Cocaine acute "binge" administration results in altered thalamocortical interactions in mice

Mostrar otras versiones (1)

Background: Abnormalities in both thalamic and cortical areas have been reported in human cocaine addicts with noninvasive functional magnetic resonance imaging. Given the substantial involvement of the thalamocortical system in sensory processing and perception, we defined electrophysiology-based p...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autor principal: Urbano, F.J
Otros Autores: Bisagno, V., Wikinski, S.I, Uchitel, O.D, Llinás, R.R
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: Elsevier USA 2009
Acceso en línea:Registro en Scopus
DOI
Handle
Registro en la Biblioteca Digital
Aporte de:Registro referencial: Solicitar el recurso aquí
Biblioteca Central Dr. Luis F. Leloir (FCEN) de Universidad de Buenos Aires
LEADER 24545caa a22018977a 4500
001 PAPER-23061
003 AR-BaUEN
005 20230518205442.0
008 190411s2009 xx ||||fo|||| 00| 0 eng|d
024 7 |2 scopus  |a 2-s2.0-74049107863 
024 7 |2 cas  |a 2 amino 5 phosphonovaleric acid, 76726-92-6; 6 cyano 7 nitro 2,3 quinoxalinedione, 115066-14-3; cesium, 7440-46-2; cocaine, 50-36-2, 53-21-4, 5937-29-1; picrotoxin, 124-87-8; potassium ion, 24203-36-9; tetrodotoxin, 4368-28-9, 4664-41-9; Cocaine, 50-36-2; Receptors, GABA-A 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a BIPCB 
100 1 |a Urbano, F.J. 
245 1 0 |a Cocaine acute "binge" administration results in altered thalamocortical interactions in mice 
260 |b Elsevier USA  |c 2009 
270 1 0 |m Urbano, F. J.; LFBM, IFIBYNE, UBA-CONICET, Intendente Guiraldes 2670, C1428BGA Buenos. Aires, Argentina; email: fjurbano@fbmc.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
504 |a Aharonovich, E., Nunes, E., Hasin, D., Cognitive impairment, retention and abstinence among cocaine abusers in cognitive- behavioral treatment (2003) Drug Alcohol Depend, 71, pp. 207-211 
504 |a Tomasi, D., Goldstein, R.Z., Telang, F., Maloney, T., Alia-Klein, N., Caparelli, E.C., Volkow, N.D., Thalamo-cortical dysfunction in cocaine abusers: Implications in attention and perception (2007) Psychiatry Res, 155, pp. 189-201 
504 |a Jones, E.G., Principles of thalamic organization (2007) The Thalamus, pp. 87-165. , Jones EG, editor. 2nd ed. Cambridge: Cambridge University Press 
504 |a Llinás, R.R., Paré, D., Of dreaming and wakefulness (1991) Neuroscience, 44, pp. 521-535 
504 |a Llinás, R., Ribary, U., Coherent 40-Hz oscillation characterizes dream state in humans (1993) Proc Natl Acad Sci U S A, 90, pp. 2078-2081 
504 |a Llinás, R., Ribary, U., Contreras, D., Pedroarena, C., The neuronal basis for consciousness (1998) Philos Trans R Soc Lond B Biol Sci, 353, pp. 1841-1849 
504 |a Steriade, M., Jones, E.G., McCormik, D.A., (1997) The Thalamus, Vol 1. Organization and Function, , Amsterdam: Elsevier 
504 |a Steriade, M., Llinás, R.R., The functional states of the thalamus and the associated neuronal interplay (1988) Physiol Rev, 68, pp. 649-742 
504 |a Zhu, J.J., Connors, B.W., Intrinsic firing patterns and whisker-evoked synaptic responses of neurons in the rat barrel cortex (1999) J Neurophysiol, 81, pp. 1171-1183 
504 |a Peden, D.R., Petitjean, C.M., Herd, M.B., Durakoglugil, M.S., Rosahl, T.W., Wafford, K., Developmental maturation of synaptic and extrasynaptic GABAA receptors in mouse thalamic ventrobasal neurons (2008) J Physiol Lond, 586, pp. 965-987 
