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Article ; Online: Vasopressin and alcohol: a multifaceted relationship.

Harper, Kathryn M / Knapp, Darin J / Criswell, Hugh E / Breese, George R

2018 Volume 235, Issue 12, Page(s) 3363–3379

Abstract: Background: Arginine vasopressin (VP) has been implicated in a number of neuropsychiatric disorders with an emphasis on situations where stress increased the severity of the disorder. Based on this hypothesized role for VP in neuropsychiatric disorders, ...

Abstract	Background: Arginine vasopressin (VP) has been implicated in a number of neuropsychiatric disorders with an emphasis on situations where stress increased the severity of the disorder. Based on this hypothesized role for VP in neuropsychiatric disorders, much research is currently being undertaken in humans and animals to test VP as a target for treatment of a number of these disorders including alcohol abuse. Objectives: To provide a summary of the literature regarding the role of VP in alcohol- and stress-related behaviors including the use of drugs that target VP in clinical trials. Results: Changes in various components of the VP system occur with alcohol and stress. Manipulating VP or its receptors can alter alcohol- and stress-related behaviors including tolerance to alcohol, alcohol drinking, and anxiety-like behavior. Finally, the hypothalamic-pituitary-adrenal axis response to alcohol is also altered by manipulating the VP system. However, clinical trials of VP antagonists have had mixed results. Conclusions: A review of VP's involvement in alcohol's actions demonstrates that there is much to be learned about brain regions involved in VP-mediated effects on behavior. Thus, future work should focus on elucidating relevant brain regions. By using previous knowledge of the actions of VP and determining the brain regions and/or systems involved in its different behavioral effects, it may be possible to identify a specific receptor subtype target, drug treatment combination, or specific clinical contexts that may point toward a more successful treatment.
MeSH term(s)	Alcohol Drinking/drug therapy ; Alcohol Drinking/metabolism ; Alcohol Drinking/psychology ; Alcoholism/drug therapy ; Alcoholism/metabolism ; Alcoholism/psychology ; Animals ; Antidiuretic Hormone Receptor Antagonists/pharmacology ; Anxiety/drug therapy ; Anxiety/metabolism ; Anxiety/psychology ; Arginine Vasopressin/antagonists & inhibitors ; Arginine Vasopressin/metabolism ; Ethanol/administration & dosage ; Ethanol/toxicity ; Humans ; Hypothalamo-Hypophyseal System/drug effects ; Hypothalamo-Hypophyseal System/metabolism ; Neurophysins/antagonists & inhibitors ; Neurophysins/metabolism ; Pituitary-Adrenal System/drug effects ; Pituitary-Adrenal System/metabolism ; Protein Precursors/antagonists & inhibitors ; Protein Precursors/metabolism ; Stress, Psychological/drug therapy ; Stress, Psychological/metabolism ; Stress, Psychological/psychology ; Vasopressins/antagonists & inhibitors ; Vasopressins/metabolism
Chemical Substances	AVP protein, human ; Antidiuretic Hormone Receptor Antagonists ; Neurophysins ; Protein Precursors ; Vasopressins (11000-17-2) ; Arginine Vasopressin (113-79-1) ; Ethanol (3K9958V90M)
Language	English
Publishing date	2018-11-03
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-018-5099-x
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Article: Phenotyping CCL2 Containing Central Amygdala Neurons Controlling Alcohol Withdrawal-Induced Anxiety.

Harper, Kathryn M / Knapp, Darin J / Todd, Caroline A / Balan, Irina / Aurelian, Laure / Criswell, Hugh E / Breese, George R

Frontiers in cellular neuroscience

2020 Volume 14, Page(s) 580583

Abstract: Chemokines such as chemokine (C-C motif) ligand 2 (CCL2) play a role in several behaviors, including anxiety-like behavior, but whether neurons are an important source of CCL2 for behavior and how neuronal CCL2 may work to affect behavior are still ... ...

