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Article ; Online: Detection and quantification of neurotransmitters in dialysates.

Zapata, Agustin / Chefer, Vladimir I / Parrot, Sandrine / Denoroy, Luc

Current protocols in neuroscience

2013 Volume Chapter 7, Page(s) Unit7.4

Abstract: Sensitive analytical methods are needed for the separation and quantification of neurotransmitters obtained in microdialysate studies. This unit describes methods that permit quantification of nanomolar concentrations of monoamines and their metabolites ( ...

Abstract	Sensitive analytical methods are needed for the separation and quantification of neurotransmitters obtained in microdialysate studies. This unit describes methods that permit quantification of nanomolar concentrations of monoamines and their metabolites (high-performance liquid chromatography [HPLC] electrochemical detection), acetylcholine (HPLC-coupled to an enzyme reactor), and amino acids (HPLC-fluorescence detection, capillary electrophoresis with laser-induced fluorescence detection).
MeSH term(s)	Amino Acids/metabolism ; Animals ; Chromatography, High Pressure Liquid ; Dialysis Solutions/chemistry ; Dialysis Solutions/metabolism ; Electrochemical Techniques ; Electrophoresis, Capillary ; Fluorescence ; Humans ; Lasers ; Microdialysis/methods ; Neurotransmitter Agents/metabolism
Chemical Substances	Amino Acids ; Dialysis Solutions ; Neurotransmitter Agents
Language	English
Publishing date	2013-04
Publishing country	United States
Document type	Journal Article
ISSN	1934-8576
ISSN (online)	1934-8576
DOI	10.1002/0471142301.ns0704s63
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Article ; Online: Basolateral amygdala-driven augmentation of medial prefrontal cortex GABAergic neurotransmission in response to environmental stimuli associated with cocaine administration.

Chefer, Vladimir I / Wang, Ruizhong / Shippenberg, Toni S

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2011 Volume 36, Issue 10, Page(s) 2018–2029

Abstract: Basolateral amygdala (BLA) and medial prefrontal cortex (mPFC) interactions have been implicated in cue-elicited craving and drug seeking. However, the neurochemical mechanisms underlying drug/environment associations are ill-defined. We used in vivo ... ...

Abstract	Basolateral amygdala (BLA) and medial prefrontal cortex (mPFC) interactions have been implicated in cue-elicited craving and drug seeking. However, the neurochemical mechanisms underlying drug/environment associations are ill-defined. We used in vivo microdialysis and pharmacological inactivation techniques to identify alterations in mPFC glutamate (GLU) and gamma-aminobutyric acid (GABA) transmission in response to cues previously associated with experimenter-administered cocaine (COC) and the BLA contribution to these effects. Rats received alternate day injections of COC and saline (SAL) paired with a distinct environment for 6 days. Behavioral, neurochemical and immunohistochemical studies were conducted, in drug-free animals, 24 h after the last conditioning session. Animals exposed to a COC-paired environment demonstrated an augmented locomotor activity (LMA) relative to those exposed to the SAL-paired environment. mPFC GABA neurotransmission in the COC-paired environment was significantly increased, whereas GLU overflow was unaltered. Dual labeling of cFos and glutamic acid decarboxylase 67 immunoreactivity in mPFC neurons revealed significantly greater colocalization of these proteins following exposure to the COC-associated environment (CAE) relative to pseudo-conditioned rats or rats exposed to the SAL-associated environment indicating that the conditioned neurochemical response to the COC-paired environment is associated with activation of intrinsic mPFC GABA neurons. BLA inactivation prevented the increase in LMA and the augmentation of mPFC GABA transmission produced by cue exposure. Intra-mPFC application of the AMPA/KA receptor antagonist, NBQX, produced similar effects. These findings indicate that exposure to a CAE increases mPFC GABA transmission by enhancing excitatory drive from the BLA and activation of AMPA/KA receptors on mPFC GABA neurons.
MeSH term(s)	Amygdala/drug effects ; Amygdala/physiology ; Animals ; Cocaine/administration & dosage ; Environment ; GABAergic Neurons/drug effects ; GABAergic Neurons/physiology ; Male ; Motor Activity/drug effects ; Motor Activity/physiology ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/physiology ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology
Chemical Substances	Cocaine (I5Y540LHVR)
Language	English
Publishing date	2011-06-01
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2011.89
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Article ; Online: Kappa opioid receptors on dopaminergic neurons are necessary for kappa-mediated place aversion.

