Home About us Contact
|
Home About us Contact | ||
|
|
||
Electrophysiological Methods (electrophysiological + methods)
Selected AbstractsLow-level defective processing of non-verbal sounds in dyslexic childrenDYSLEXIA, Issue 2 2009Paulino Uclés Abstract We compared processing of non-verbal auditory stimuli by dyslexic and non-dyslexic children using electrophysiological methods. The study included 39 children (17 with dyslexia plus 22 controls) assessed via frontal, central, parietal, and temporal electrodes. As an extension of previous P300 event-related potential studies, we analysed variations in the power values of 40-Hz oscillations (gamma-band oscillations involved in cognitive processing) during a specific time window in response to the auditory ,oddball' paradigm that entail target (random 2,kHz) and standard (frequent 1,kHz) stimuli. Dyslexic children differed significantly from controls (P<0.001) in the mean power of the wavelet-transformed 40-Hz oscillation in a time interval starting at 25 ms after stimulus onset up to 50 ms. This means defective processing of sounds. Within groups, standard and target tones elicited significantly different power values (P<0.001). Correlations of values between standard and target responses at each electrode position were not significant within either group, although dyslexics showed a lower correlation than controls. Significant differences in the mean power of these oscillations detected at very early stages of auditory processing in dyslexic children and the wide range of mean values reveal impairment in processing non-verbal sounds in dyslexia. Our results also support recent findings using behavioural and electrophysiological methods suggesting that dyslexia is a general auditory deficit instead of a speech-specific deficit. Copyright © 2008 John Wiley & Sons, Ltd. [source] Multi-level analysis of cultural phenomena: The role of ERPs approach to prejudiceJOURNAL FOR THE THEORY OF SOCIAL BEHAVIOUR, Issue 1 2009AGUSTÍN IBÁÑEZ Brain processes and social processes are not as separated as many of our Social Psychology and Neuroscience departments. This paper discusses the potential contribution of social neuroscience to the development of a multi-level, dynamic, and context-sensitive approach to prejudice. Specifically, the authors review research on event related potentials during social bias, stereotypes, and social attitudes measurements, showing that electrophysiological methods are powerful tools for analyzing the temporal fine-dynamics of psychological processes involved in implicit and explicit prejudice. Meta-theoretical implications are drawn regarding the social psychological modeling of social attitudes, and for the integration of social neuroscience into a multi-level account of cultural behavior. [source] Acute and Chronic Ethanol Modulate Dopamine D2-Subtype Receptor Responses in Ventral Tegmental Area GABA NeuronsALCOHOLISM, Issue 5 2009Kimberly H. Ludlow Background:, Ventral tegmental area (VTA) ,-aminobutyric acid (GABA) neurons appear to be critical substrates underlying the acute and chronic effects of ethanol on dopamine (DA) neurotransmission in the mesocorticolimbic system implicated in drug reward. VTA GABA neuron firing rate is reduced by acute ethanol and enhanced by DA via D2 receptor activation. The objective of this study was to evaluate the role of D2 receptors in acute ethanol inhibition of VTA GABA neuron activity, as well as the adaptation of D2 receptors by chronic ethanol consumption. Methods:, Using electrophysiological methods, we evaluated the effects of intraperitoneal ethanol on DA activation of VTA GABA neurons, the effects of DA antagonists on ethanol inhibition of their firing rate, as well as adaptations in firing rate following chronic ethanol consumption. Using single cell quantitative RT-polymerase chain reaction (PCR), we evaluated the expression of VTA GABA neuron D2 receptors in rats consuming ethanol versus pair-fed controls. Results:, In acute ethanol studies, microelectrophoretic activation of VTA GABA neurons by DA was inhibited by acute intraperitoneal ethanol, and intravenous administration of the D2 antagonist eticlopride blocked ethanol suppression of VTA GABA neuron firing rate. In chronic ethanol studies, while there were no signs of withdrawal at 24 hours, or significant adaptation in firing rate or response to acute ethanol, there was a significant down-regulation in the expression of D2 receptors in ethanol-consuming rats versus pair-fed controls. Conclusions:, Inhibition of DA activation