ; Humans ; Male ; Pyridines/administration & dosage ; Receptors, Nicotinic/analysis ; Smoking ; Tomography, Emission-Computed, Single-Photon
Chemical Substances	5-iodo-3-(2-azetidinylmethoxy)pyridine ; Azetidines ; Pyridines ; Receptors, Nicotinic ; nicotinic receptor beta2
Language	English
Publishing date	2013-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2013.04.004
Database	MEDical Literature Analysis and Retrieval System OnLINE

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