Chefer, Vladimir I / Bäckman, Cristina M / Gigante, Eduardo D / Shippenberg, Toni S

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2013 Volume 38, Issue 13, Page(s) 2623–2631

Abstract: Kappa-opioid receptor (KOR) agonists have dysphoric properties in humans and are aversive in rodents. This has been attributed to the activation of KORs within the mesolimbic dopamine (DA) system. However, the role of DA in KOR-mediated aversion and ... ...

Abstract	Kappa-opioid receptor (KOR) agonists have dysphoric properties in humans and are aversive in rodents. This has been attributed to the activation of KORs within the mesolimbic dopamine (DA) system. However, the role of DA in KOR-mediated aversion and stress remains divisive as recent studies have suggested that activation of KORs on serotonergic neurons may be sufficient to mediate aversive behaviors. To address this question, we used conditional knock-out (KO) mice with KORs deleted on DA neurons (DAT(Cre/wt)/KOR(loxp/loxp), or DATCre-KOR KO). In agreement with previous findings, control mice (DAT(Cre/wt)/KOR(wt/wt) or WT) showed conditioned place aversion (CPA) to the systemically administered KOR agonist U69,593. In contrast, DATCre-KOR KO mice did not exhibit CPA with this same agonist. In addition, in vivo microdialysis showed that systemic U69,593 decreased overflow of DA in the nucleus accumbens (NAc) in WT mice, but had no effect in DATCre-KOR KO mice. Intra- ventral tegmental area (VTA) delivery of KORs using an adeno-associated viral gene construct, resulted in phenotypic rescue of the KOR-mediated NAc DA response and aversive behavior in DATCre-KOR KO animals. These results provide evidence that KORs on VTA DA neurons are necessary to mediate KOR-mediated aversive behavior. Therefore, our data, along with recent findings, suggest that the neuronal mechanisms of KOR-mediated aversive behavior may include both dopaminergic and serotonergic components.
MeSH term(s)	Analgesics/pharmacology ; Animals ; Avoidance Learning/drug effects ; Avoidance Learning/physiology ; Benzeneacetamides/pharmacology ; Conditioning, Operant/drug effects ; Conditioning, Operant/physiology ; Dopamine Plasma Membrane Transport Proteins/genetics ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/metabolism ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microdialysis ; Microinjections ; Nucleus Accumbens/cytology ; Nucleus Accumbens/metabolism ; Olfactory Bulb/cytology ; Pyrrolidines/pharmacology ; Receptors, Opioid, kappa/deficiency ; Receptors, Opioid, kappa/metabolism ; Transduction, Genetic ; Ventral Tegmental Area/cytology
Chemical Substances	Analgesics ; Benzeneacetamides ; Dopamine Plasma Membrane Transport Proteins ; Pyrrolidines ; Receptors, Opioid, kappa ; Slc6a3 protein, mouse ; Green Fluorescent Proteins (147336-22-9) ; U 69593 (J5S4K6TKTG)
Language	English
Publishing date	2013-07-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2013.171
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Article ; Online: Microdialysis in rodents.

Zapata, Agustin / Chefer, Vladimir I / Shippenberg, Toni S

Current protocols in neuroscience

2009 Volume Chapter 7, Page(s) Unit7.2

Abstract: Microdialysis is an in vivo sampling technique that permits the quantification of various substances (e.g., neurotransmitters, peptides, electrolytes) in blood and tissue. It is also used to infuse substances into the brain and spinal cord. This unit ... ...