Abstract	Chemokines such as chemokine (C-C motif) ligand 2 (CCL2) play a role in several behaviors, including anxiety-like behavior, but whether neurons are an important source of CCL2 for behavior and how neuronal CCL2 may work to affect behavior are still debated. When a herpes simplex virus (HSV) vector was used to knockdown CCL2 mRNA in neurons of the central nucleus of the amygdala (CeA) in rats experiencing multiple withdrawals from low dose ethanol, anxiety-like behavior appeared in the social interaction task. To examine this finding further Fractalkine (CX3CL1), a chemokine that is often found to have an opposing function to CCL2 was measured in these rats. Both alcohol withdrawal and CCL2 knockdown increased the levels of the anti-inflammatory protein CX3CL1. The combination of alcohol withdrawal and CCL2 knockdown decreased CX3CL1 and may alter pro-inflammatory/anti-inflammatory balance, and thus highlights the potential importance of CCL2 and CCL2/CX3CL1 balance in anxiety. To find a mechanism by which neuronal chemokines like CCL2 could affect behavior, retrograde tracing with fluorescent nanobeads was done in two brain regions associated with anxiety the bed nucleus of the stria terminalis (BNST) and the ventral periaqueductal gray (VPAG). These studies identified CeA projection neurons to these brain regions that contain CCL2. To demonstrate that CCL2 can be transported
Language	English
Publishing date	2020-09-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2020.580583
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Article ; Online: Viral Vector Reprogramming of Adult Resident Striatal Oligodendrocytes into Functional Neurons.

Weinberg, Marc S / Criswell, Hugh E / Powell, Sara K / Bhatt, Aadra P / McCown, Thomas J

Molecular therapy : the journal of the American Society of Gene Therapy

2017 Volume 25, Issue 4, Page(s) 928–934

Abstract: Recent advances suggest that in vivo reprogramming of endogenous cell populations provides a viable alternative for neuron replacement. Astrocytes and oligodendrocyte precursor cells can be induced to transdifferentiate into neurons in the CNS, but, in ... ...

Abstract	Recent advances suggest that in vivo reprogramming of endogenous cell populations provides a viable alternative for neuron replacement. Astrocytes and oligodendrocyte precursor cells can be induced to transdifferentiate into neurons in the CNS, but, in these instances, reprogramming requires either transgenic mice or retroviral-mediated gene expression. We developed a microRNA (miRNA)-GFP construct that in vitro significantly reduced the expression of polypyrimidine tract-binding protein, and, subsequently, we packaged this construct in a novel oligodendrocyte preferring adeno-associated virus vector. Ten days after rat striatal transduction, the vast majority of the GFP-positive cells were oligodendrocytes, but 6 weeks to 6 months later, the majority of GFP-positive cells exhibited neuronal morphology and co-localized with the neuronal marker NeuN. Patch-clamp studies on striatal slices established that the GFP-positive cells exhibited electrophysiological properties indicative of mature neurons, such as spontaneous action potentials and spontaneous inhibitory postsynaptic currents. Also, 3 months after striatal vector administration, GFP-positive terminals in the ipsilateral globus pallidus or substantia nigra retrogradely transported fluorescent beads back to GFP-positive striatal cell bodies, indicating the presence of functional presynaptic terminals. Thus, this viral vector approach provides a potential means to harness resident oligodendrocytes as an endogenous source for in vivo neuronal replacement.
MeSH term(s)	Animals ; Cell Line ; Cell Transdifferentiation/genetics ; Cellular Reprogramming/genetics ; Corpus Striatum/cytology ; Dependovirus/genetics ; Genetic Vectors/genetics ; Humans ; Neurons/cytology ; Neurons/metabolism ; Oligodendroglia/cytology ; Oligodendroglia/metabolism ; RNA Interference ; RNA, Small Interfering ; Rats
Chemical Substances	RNA, Small Interfering
Language	English
Publishing date	2017-04-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2017.01.016
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Article ; Online: Amygdala Arginine Vasopressin Modulates Chronic Ethanol Withdrawal Anxiety-Like Behavior in the Social Interaction Task.

Harper, Kathryn M / Knapp, Darin J / Butler, Ryan K / Cook, Cory A / Criswell, Hugh E / Stuber, Garret D / Breese, George R

Alcoholism, clinical and experimental research

2019 Volume 43, Issue 10, Page(s) 2134–2143

Abstract: Background: Chronic ethanol (EtOH) exposure induces neurobehavioral maladaptations in the brain though the precise changes have not been fully explored. The central nucleus of the amygdala (CEA) regulates anxiety-like behavior induced by withdrawal from ...