504 |a Rutter, J.J., Baumann, M.H., Waterhouse, B.D., Systemically administered cocaine alters stimulus-evoked responses of thalamic somatosensory neurons to perithreshold vibrissae stimulation (1998) Brain Res, 798, pp. 7-17 
504 |a Rutter, J.J., Devilbiss, D.M., Waterhouse, B.D., Effects of systemically administered cocaine on sensory responses to peri-threshold vibrissae stimulation: Individual cells, ensemble activity, and animal behaviour (2005) Eur J Neurosci, 22, pp. 3205-3216 
504 |a Jeanmonod, D., Schulman, J., Ramirez, R., Cancro, R., Lanz, M., Morel, A., Neuropsychiatric thalamocortical dysrhythmia: Surgical implications (2003) Neurosurg Clin North Am, 14, pp. 251-265 
504 |a Llinás, R.R., Ribary, U., Jeanmonod, D., Kronberg, E., Mitra, P.P., Thalamocortical dysrhythmia: A neurological and neuropsychiatric syndrome characterized by magnetoencephalography (1999) Proc Natl Acad Sci U S A, 96, pp. 15222-15227 
504 |a Llinás, R., Urbano, F.J., Leznik, E., Ramírez, R.R., Van Marle, H.J., Rhythmic and dysrhythmic thalamocortical dynamics: GABA systems and the edge effect (2005) Trends Neurosci, 28, pp. 325-333 
504 |a Schramm-Sapyta, N.L., Pratt, A.R., Winder, D.G., Effects of periadolescent versus adult cocaine exposure on cocaine conditioned place preference and motor sensitization in mice (2004) Psychopharmacology, 173, pp. 41-48 
504 |a Schlussman, S.D., Zhang, Y., Kane, S., Stewart, C.L., Ho, A., Kreek, M.J., Locomotion, stereotypy, and dopamine D1 receptors after chronic "binge" cocaine in C57BL/6J and 129/joules mice (2003) Pharmacol Biochem Behav, 75, pp. 123-131 
504 |a Riespangler, R., Unterwald, E.M., Kreek, M.J., "Binge" cocaine administration induces a sustained increase of prodynorphin mRNA in rat caudate-putamen (1993) Brain Res Mol Brain Res, 19, pp. 323-327 
504 |a Zhou, Y., Spangler, R., Yuferov, V.P., Schlussmann, S.D., Ho, A., Kreek, M.J., Effects of selective D1- or D2-like dopamine receptor antagonists with acute "binge" pattern cocaine on corticotrophin-releasing hormone and proopiomelanocortin mRNA levels in the hypothalamus (2004) Mol Brain Res, 130, pp. 61-67 
504 |a Isoardi, N.A., Bertotto, M.E., Martijena, I.D., Molina, V.A., Carrer, H.F., Lack of feedback inhibition on rat basolateral amygdala following stress or withdrawal from sedative-hypnotic drugs (2007) Eur J Neurosci, 26, pp. 1036-1044 
504 |a Llinás, R.R., Choi, S., Urbano, F.J., Shin, H.S., Gamma-band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice (2007) Proc Natl Acad Sci U S A, 104, pp. 17819-17824 
504 |a Alper, K.R., Chabot, R.J., Kim, A.H., Prichep, L.S., John, E.R., Quantitative EEG correlates of crack cocaine dependence (1990) Psychiatry Res Neuroimaging, 35, pp. 95-105 
504 |a Prichep, L.S., Alper, K.R., Kowalik, S.C., Vaysblat, L.S., Merkin, H.A., Tom, M.L., Prediction of treatment outcome in cocaine dependent males using quantitative EEG (1999) Drug Alcohol Depend, 54, pp. 35-43 
504 |a Reid, M.S., Flammino, F., Howard, B., Nilsen, D., Prichep, L.S., Cocaine cue versus cocaine dosing in humans: Evidence for distinct neurophysiological response profiles (2008) Pharmacol Biochem Behav, 91, pp. 155-164 
504 |a Rausell, E., Bickford, L., Manger, P.R., Woods, T.M., Jones, E.G., Extensive divergence and convergence in the thalamocortical projection to monkey somatosensory cortex (1998) J Neurosci, 18, pp. 4216-4232 
504 |a Pedroarena, C., Llinas, R., Dendritic calcium conductances generate high-frequency oscillation in thalamocortical neurons (1997) Proc Natl Acad Sci U S A, 94, pp. 724-728 