Abstract	Microdialysis is an in vivo sampling technique that permits the quantification of various substances (e.g., neurotransmitters, peptides, electrolytes) in blood and tissue. It is also used to infuse substances into the brain and spinal cord. This unit describes methods for the construction and stereotaxic implantation of microdialysis probes into discrete brain regions of the rat and mouse. Procedures for the conduct of conventional and quantitative microdialysis experiments in the awake and anesthetized rodent are also provided.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/metabolism ; Brain Chemistry/drug effects ; Brain Chemistry/physiology ; Equipment Design ; Microdialysis/instrumentation ; Microdialysis/methods ; Microelectrodes ; Models, Animal ; Rodentia
Language	English
Publishing date	2009-04-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2179072-3
ISSN	1934-8576 ; 1934-8584
ISSN (online)	1934-8576
ISSN	1934-8584
DOI	10.1002/0471142301.ns0702s47
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Article ; Online: Dopamine in the dorsal hippocampus impairs the late consolidation of cocaine-associated memory.

Kramar, Cecilia P / Chefer, Vladimir I / Wise, Roy A / Medina, Jorge H / Barbano, M Flavia

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2014 Volume 39, Issue 7, Page(s) 1645–1653

Abstract: Cocaine is thought to be addictive because it elevates dopamine levels in the striatum, reinforcing drug-seeking habits. Cocaine also elevates dopamine levels in the hippocampus, a structure involved in contextual conditioning as well as in reward ... ...

Abstract	Cocaine is thought to be addictive because it elevates dopamine levels in the striatum, reinforcing drug-seeking habits. Cocaine also elevates dopamine levels in the hippocampus, a structure involved in contextual conditioning as well as in reward function. Hippocampal dopamine promotes the late phase of consolidation of an aversive step-down avoidance memory. Here, we examined the role of hippocampal dopamine function in the persistence of the conditioned increase in preference for a cocaine-associated compartment. Blocking dorsal hippocampal D1-type receptors (D1Rs) but not D2-type receptors (D2Rs) 12 h after a single training trial extended persistence of the normally short-lived memory; conversely, a general and a specific phospholipase C-coupled D1R agonist (but not a D2R or adenylyl cyclase-coupled D1R agonist) decreased the persistence of the normally long-lived memory established by three-trial training. These effects of D1 agents were opposite to those previously established in a step-down avoidance task, and were here also found to be opposite to those in a lithium chloride-conditioned avoidance task. After returning to normal following cocaine injection, dopamine levels in the dorsal hippocampus were found elevated again at the time when dopamine antagonists and agonists were effective: between 13 and 17 h after cocaine injection. These findings confirm that, long after the making of a cocaine-place association, hippocampal activity modulates memory consolidation for that association via a dopamine-dependent mechanism. They suggest a dynamic role for dorsal hippocampal dopamine in this late-phase memory consolidation and, unexpectedly, differential roles for late consolidation of memories for places that induce approach or withdrawal because of a drug association.
MeSH term(s)	Animals ; Association Learning/drug effects ; Brain-Derived Neurotrophic Factor/metabolism ; Cocaine/administration & dosage ; Conditioning, Operant/drug effects ; Disease Models, Animal ; Dopamine/metabolism ; Dopamine/toxicity ; Dopamine Agents/pharmacology ; Dopamine Uptake Inhibitors/administration & dosage ; Dose-Response Relationship, Drug ; Drug Administration Routes ; Hippocampus/drug effects ; Lithium Chloride/administration & dosage ; MAP Kinase Signaling System/drug effects ; Male ; Memory Disorders/chemically induced ; Rats ; Rats, Sprague-Dawley ; Receptor, trkB/metabolism ; Time Factors
Chemical Substances	Brain-Derived Neurotrophic Factor ; Dopamine Agents ; Dopamine Uptake Inhibitors ; Receptor, trkB (EC 2.7.10.1) ; Lithium Chloride (G4962QA067) ; Cocaine (I5Y540LHVR) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2014-01-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2014.11
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Article ; Online: Delta-opioid receptor antagonists prevent sensitization to the conditioned rewarding effects of morphine.

Shippenberg, Toni S / Chefer, Vladimir I / Thompson, Alexis C

Biological psychiatry

2008 Volume 65, Issue 2, Page(s) 169–174

Abstract: Background: Functional interactions between mu- and delta-opioid receptors (MOPr and DOPr, respectively) are implicated in morphine tolerance and dependence. The contribution of DOPr to the conditioned rewarding effects of morphine and the enhanced ... ...