Abstract	Background: Chronic ethanol (EtOH) exposure induces neurobehavioral maladaptations in the brain though the precise changes have not been fully explored. The central nucleus of the amygdala (CEA) regulates anxiety-like behavior induced by withdrawal from chronic intermittent EtOH (CIE) exposure, and the arginine vasopressin (AVP) system within the CEA regulates many anxiety-like behaviors. Thus, adaptations occur in the CEA AVP system due to chronic EtOH exposure, which lead to anxiety-like behaviors in rats. Methods: Chronic exposure to a low-dose EtOH (4.5% wt/vol) induces anxiety-like behavior in rats. Wistar or Sprague Dawley rats were exposed to a modified CIE or CIE, while intra-CEA microinjections of AVP or a V1b receptor antagonist were used to elicit or block withdrawal-induced anxiety. Additionally, AVP microinjections into the CEA were given 24 hours following 15 days of continuous high-dose EtOH (7% wt/vol), a time period when rats no longer express anxiety. Chemogenetics was also used to activate the basolateral amygdala (BLA) or deactivate the dorsal periaqueductal gray=(dm/dlPAG) therefore PAG=periaqueductal gray to elicit or block withdrawal-induced anxiety. Results: AVP microinjected into the CEA in lieu of exposure to the first 2 cycles of CIE was sufficient to induce anxiety-like behavior in these commonly used rat strains. The V1b receptor antagonist, but not an oxytocin receptor agonist, into the CEA during the first 2 withdrawal cycles suppressed anxiety. However, activation of the BLA in lieu of exposure to the first 2 cycles of CIE was insufficient to induce anxiety-like behavior. AVP microinjection into the CEA 24 hours into withdrawal reelicited anxiety-like behavior, and deactivation of the dm/dlPAG reduced this effect of CEA AVP. Conclusions: Taken together, this study demonstrates a role of CEA AVP and a CEA-dm/dlPAG circuit in the development of anxiety induced by CIE. Such information is valuable for identifying novel therapeutic targets for alcohol- and anxiety-associated disorders.
MeSH term(s)	Amygdala/drug effects ; Animals ; Anxiety/etiology ; Anxiety/physiopathology ; Anxiety/psychology ; Arginine Vasopressin/administration & dosage ; Arginine Vasopressin/pharmacology ; Behavior, Animal ; Central Nervous System Depressants ; Ethanol ; Interpersonal Relations ; Male ; Microinjections ; Periaqueductal Gray/drug effects ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Receptors, Vasopressin/drug effects ; Substance Withdrawal Syndrome/complications ; Substance Withdrawal Syndrome/physiopathology ; Substance Withdrawal Syndrome/psychology
Chemical Substances	Central Nervous System Depressants ; Receptors, Vasopressin ; Arginine Vasopressin (113-79-1) ; Ethanol (3K9958V90M)
Language	English
Publishing date	2019-08-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.14163
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Zs.A 1375: Show issues

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Article ; Online: Evidence for TNFα action on excitatory and inhibitory neurotransmission in the central amygdala: a brain site influenced by stress.

Ming, Zhen / Criswell, Hugh E / Breese, George R

Brain, behavior, and immunity

2013 Volume 33, Page(s) 102–111

Abstract: Anxiety-like responses to stress are accompanied by elevation of brain cytokine-mRNAs. Because cytokines microinjected into central-amygdala (CeA) substitute for stress in a behavioral paradigm, the possibility was raised that cytokines increased by ... ...