504 |a Bauer, L.O., Kranzler, H.R., Electroencephalographic activity and mood in cocaine-dependent outpatients: Effects of cocaine cue exposure (1994) Biol Psychiatry, 36, pp. 189-197 
504 |a Volkow, N.D., Mullani, N., Gould, K.L., Adler, S., Krajewski, K., Cerebral blood flow in chronic cocaine users: A study with positron emission tomography (1988) Br J Psychiatry, 152, pp. 641-648 
504 |a Pascual-Leone, A., Dhuna, A., Anderson, D.C., Cerebral atrophy in habitual cocaine abusers: A planimetric CT study (1991) Neurology, 41, pp. 34-38 
504 |a Liu, X.B., Warren, R.A., Jones, E.G., Synaptic distribution of afferents from the reticular nucleus in ventroposterior nucleus of cat thalamus (1995) J Comp Neurol, 352, pp. 187-202 
504 |a Wang, S., Bickford, M.E., Van Horn, S.C., Erisir, A., Godwin, D.W., Sherman, S.M., Synaptic targets of thalamic reticular nucleus terminals in the visual thalamus of the cat (2001) J Comp Neurol, 440, pp. 321-341 
504 |a Warren, R.A., Agmon, A., Jones, E.G., Oscillatory synaptic interactions between ventroposterior and reticular neurons in mouse thalamus in vitro (1994) J Neurophysiol, 72, pp. 1993-2003 
504 |a Jahnsen, H., Llinás, R., Electrophysiological properties of guinea-pig thalamic neurones: An in vitro study (1984) J Physiol Lond, 349, pp. 205-226 
504 |a Jahnsen, H., Llinas, R., Ionic basis for the electroresponsiveness and oscillatory properties of guinea-pig thalamic neurones in vitro (1984) Journal of Physiology, VOL. 349, pp. 227-247 
504 |a Coulter, D.A., Huguenard, J.R., Prince, D.A., Calcium currents in rat thalamocortical relay neurones: Kinetic properties of the transient, lowthreshold current (1989) J Physiol Lond, 414, pp. 587-604 
504 |a Huguenard, J.R., Prince, D.A., A novel T-type current underlies prolonged Ca(2+)-dependent burst firing in GABAergic neurons of rat thalamic reticular nucleus (1992) J Neurosci, 12, pp. 3804-3817 
504 |a Llinás, R., Geijo-Barrientos, E., In vitro studies of mammalian thalamic and reticularis thalami neurons (1988) Cellular Thalamic Mechanisms, pp. 23-33. , Bentivoglio M, Spreafico R, editors. Amsterdam: Elsevier/Holland 
504 |a Benuck, M., Lajtha, A., Reith, M.E., Pharmacokinetics of systemically administered cocaine and locomotor stimulation in mice (1987) J Pharmacol Exp Ther, 243, pp. 144-149 
504 |a Wilson, M.C., Holbrook, J.M., Actometric effects of intravenous cocaine in rats (1979) Arch Int Pharmacodyn Ther, 238, pp. 244-256 
504 |a Wise, R.A., Ma, B., A psychomotor stimulant theory of addiction (1987) Psychol Rev, 94, pp. 469-492 
504 |a Ritz, M.C., Lamb, R.J., Goldberg, S.R., Kuhar, M.J., Cocaine receptors on dopamine transporters are related to self-administration of cocaine (1987) Science, 237, pp. 1219-1223 
504 |a Howes, S.R., Dalley, J.W., Ch, M., Robbins, T.W., Everitt, B.J., Leftward shift in the acquisition of cocaine self-administration in isolationreared rats: Relationship to extracellular levels of dopamine, serotonin and glutamate in the nucleus accumbens and amygdala-striatal FOS expression (2000) Psychopharmacology (Berl), 151, pp. 55-63 
504 |a Glowinski, J., Axelrod, J., Effects of drugs on the disposition of H-3-norepinephrine in the rat brain (1966) Pharmacol Rev, 18, pp. 775-785 
504 |a Ross, S.B., Renyi, A.L., Inhibition of the uptake of tritiated 5-hydroxytryptamine in brain tissue (1969) Eur J Pharmacol, 7, pp. 270-277 
504 |a McCormick, D.A., Bal, T., Sleep and arousal: Thalamocortical mechanisms (1997) Annu Rev Neurosci, 20, pp. 185-215 
504 |a McCormick, D.A., Feeser, H.R., Functional implications of burst firing and single spike activity in lateral geniculate relay neurons (1990) Neuroscience, 39, pp. 103-113 