Abstract	Background: Functional interactions between mu- and delta-opioid receptors (MOPr and DOPr, respectively) are implicated in morphine tolerance and dependence. The contribution of DOPr to the conditioned rewarding effects of morphine and the enhanced conditioned response that occurs after repeated morphine administration is unknown. This issue was addressed with the conditioned place preference procedure (CPP). Methods: Rats received home cage injections of saline or morphine (5.0 mg/kg/day x 5 days) before conditioning. For sensitization studies, DOPr antagonists (DOPr1/2: naltrindole, DOPr2: naltriben, DOPr1: 7-benzylidenenaltrexone) were administered before morphine injections. Conditioning sessions (2 morphine; 2 saline) commenced 3 days later. To assess the influence of acute DOPr blockade on the conditioning of morphine reward in naïve animals, 3 morphine and 3 saline conditioning sessions were employed. Antagonists were administered before morphine conditioning sessions. Results: Morphine was ineffective as a conditioning stimulus after two conditioning sessions in naïve rats. However, doses > or = 3.0 mg/kg produced significant CPP in morphine pre-exposed rats, confirming that sensitization develops to the conditioned rewarding effects of morphine. In animals that received morphine pre-exposure with naltrindole or naltriben but not 7-benzylidenenaltrexone, sensitization was prevented. No attenuation of morphine CPP was observed in animals that received DOPr antagonists acutely, before conditioning sessions. Conclusions: These data indicate a critical role of DOPr systems in mediating sensitization to the conditioned rewarding effects of morphine. The efficacy of naltrindole and naltriben in preventing the enhanced response to morphine suggest the specific involvement of DOPr2 in the sensitization process.
MeSH term(s)	Analysis of Variance ; Animals ; Association Learning/drug effects ; Behavior, Animal/drug effects ; Benzylidene Compounds/pharmacology ; Conditioning, Classical/drug effects ; Disease Models, Animal ; Male ; Morphine Dependence/physiopathology ; Naltrexone/analogs & derivatives ; Naltrexone/pharmacology ; Narcotic Antagonists/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptor Cross-Talk/drug effects ; Receptors, Opioid, delta/antagonists & inhibitors ; Receptors, Opioid, mu/drug effects ; Reinforcement (Psychology) ; Statistics, Nonparametric
Chemical Substances	Benzylidene Compounds ; Narcotic Antagonists ; Receptors, Opioid, delta ; Receptors, Opioid, mu ; naltrindole benzofuran (111555-58-9) ; 7-benzylidenenaltrexone (129468-28-6) ; Naltrexone (5S6W795CQM) ; naltrindole (G167Z38QA4)
Language	English
Publishing date	2008-10-31
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2008.09.009
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Article: Effects of acute and repeated administration of salvinorin A on dopamine function in the rat dorsal striatum.

Gehrke, Brenda J / Chefer, Vladimir I / Shippenberg, Toni S

Psychopharmacology

2008 Volume 197, Issue 3, Page(s) 509–517

Abstract: Rationale: Acute systemic administration of salvinorin A, a naturally occurring kappa-opioid receptor (KOPr) agonist, decreases locomotion and striatal dopamine (DA) overflow.: Objectives: Conventional and quantitative microdialysis techniques were ... ...