of VTA GABA neuron firing rate by ethanol, as well as eticlopride block of ethanol inhibition of VTA GABA neuron firing rate, suggests an interaction between ethanol and DA neurotransmission via D2 receptors, perhaps via enhanced DA release in the VTA subsequent to ethanol inhibition of GABA neurons. Down-regulation of VTA GABA neuron D2 receptors by chronic ethanol might result from persistent DA release onto GABA neurons. [source] Presynaptic modulation of cholinergic and non-cholinergic fast synaptic transmission in the myenteric plexus of guinea pig ileumNEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2004K. J. LePard Abstract, These studies investigated receptors modulating release of mediators of fast excitatory postsynaptic potentials (fEPSPs) in guinea pig ileum myenteric plexus using electrophysiological methods. Fast EPSPs inhibited by >95% by hexamethonium (100 ,mol L,1) were cholinergic; mixed fEPSPs were inhibited <95% by hexamethonium. Non-cholinergic fEPSPs were studied in the presence of hexamethonium. The ,2-adrenergic receptor agonist UK 14304 inhibited cholinergic (maximum inhibition = 76%, EC50 = 18 nmol L,1), mixed (81%, 21 nmol L,1) and non-cholinergic (76%, 44 nmol L,1) fEPSPs equally. The 5-HT1 receptor agonist 5-carboxamidotryptamine inhibited cholinergic, mixed and non-cholinergic fEPSPs equally. Renzapride, increased non-cholinergic (33%) less than mixed (97%, 13 ,mol L,1) fEPSPs. Renzapride inhibited the purely cholinergic fEPSPs (,29%) but potentiated the cholinergic component of mixed fEPSPs (39%). Prucalopride potentiated all fEPSPs equally (30,33%). 5-HT (0.1 ,mol L,1) induced potentiation of cholinergic (75%), mixed (97%) and non-cholinergic (84%) fEPSPs was not statistically different. The potentiating effects of renzapride and 5-HT on fEPSPs were inhibited by the 5-HT4 receptor antagonist, SB 204070 (10 nmol L,1). Renzapride (0.3 ,mol L,1) blocked 5-HT-induced increases in cholinergic fEPSPs. ,2-Adrenergic and 5-HT1 receptors mediate inhibition of transmitter release from cholinergic and mixed terminals. 5-HT and prucalopride, acting at 5-HT4 receptors, facilitate all fEPSPs; renzapride facilitates the cholinergic and non-cholinergic components of mixed fEPSPs but not purely cholinergic fEPSPs. Cholinergic synapses may express few 5-HT4 receptors or a renzapride-insensitive 5-HT4 receptor isoform. [source] Region-specific effects of N,N,-dodecane-1,12-diyl-bis-3-picolinium dibromide on nicotine-induced increase in extracellular dopamine in vivoBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2008S Rahman Background and purpose: Systemic administration of N,N,-dodecane-1,12-diyl-bis-3-picolinium dibromide (bPiDDB), an antagonist of nicotinic acetylcholine receptors (nAChRs) attenuated the nicotine-induced increase in dopamine levels in nucleus accumbens (NAcc). Experimental approach: Using in vivo microdialysis, we investigated the effects of local perfusion of the novel nAChR antagonist bPiDDB into the NAcc or ventral tegmental area (VTA) on increased extracellular dopamine in NAcc, induced by systemic nicotine. We also examined the concentration-dependent effects of bPiDDB on the acetylcholine (ACh)-evoked response of specific recombinant neuronal nAChR subtypes expressed in Xenopus oocytes, using electrophysiological methods. Key results: Nicotine (0.4 mg kg,1, s.c.) increased extracellular dopamine in NAcc, which was attenuated by intra-VTA perfusion of mecamylamine (100 ,M). Intra-VTA perfusion of bPiDDB (1 and 10 ,M) reduced nicotine-induced increases in extracellular dopamine in NAcc. In contrast, intra-NAcc perfusion of bPiDDB (1 or 10 ,M) failed to alter the nicotine-induced increase in dopamine in NAcc. Intra-VTA perfusion of bPiDDB alone did not alter basal dopamine levels, compared to control, nor the increased dopamine in NAcc following amphetamine (0.5 mg kg,1, s.c.). Using Xenopus oocytes, bPiDDB (0.01,100 ,M) inhibited the response to ACh on specific combinations of rat neuronal nAChR subunits, with highest potency at ,3,4,3 and lowest potency at ,6/3,2,3. Conclusions and implications: bPiDDB-Sensitive nAChRs involved in regulating nicotine-induced dopamine release are located in the VTA, rather than in the NAcc. As bPiDDB has properties different from the prototypical nAChR antagonist mecamylamine, further development may lead to novel nAChR antagonists for the treatment of tobacco dependence. British Journal of Pharmacology (2008) 153, 792,804; doi:10.1038/sj.bjp.0707612; published online 3 December 2007 [source] | |||||||||||||