504 |a Llinás, R.R., Steriade, M., Bursting of thalamic neurons and states of vigilance (2006) J Neurophysiol, 95, pp. 3297-3308 
504 |a McCormick, D.A., Wang, Z., Serotonin and noradrenaline excite GABAergic neurones of the guinea-pig and cat nucleus reticularis thalami (1991) J Physiol (Lond), 442, pp. 235-255 
504 |a Pape, H.C., McCormick, D.A., Noradrenaline and serotonin selectively modulate thalamic burst firing by enhancing a hyperpolarizationactivated cation current (1989) Nature, 340, pp. 715-718 
504 |a McCormick, D.A., Pape, H.C., Noradrenergic and serotonergic modulation of a hyperpolarization- activated cation current in thalamic relay neurones (1990) J Physiol (Lond), 431, pp. 319-342 
504 |a Talley, E.M., Cribbs, L.L., Lee, J.-H., Daud, A., Perez-Reyes, E., Bayliss, D.A., Differential distribution of three members of a gene family encoding low voltage-activated (T-type) calcium channels (1999) J Neurosci, 19, pp. 1895-1911 
504 |a Berger, A.J., Takahashi, T., Serotonin enhances a low-voltage-activated calcium current in rat spinal motoneurons (1990) J Neurosci, 10, pp. 1922-1928 
504 |a Fraser, D.D., MacVicar, B.A., Low-threshold transient calcium current in rat hippocampal lacunosum-moleculare interneurons: Kinetics and modulation by neurotransmitters (1991) J Neurosci, 11, pp. 2812-2820 
504 |a Fisher, R., Johnston, D., Differential modulation of single voltage gated calcium channels by cholinergic and adrenergic agonists in adult hippocampal neurons (1990) J Neurophysiol, 64, pp. 1291-1302 
520 3 |a Background: Abnormalities in both thalamic and cortical areas have been reported in human cocaine addicts with noninvasive functional magnetic resonance imaging. Given the substantial involvement of the thalamocortical system in sensory processing and perception, we defined electrophysiology-based protocols to attempt a characterization of cocaine effects on thalamocortical circuits. Methods: Thalamocortical function was studied in vivo and in vitro in mice after cocaine "binge" administration. In vivo awake electroencephalography (EEG) was implemented in mice injected with saline, 1 hour or 24 hours after the last cocaine "binge" injection. In vitro current- and voltage-clamp whole-cell patch-clamp recordings were performed from slices including thalamic relay ventrobasal (VB) neurons. Results: In vivo EEG recordings after cocaine "binge" administration showed a significant increment, compared with saline, in low frequencies while observing no changes in high-frequency γ activity. In vitro patch recordings from VB neurons after cocaine "binge" administration showed low threshold spikes activation at more negative membrane potentials and increments in both lh and low voltage activated T-type calcium currents. Also, a 10-mV negative shift on threshold activation level of T-type current and a remarkable increment in both frequency and amplitudes of γ-aminobutyric acid-A-mediated minis were observed. Conclusions: Our data indicate that thalamocortical dysfunctions observed in cocaine abusers might be due to two distinct but additive events: 1) increased low frequency oscillatory thalamocortical activity, and 2) overinhibition of VB neurons that can abnormally "lock" the whole thalamocortical system at low frequencies. © 2009 Society of Biological Psychiatry.  |l eng 
536 |a Detalles de la financiación: Agencia Nacional de Promoción Científica y Tecnológica 