Abstract	Anxiety-like responses to stress are accompanied by elevation of brain cytokine-mRNAs. Because cytokines microinjected into central-amygdala (CeA) substitute for stress in a behavioral paradigm, the possibility was raised that cytokines increased by stress influence behavior by affecting CeA-neural activity. Previously, cytokines increased firing-rate of CeA-neurons comparable to that induced by corticotropin-releasing factor (CRF). In this investigation, tumor-necrosis-factor-α (TNFα) increased amplitude, but not frequency of mEPSCs from CeA-neurons. Additionally, TNFα decreased the threshold for triggering action potentials from CeA-neurons without altering membrane-properties during current-clamp recording. Glutamate-receptor-antagonist blockade of mEPSCs and the TNFα-induced reduction in firing threshold implicated glutamate in these changes. A phosphatidyl-inositol-3-kinase-antagonist prevented the TNFα-induced increased in amplitude of mEPSCs, documenting a TNFα intracellular influence. Additionally, TNFα increased frequency, but not amplitude of mIPSCs. CRF-receptor-antagonists were found to prevent the TNFα-induced increase in mIPSC-frequency, without altering the TNFα-induced amplitude increase in mEPSCs or the reduced threshold for action-potentials by TNFα. To clarify how TNFα was increasing CRF-release in the presence of tetrodotoxin, the possibility tested was whether preventing glial-activation would prevent this elevated mIPSC-frequency blocked by CRF-receptor antagonists. Minocycline, which blocks glial activation, prevented the TNFα-induced increase in mIPSC-frequency - a finding consistent with glia contributing to the CRF-involvement in this TNFα action. To fully understand the means by which a CRF1-receptor-antagonist and minocycline prevent TNFα from increasing mIPSC-frequency will require further clarification. Nonetheless, these data provide convincing evidence that release of TNFα by stress could alter neural activity of CeA-neurons by influencing GABA-and glutamate function.
MeSH term(s)	Amygdala/cytology ; Amygdala/immunology ; Amygdala/metabolism ; Animals ; Excitatory Postsynaptic Potentials/immunology ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/immunology ; Induced Pluripotent Stem Cells/metabolism ; Neural Inhibition/immunology ; Neurons/cytology ; Neurons/immunology ; Neurons/metabolism ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological/immunology ; Synaptic Transmission/immunology ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/physiology
Chemical Substances	Tumor Necrosis Factor-alpha
Language	English
Publishing date	2013-06-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2013.06.001
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Article ; Online: Ethanol-enhanced GABA release: a focus on G protein-coupled receptors.

Kelm, M Katherine / Criswell, Hugh E / Breese, George R

Brain research reviews

2010 Volume 65, Issue 2, Page(s) 113–123

Abstract: While research on the actions of ethanol at the GABAergic synapse has focused on postsynaptic mechanisms, recent data have demonstrated that ethanol also facilitates GABA release from presynaptic terminals in many, but not all, brain regions. The ability ...

Abstract	While research on the actions of ethanol at the GABAergic synapse has focused on postsynaptic mechanisms, recent data have demonstrated that ethanol also facilitates GABA release from presynaptic terminals in many, but not all, brain regions. The ability of ethanol to increase GABA release can be regulated by different G protein-coupled receptors (GPCRs), such as the cannabinoid-1 receptor, corticotropin-releasing factor 1 receptor, GABA(B) receptor, and the 5-hydroxytryptamine 2C receptor. The intracellular messengers linked to these GPCRs, including the calcium that is released from internal stores, also play a role in ethanol-enhanced GABA release. Hypotheses are proposed to explain how ethanol interacts with the GPCR pathways to increase GABA release and how this interaction contributes to the brain region specificity of ethanol-enhanced GABA release. Defining the mechanism of ethanol-facilitated GABA release will further our understanding of the GABAergic profile of ethanol and increase our knowledge of how GABAergic neurotransmission may contribute to the intoxicating effects of alcohol and to alcohol dependence.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/metabolism ; Central Nervous System Depressants/pharmacology ; Ethanol/pharmacology ; Humans ; Receptors, G-Protein-Coupled/physiology ; Receptors, GABA/physiology ; Synapses/drug effects ; Synapses/metabolism ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Central Nervous System Depressants ; Receptors, G-Protein-Coupled ; Receptors, GABA ; Ethanol (3K9958V90M) ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2010-09-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	423722-5
ISSN	1872-6321 ; 0165-0173
ISSN (online)	1872-6321
ISSN	0165-0173
DOI	10.1016/j.brainresrev.2010.09.003
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Article: A conceptualization of integrated actions of ethanol contributing to its GABAmimetic profile: a commentary.