Abstract	Rationale: Acute systemic administration of salvinorin A, a naturally occurring kappa-opioid receptor (KOPr) agonist, decreases locomotion and striatal dopamine (DA) overflow. Objectives: Conventional and quantitative microdialysis techniques were used to determine whether salvinorin A infusion into the dorsal striatum (DSTR) decreases DA overflow by altering DA uptake or release. The influence of repeated salvinorin A administration on basal DA dynamics and cocaine-evoked alterations in DA overflow and locomotion was also assessed. Materials and methods: Salvinorin A was administered via the dialysis probe (0; 20-200 nM) or via intraperitoneal (i.p.) injection (1.0 or 3.2 mg/kg per day x 5 days). The effects of a challenge dose of cocaine were examined 48 h after repeated salvinorin treatment. Results: Retrodialysis of salvinorin A produced a dose-related, KOPr antagonist reversible, decrease in DA levels. Extracellular DA levels were decreased whereas DA extraction fraction, which provides an estimate of DA uptake, was unaltered. In contrast to its acute administration, repeated salvinorin A administration did not modify dialysate DA levels. Similarly, neither basal extracellular DA levels nor DA uptake was altered. Unlike synthetic KOPr agonists, prior repeated administration of salvinorin A did not attenuate the locomotor activating effects of an acute cocaine (20 mg/kg, i.p.) challenge. However, cocaine-evoked DA overflow was enhanced. Conclusions: These data demonstrate that acute, but not repeated, salvinorin A administration decreases mesostriatal neurotransmission and that activation of DSTR KOPr is sufficient for this effect. Differences in the interaction of salvinorin and synthetic KOPr agonists with cocaine suggest that the pharmacology of these agents may differ.
MeSH term(s)	Animals ; Brain Mapping ; Cocaine/pharmacology ; Corpus Striatum/drug effects ; Corpus Striatum/pathology ; Diterpenes, Clerodane/pharmacology ; Dopamine/metabolism ; Drug Administration Schedule ; Drug Interactions ; Hallucinogens/pharmacology ; Injections, Intraperitoneal ; Male ; Microdialysis ; Motor Activity/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, kappa/agonists
Chemical Substances	Diterpenes, Clerodane ; Hallucinogens ; Receptors, Opioid, kappa ; Cocaine (I5Y540LHVR) ; salvinorin A (T56W91NG6J) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2008-02-02
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-007-1067-6
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Article ; Online: The effects of kappa-opioid receptor ligands on prepulse inhibition and CRF-induced prepulse inhibition deficits in the rat.

Tejeda, Hugo A / Chefer, Vladimir I / Zapata, Agustin / Shippenberg, Toni S

Psychopharmacology

2010 Volume 210, Issue 2, Page(s) 231–240

Abstract: Rationale: Kappa-opioid receptor (KOR) agonists produce dysphoria and psychotomimesis in humans. KORs are enriched in the prefrontal cortex and other brain regions that regulate mood and cognitive function. Dysregulation of the dynorphin/KOR system has ... ...

Abstract	Rationale: Kappa-opioid receptor (KOR) agonists produce dysphoria and psychotomimesis in humans. KORs are enriched in the prefrontal cortex and other brain regions that regulate mood and cognitive function. Dysregulation of the dynorphin/KOR system has been implicated in the pathogenesis of schizophrenia, depression, and bipolar disorder. Prepulse inhibition of the acoustic startle reflex (PPI), a sensorimotor gating process, is disrupted in many psychiatric disorders. Objectives: The present study determined whether KOR ligands alter PPI in rats. Results: Utilizing a range of doses of the synthetic KOR agonists (+/-) U50,488, (-) U50,488, and U69,593 and the naturally occurring KOR agonist, Salvinorin A, we demonstrate that KOR activation does not alter PPI or startle reactivity in rats. Similarly, selective KOR blockade using the long-acting antagonist nor-binaltorphimine (nor-BNI) was without effect. In contrast to KOR ligands, MK-801 and quinpirole produced deficits in PPI. Stress and corticotropin-releasing factor (CRF) decrease PPI levels. The dynorphin/KOR system has been suggested to be a key mediator of various behavioral effects produced by stress and CRF. We therefore examined the contribution of KORs to CRF-induced alterations in PPI. Intracerebroventricular infusion of CRF decreased PPI. Administration of nor-BNI failed to affect the CRF-evoked disruption in PPI. Conclusions: Together, these results provide no evidence of a link between the dynorphin/KOR system and deficits in sensory gating processes. Additional studies, however, examining whether dysregulation of this opioid system contributes to cognitive deficits and other behavioral abnormalities associated with psychiatric disorders are warranted.
MeSH term(s)	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer/pharmacology ; Animals ; Benzeneacetamides/pharmacology ; Corticotropin-Releasing Hormone/pharmacology ; Diterpenes, Clerodane/pharmacology ; Dose-Response Relationship, Drug ; Ligands ; Male ; Naltrexone/analogs & derivatives ; Naltrexone/pharmacology ; Neural Inhibition ; Pyrrolidines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, kappa/agonists ; Receptors, Opioid, kappa/antagonists & inhibitors ; Reflex, Startle/drug effects
Chemical Substances	Benzeneacetamides ; Diterpenes, Clerodane ; Ligands ; Pyrrolidines ; Receptors, Opioid, kappa ; norbinaltorphimine (36OOQ86QM1) ; Naltrexone (5S6W795CQM) ; 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer (67198-13-4) ; Corticotropin-Releasing Hormone (9015-71-8) ; U 69593 (J5S4K6TKTG) ; salvinorin A (T56W91NG6J)
Language	English
Publishing date	2010-03-16
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-010-1799-6
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Article ; Online: Detection and quantification of neurotransmitters in dialysates.