536 |a Detalles de la financiación: Secretaría de Ciencia y Técnica, Universidad de Buenos Aires, 171, X223 
536 |a Detalles de la financiación: Wellcome Trust, 068941/Z/02/Z 
536 |a Detalles de la financiación: 6220 
536 |a Detalles de la financiación: Fondo para la Investigación Científica y Tecnológica 
536 |a Detalles de la financiación: Agencia Nacional de Promoción Científica y Tecnológica, PICT 2007-01009, BID 1728 OC.AR 
536 |a Detalles de la financiación: Thalamic ventrobasal nucleus (VB) is known to be densely innervated by GABAergic terminals from reticular neurons ( 8,30,31 ) that exert a finely regulated inhibitory control of all relay thalamic neurons through GABA receptors ( 32 ). Both reticular and VB neurons have T-type calcium currents mediated LTS ( 33–36 ). The T-type currents described for VB neurons activate at more hyperpolarized potentials than their reticular neuron counterpart, whereas T channels from the latter have a longer open probability duration generating longer action potential burst ( 36,37 ). It was suggested that such difference in threshold for T-type currents would prevent thalamic nuclei (and therefore the whole thalamocortical system) from being “locked” at GABA-A–driven low-frequency interactions. The increased activation of T-type channels on VB neurons at resting membrane potentials would generate abnormally prominent low-frequency excitatory inputs to the reticular nucleus that in turn would enhance GABAergic feed-back transmission from reticular to VB neurons, as shown in this study. Indeed, bath-applied octanol (50 μmol/L) significantly reduced cocaine “binge”-induced GABAergic minis frequency (data not shown), thus suggesting that the frequency enhancement on VB's GABA-A minis shown here resulted from higher T-currents–mediated LTS bursts at reticular neuron terminals. Although cocaine half-life is relatively short, 30–45 min ( 38 ), cocaine accumulation in plasma/brain is expected after a cocaine “binge” administration (because the three cocaine injections were administered <2 half-lives apart). Cocaine increase would ultimately result in the inhibition of monoamine transporters (dopamine transporter, serotonin transporter, and norepinephrine transporter), elevating synaptic levels of dopamine ( 39–42 ), noradrenaline, and serotonin ( 42–44 ). Indeed, drastic increments in extracellular serotonin and noradrenaline levels on VB nucleus have been reported after cocaine injection ( 11 ). Here we showed persistent changes in GABA-A minis amplitude and frequency values 24 hours after last cocaine “binge” injection, suggesting that cocaine effects on VB/reticular neurons might be related to long-lasting activation of intracellular phosphorylation pathways, triggered by the interaction of monoamines with their pre- and/or postsynaptic receptors. VB neurons are capable of integrating a variety of neuromodulators ( 45 ) that can ultimately affect their glutamatergic and/or GABAergic inputs. The rapid transitions of VB between low ( 33,34,46 ) and high frequency ( 26 ) are modulated by a variety of neurotransmitters ( 8,47 ). Serotonin was reported to have direct excitatory action on GABAergic neurons in the thalamic reticular nucleus ( 48 ) and mediates an enhancement of I h -currents present on thalamic specific neurons ( 49,50 ). Our results suggest that cocaine “binge”-induced effects on VB and reticular neurons might be mediated by serotonin. Accordingly, serotonin could be reducing VB neurons input resistance while incrementing I h -current density