Criswell, Hugh E / Breese, George R

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2005 Volume 30, Issue 8, Page(s) 1407–1425

Abstract: Early behavioral investigations supported the contention that systemic ethanol displays a GABAmimetic profile. Microinjection of GABA agonists into brain and in vivo electrophysiological studies implicated a regionally specific action of ethanol on GABA ... ...

Abstract	Early behavioral investigations supported the contention that systemic ethanol displays a GABAmimetic profile. Microinjection of GABA agonists into brain and in vivo electrophysiological studies implicated a regionally specific action of ethanol on GABA function. While selectivity of ethanol to enhance the effect of GABA was initially attributed an effect on type-I-benzodiazepine (BZD)-GABA(A) receptors, a lack of ethanol's effect on GABA responsiveness from isolated neurons with this receptor subtype discounted this contention. Nonetheless, subsequent work identified GABA(A) receptor subtypes, with limited distribution in brain, sensitive to enhancement of GABA at relevant ethanol concentrations. In view of these data, it is hypothesized that the GABAmimetic profile for ethanol is due to activation of mechanisms associated with GABA function, distinct from a direct action on the majority of postsynaptic GABA(A) receptors. The primary action proposed to account for ethanol's regional specificity on GABA transmission is its ability to release GABA from some, but not all, presynaptic GABAergic terminals. As systemic administration of ethanol increases neuroactive steroids, which can enhance GABA responsiveness, this elevated level of neurosteroids is proposed to magnify the effect of GABA released by ethanol. Additional factors contributing to the degree to which ethanol interacts with GABA function include an involvement of GABA(B) and other receptors that influence ethanol-induced GABA release, an effect of phosphorylation on GABA responsiveness, and a regional reduction of glutamatergic tone. Thus, an integration of these consequences induced by ethanol is proposed to provide a logical basis for its in vivo GABAmimetic profile.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/metabolism ; Central Nervous System Depressants/pharmacology ; Drug Interactions ; Ethanol/pharmacology ; GABA Agonists/pharmacology ; Humans ; Models, Biological ; Receptors, GABA/classification ; Receptors, GABA/physiology ; gamma-Aminobutyric Acid/metabolism ; gamma-Aminobutyric Acid/pharmacology
Chemical Substances	Central Nervous System Depressants ; GABA Agonists ; Receptors, GABA ; Ethanol (3K9958V90M) ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2005-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/sj.npp.1300750
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Article: The role of protein kinase A in the ethanol-induced increase in spontaneous GABA release onto cerebellar Purkinje neurons.

Kelm, M Katherine / Criswell, Hugh E / Breese, George R

Journal of neurophysiology

2008 Volume 100, Issue 6, Page(s) 3417–3428

Abstract: Ethanol increases miniature inhibitory postsynaptic current frequency and decreases the paired-pulse ratio, which suggests that ethanol increases both spontaneous and evoked GABA release, respectively. We have shown previously that ethanol increases GABA ...