Zapata, Agustin / Chefer, Vladimir I / Shippenberg, Toni S / Denoroy, Luc

Current protocols in neuroscience

2009 Volume Chapter 7, Page(s) Unit 7.4.1–30

Abstract	Sensitive analytical methods are needed for the separation and quantification of neurotransmitters obtained in microdialysate studies. This unit describes methods that permit quantification of nanomolar concentrations of monoamines and their metabolites (high-pressure liquid chromatography electrochemical detection), acetylcholine (HPLC-coupled to an enzyme reactor), and amino acids (HPLC-fluorescence detection; capillary electrophoresis with laser-induced fluorescence detection).
MeSH term(s)	Animals ; Chromatography, High Pressure Liquid/methods ; Chromatography, Micellar Electrokinetic Capillary/methods ; Humans ; Neurotransmitter Agents/analysis
Chemical Substances	Neurotransmitter Agents
Language	English
Publishing date	2009-07-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2179072-3
ISSN	1934-8576 ; 1934-8584
ISSN (online)	1934-8576
ISSN	1934-8584
DOI	10.1002/0471142301.ns0704s48
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Article ; Online: Overview of brain microdialysis.

Chefer, Vladimir I / Thompson, Alexis C / Zapata, Agustin / Shippenberg, Toni S

Current protocols in neuroscience

2009 Volume Chapter 7, Page(s) Unit7.1

Abstract: The technique of microdialysis enables sampling and collecting of small-molecular-weight substances from the interstitial space. It is a widely used method in neuroscience and is one of the few techniques available that permits quantification of ... ...

Abstract	The technique of microdialysis enables sampling and collecting of small-molecular-weight substances from the interstitial space. It is a widely used method in neuroscience and is one of the few techniques available that permits quantification of neurotransmitters, peptides, and hormones in the behaving animal. More recently, it has been used in tissue preparations for quantification of neurotransmitter release. This unit provides a brief review of the history of microdialysis and its general application in the neurosciences. The authors review the theoretical principles underlying the microdialysis process, methods available for estimating extracellular concentration from dialysis samples (i.e., relative recovery), the various factors that affect the estimate of in vivo relative recovery, and the importance of determining in vivo relative recovery to data interpretation. Several areas of special note, including impact of tissue trauma on the interpretation of microdialysis results, are discussed. Step-by-step instructions for the planning and execution of conventional and quantitative microdialysis experiments are provided.
MeSH term(s)	Algorithms ; Animals ; Brain/drug effects ; Brain/metabolism ; Brain Chemistry/drug effects ; Brain Chemistry/physiology ; Brain Injuries/etiology ; Brain Injuries/metabolism ; Humans ; Microdialysis/adverse effects ; Microdialysis/instrumentation ; Microdialysis/methods ; Microelectrodes
Language	English
Publishing date	2009-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2179072-3
ISSN	1934-8576 ; 1934-8584
ISSN (online)	1934-8576
ISSN	1934-8584
DOI	10.1002/0471142301.ns0701s47
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In stock of ZB MED Cologne/Königswinter

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Kategorien

In stock of ZB MED Cologne/Königswinter

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Full text online

More links

Kategorien

Order via subito

Full text online

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Kategorien

Order via subito