and overexciting reticular nucleus to induce the GABA-A–mediated increased inhibition of VB nucleus. Concerning the differential distribution of T-type (Ca v 3) calcium channels among thalamic nuclei, it is widely accepted that Ca V 3.1, nickel-resistant T-channels are present in VB neurons, whereas Ca V 3.2, nickel-sensitive T-channels are all present on reticular neurons ( 51 ). Moreover, serotonin is known to increase Ca V 3.1, nickel-resistant T-channels–mediated currents present in spinal motoneurons (approximately 65%; in slices) ( 52 ) and in hippocampal interneurons (approximately 60%) ( 53 ). Interestingly, in hippocampal interneurons serotonin shifts (approximately 5 mV) the I–V curve of Ca V 3.1 channels toward more hyperpolarizing values ( 53 ). By contrast, adrenergic agonists had no effect on T-channels in CA3 pyramidal neurons from adult guinea pigs ( 54 ). Importantly, CA3 pyramids contain all Ca V 3.1, 3.2, and 3.3 subunits ( 51 ), strongly suggesting that adrenergic receptors do not affect neuronal T channels. Therefore, cocaine “binge”-dependent increments in T-channels currents density as well as I–V shift toward hyperpolarizing values observed in this study agrees with serotonin-mediated enhancement Ca V 3.1, T-channels that might be present on both presynaptic terminals from reticular neurons and postsynaptic VB neurons. If sustained in time, such increment would lead thalamocortical circuitry to a self-destruction due to deleterious effects of the persistent calcium entry. As for the basic mechanisms underneath thalamocortical dysrhythmia syndromes, it has been proposed that increased low-frequency oscillatory activity of reticular GABAergic neurons, enhanced by an excessive hyperpolarization through overactivation of thalamic relay T-type calcium currents, would result in abnormal interactions between low and high frequencies during awake states ( 13–15 ). As far as we know, this is the first study that shows the existence of both thalamic GABAergic overactivation and an increase in T-type calcium currents density, suggesting that acute cocaine administration induces a thalamocortical dysrhythmia-like state. In conclusion, data presented here illustrated two distinct but additive cocaine mediated events: 1) increase in the low-threshold calcium and I h conductance of cortical projecting VB neurons, leading to a direct increase in low-frequency thalamocortical oscillations; and 2) GABAergic-mediated, low-rhythm overinhibition due to the excessive activation of both I h and T-type currents in reticular thalamic neurons. The interaction among both phenomena would “lock” the whole thalamocortical system at low frequencies, ultimately inducing a thalamocortical dysrhythmia-like state. We report no conflict of interest related directly or indirectly to this work. Dr. Bisagno has been authorized to study drug abuse substances in animal models by A.N.M.A.T. (Ministerio de Salud, Argentina). We would like to thank Maria Eugenia Martin for excellent technical assistance. This work was supported by Grants from: FONCYT Agencia Nacional de Promoción Científica y Tecnológica, BID 1728 OC.AR. PICT 2007-01009 (FJU), Wellcome Trust, Grant #068941/Z/02/Z; ANCyT; Grant #6220; UBACYT; Grant #X171, and X223; FONCYT, Agencia Nacional de Promoción Científica y Tecnológica, BID 1728 OC.AR. PICT2005 #32113 and #13367; and BID 1728 OC.AR. PICT 2006 #199 (ODU), National Institutes of Health NS13742 (RRL) and PICT 31,953 (ANPCyT), PIP 5870 (CONICET), and UBACYT M073 (SIW). 