Abstract	Ethanol increases miniature inhibitory postsynaptic current frequency and decreases the paired-pulse ratio, which suggests that ethanol increases both spontaneous and evoked GABA release, respectively. We have shown previously that ethanol increases GABA release at the rat interneuron-Purkinje cell synapse and that this ethanol effect involves calcium release from internal stores; however, further exploration of the mechanism responsible for ethanol-enhanced GABA release was needed. We found that a cannabinoid receptor 1 (CB1) agonist, WIN-55212, and a GABA(B) receptor agonist, baclofen, decreased baseline spontaneous GABA release and prevented ethanol from increasing spontaneous GABA release. The CB1 receptor and GABA(B) receptor are Galpha i-linked G protein-coupled receptors with common downstream messengers that include adenylate cyclase and protein kinase A (PKA). Adenylate cyclase and PKA antagonists blocked ethanol from increasing spontaneous GABA release, whereas a PKA antagonist limited to the postsynaptic neuron did not block ethanol from increasing spontaneous GABA release. These results suggest that presynaptic PKA plays an essential role in ethanol-enhanced spontaneous GABA release. Similar to ethanol, we found that the mechanism of the cannabinoid-mediated decrease in spontaneous GABA release involves internal calcium stores and PKA. A PKA antagonist decreased baseline spontaneous GABA release. This effect was reduced after incubating the slice with a calcium chelator, BAPTA-AM, but was unaffected when BAPTA was limited to the postsynaptic neuron. This suggests that the PKA antagonist is acting through a presynaptic, calcium-dependent mechanism to decrease spontaneous GABA release. Overall, these results suggest that PKA activation is necessary for ethanol to increase spontaneous GABA release.
MeSH term(s)	Animals ; Animals, Newborn ; Baclofen/pharmacology ; Benzoxazines/pharmacology ; Benzylamines/pharmacology ; Calcium/metabolism ; Central Nervous System Depressants/pharmacology ; Cerebellum/cytology ; Dose-Response Relationship, Drug ; Electric Stimulation/methods ; Enzyme Inhibitors/pharmacology ; Ethanol/pharmacology ; GABA Agents/pharmacology ; In Vitro Techniques ; Inhibitory Postsynaptic Potentials/drug effects ; Inhibitory Postsynaptic Potentials/physiology ; Membrane Potentials/drug effects ; Membrane Potentials/physiology ; Morpholines/pharmacology ; Naphthalenes/pharmacology ; Patch-Clamp Techniques ; Phosphinic Acids/pharmacology ; Protein Kinase C/physiology ; Purkinje Cells/drug effects ; Rats ; Rats, Sprague-Dawley ; Sodium Channel Blockers/pharmacology ; Tetrodotoxin/pharmacology ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Benzoxazines ; Benzylamines ; Central Nervous System Depressants ; Enzyme Inhibitors ; GABA Agents ; Morpholines ; Naphthalenes ; Phosphinic Acids ; Sodium Channel Blockers ; CGP 52432 (139667-74-6) ; Ethanol (3K9958V90M) ; Tetrodotoxin (4368-28-9) ; gamma-Aminobutyric Acid (56-12-2) ; (3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanone (5H31GI9502) ; Protein Kinase C (EC 2.7.11.13) ; Baclofen (H789N3FKE8) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2008-10-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80161-6
ISSN	1522-1598 ; 0022-3077
ISSN (online)	1522-1598
ISSN	0022-3077
DOI	10.1152/jn.90970.2008
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Article ; Online: The PLC/IP 3 R/PKC pathway is required for ethanol-enhanced GABA release.

Kelm, M Katherine / Weinberg, Richard J / Criswell, Hugh E / Breese, George R

Neuropharmacology

2010 Volume 58, Issue 7, Page(s) 1179–1186

Abstract: Research on the actions of ethanol at the GABAergic synapse has traditionally focused on postsynaptic mechanisms, but recent data demonstrate that ethanol also increases both evoked and spontaneous GABA release in many brain regions. Using whole-cell ... ...