593 |a Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY, United States 
593 |a Laboratorio de Fisiología y Biología Molecular (LFBM), Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), Ciudad Universitaria, Buenos Aires, Argentina 
593 |a Instituto de Investigaciones Farmacológicas (ININFA-UBACONICET), Buenos Aires, Argentina 
690 1 0 |a COCAINE 
690 1 0 |a GABA-A RECEPTORS 
690 1 0 |a MICE 
690 1 0 |a T-TYPE CALCIUM CHANNELS 
690 1 0 |a THALAMOCORTICAL DYSRHYTHMIA 
690 1 0 |a 2 AMINO 5 PHOSPHONOVALERIC ACID 
690 1 0 |a 4 AMINOBUTYRIC ACID A RECEPTOR 
690 1 0 |a 6 CYANO 7 NITRO 2,3 QUINOXALINEDIONE 
690 1 0 |a AMPA RECEPTOR ANTAGONIST 
690 1 0 |a CALCIUM CHANNEL T TYPE 
690 1 0 |a CESIUM 
690 1 0 |a COCAINE 
690 1 0 |a KAINIC ACID RECEPTOR ANTAGONIST 
690 1 0 |a N METHYL DEXTRO ASPARTIC ACID RECEPTOR BLOCKING AGENT 
690 1 0 |a PICROTOXIN 
690 1 0 |a POTASSIUM ION 
690 1 0 |a TETRODOTOXIN 
690 1 0 |a 4 AMINOBUTYRIC ACID A RECEPTOR 
690 1 0 |a COCAINE 
690 1 0 |a ANIMAL CELL 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL MODEL 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a BRAIN FUNCTION 
690 1 0 |a BRAIN SLICE 
690 1 0 |a COCAINE DEPENDENCE 
690 1 0 |a DRUG ABUSE 
690 1 0 |a ELECTROENCEPHALOGRAPHY 
690 1 0 |a IN VITRO STUDY 
690 1 0 |a IN VIVO STUDY 
690 1 0 |a MOUSE 
690 1 0 |a NEUROTRANSMITTER RELEASE 
690 1 0 |a NONHUMAN 
690 1 0 |a PATCH CLAMP 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a THALAMOCORTICAL TRACT 
690 1 0 |a VOLTAGE CLAMP 
690 1 0 |a ANIMAL 
690 1 0 |a BRAIN CORTEX 
690 1 0 |a C57BL MOUSE 
690 1 0 |a CELL MEMBRANE POTENTIAL 
690 1 0 |a DRUG ANTAGONISM 
690 1 0 |a DRUG EFFECT 
690 1 0 |a DRUG INTERACTION 
690 1 0 |a DRUG POTENTIATION 
690 1 0 |a METHODOLOGY 
690 1 0 |a NERVE CELL 
690 1 0 |a NERVE CELL INHIBITION 
690 1 0 |a NERVE TRACT 
690 1 0 |a PHYSIOLOGY 
690 1 0 |a THALAMUS 
690 1 0 |a ANIMALS 
690 1 0 |a CEREBRAL CORTEX 
690 1 0 |a COCAINE 
690 1 0 |a DRUG INTERACTIONS 
690 1 0 |a ELECTROENCEPHALOGRAPHY 
690 1 0 |a MEMBRANE POTENTIALS 
690 1 0 |a MICE 
690 1 0 |a MICE, INBRED C57BL 
690 1 0 |a NEURAL INHIBITION 
690 1 0 |a NEURAL PATHWAYS 
690 1 0 |a NEURONS 
690 1 0 |a PATCH-CLAMP TECHNIQUES 
690 1 0 |a RECEPTORS, GABA-A 
690 1 0 |a THALAMUS 
700 1 |a Bisagno, V. 
700 1 |a Wikinski, S.I. 
700 1 |a Uchitel, O.D. 
700 1 |a Llinás, R.R. 
773 0 |d Elsevier USA, 2009  |g v. 66  |h pp. 769-776  |k n. 8  |p Biol. Psychiatry  |x 00063223  |w (AR-BaUEN)CENRE-3966  |t Biological Psychiatry 
856 4 1 |u https://www.scopus.com/inward/record.uri?eid=2-s2.0-74049107863&doi=10.1016%2fj.biopsych.2009.04.026&partnerID=40&md5=f8b673504c9095df0adda3f56d5abe94  |y Registro en Scopus 
856 4 0 |u https://doi.org/10.1016/j.biopsych.2009.04.026  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_00063223_v66_n8_p769_Urbano  |y Handle 
856 4 0 |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00063223_v66_n8_p769_Urbano  |y Registro en la Biblioteca Digital 
961 |a paper_00063223_v66_n8_p769_Urbano  |b paper  |c PE 
962 |a info:eu-repo/semantics/article  |a info:ar-repo/semantics/artículo  |b info:eu-repo/semantics/publishedVersion 
999 |c 84014 

Ejemplares similares