Abstract	Research on the actions of ethanol at the GABAergic synapse has traditionally focused on postsynaptic mechanisms, but recent data demonstrate that ethanol also increases both evoked and spontaneous GABA release in many brain regions. Using whole-cell voltage-clamp recordings, we previously showed that ethanol increases spontaneous GABA release at the rat interneuron-Purkinje cell synapse. This presynaptic ethanol effect is dependent on calcium release from internal stores, possibly through activation of inositol 1,4,5-trisphosphate receptors (IP(3)Rs). After confirming that ethanol targets vesicular GABA release, in the present study we used electron microscopic immunohistochemistry to demonstrate that IP(3)Rs are located in presynaptic terminals of cerebellar interneurons. Activation of IP(3)Rs requires binding of IP(3), generated through activation of phospholipase C (PLC). We find that the PLC antagonist edelfosine prevents ethanol from increasing spontaneous GABA release. Diacylglycerol generated by PLC and calcium released by activation of the IP(3)R activate protein kinase C (PKC). Ethanol-enhanced GABA release was blocked by two PKC antagonists, chelerythrine and calphostin C. When a membrane impermeable PKC antagonist, PKC (19-36), was delivered intracellularly to the postsynaptic neuron, ethanol continued to increase spontaneous GABA release. Overall, these results suggest that activation of the PLC/IP(3)R/PKC pathway is necessary for ethanol to increase spontaneous GABA release from presynaptic terminals onto Purkinje cells.
MeSH term(s)	Animals ; Calcium/metabolism ; Central Nervous System Depressants/pharmacology ; Cerebellum/drug effects ; Cerebellum/metabolism ; Cerebellum/ultrastructure ; Diglycerides/metabolism ; Ethanol/pharmacology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Interneurons/drug effects ; Interneurons/metabolism ; Interneurons/ultrastructure ; Male ; Presynaptic Terminals/drug effects ; Presynaptic Terminals/metabolism ; Presynaptic Terminals/ultrastructure ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/metabolism ; Purkinje Cells/drug effects ; Purkinje Cells/metabolism ; Purkinje Cells/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Type C Phospholipases/antagonists & inhibitors ; Type C Phospholipases/metabolism ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Central Nervous System Depressants ; Diglycerides ; Inositol 1,4,5-Trisphosphate Receptors ; Ethanol (3K9958V90M) ; gamma-Aminobutyric Acid (56-12-2) ; Protein Kinase C (EC 2.7.11.13) ; Type C Phospholipases (EC 3.1.4.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2010-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2010.02.018
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Article: Calcium release from presynaptic internal stores is required for ethanol to increase spontaneous gamma-aminobutyric acid release onto cerebellum Purkinje neurons.

Kelm, M Katherine / Criswell, Hugh E / Breese, George R

The Journal of pharmacology and experimental therapeutics

2007 Volume 323, Issue 1, Page(s) 356–364

Abstract: Recent data have demonstrated that ethanol increases gamma-aminobutyric acid (GABA) release in many brain regions, but little is known about the mechanism responsible for this action. Consistent with previous results, ethanol increased miniature ... ...

Abstract	Recent data have demonstrated that ethanol increases gamma-aminobutyric acid (GABA) release in many brain regions, but little is known about the mechanism responsible for this action. Consistent with previous results, ethanol increased miniature inhibitory postsynaptic current (mIPSC) frequency at the interneuron-Purkinje cell synapse in the slice and in mechanically dissociated neurons. These data suggest that ethanol is increasing spontaneous GABA release at this synapse. It is generally accepted that ethanol increases levels of intracellular calcium and that changes in intracellular calcium can alter neurotransmitter release. Therefore, we examined the contribution of calcium-dependent pathways to the effect of ethanol on spontaneous GABA release at the interneuron-Purkinje cell synapse. Ethanol continued to increase mIPSC frequency in a nominally calcium-free extracellular solution and in the presence of a voltage-dependent calcium channel inhibitor, cadmium chloride. These data suggest that influx of extracellular calcium does not play a critical role in the mechanism of ethanol-enhanced spontaneous GABA release. However, a sarco/endoplasmic-reticulum calcium ATPase pump inhibitor (thapsigargin), an inositol 1,4,5-trisphosphate receptor antagonist (2-aminoethoxydiphenylborate) and a ryanodine receptor antagonist (ryanodine) significantly reduced the ability of ethanol to increase mIPSC frequency. In addition, ethanol was still able to increase mIPSC frequency in the presence of intracellular 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) and a cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM-251); thus, retrograde messengers are not involved in ethanol-enhanced spontaneous GABA release. Overall, these data suggest that calcium release from presynaptic internal stores plays a vital role in the mechanism of ethanol-enhanced spontaneous GABA release at the interneuron-Purkinje cell synapse.
MeSH term(s)	Animals ; Calcium/metabolism ; Cerebellum/cytology ; Cerebellum/drug effects ; Cerebellum/metabolism ; Ethanol/pharmacology ; In Vitro Techniques ; Inhibitory Postsynaptic Potentials/drug effects ; Interneurons/drug effects ; Interneurons/metabolism ; Presynaptic Terminals/metabolism ; Purkinje Cells/drug effects ; Purkinje Cells/metabolism ; Rats ; Rats, Sprague-Dawley ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Ethanol (3K9958V90M) ; gamma-Aminobutyric Acid (56-12-2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2007-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.107.126144
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