Neuroscience
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This study investigates the role of phonology in reading logographic Chinese. Specifically, whether phonological information is obligatorily activated in reading Chinese two-character compounds was examined using the masked-priming paradigm with event-related potential (ERP) recordings. Twenty-two native Cantonese Chinese speakers participated in a lexical decision experiment. ⋯ In addition, attenuation in ERP amplitudes was found in the Semantic-related condition in the window of 250-500 ms (N400). However, no significant results (neither behavioral nor ERP) were found in the Syllable-related condition. These results suggest that phonological activation is not mandatory and the role of phonology is minimal at best in reading Chinese two-character compounds.
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Multisensory integration has been widely studied in neurons of the mammalian superior colliculus (SC). This has led to the description of various determinants of multisensory integration, including those based on stimulus- and neuron-specific factors. The most widely characterized of these illustrate the importance of the spatial and temporal relationships of the paired stimuli as well as their relative effectiveness in eliciting a response in determining the final integrated output. ⋯ The results show that neuronal responsiveness changes dramatically with changes in stimulus location - highlighting a marked heterogeneity in the spatial receptive fields of SC neurons. More importantly, this receptive field heterogeneity played a major role in the integrative product exhibited by stimulus pairings, such that pairings at weakly responsive locations of the receptive fields resulted in the largest multisensory interactions. Together these results provide greater insight into the interrelationship of the factors underlying multisensory integration in SC neurons, and may have important mechanistic implications for multisensory integration and the role it plays in shaping SC-mediated behaviors.
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Allotetrahydrodeoxycorticosterone (THDOC) belongs to a class of pregnane neurosteroidal compounds that enhance brain inhibition by interacting directly with GABAA signaling, mainly through an increase in tonic inhibitory current. Here, we addressed the role of THDOC in the modulation of interictal- and ictal-like activity and associated high-frequency oscillations (HFOs, 80-500 Hz; ripples: 80-200 Hz, fast ripples: 250-500 Hz) recorded in vitro in the rat piriform cortex, a highly excitable brain structure that is implicated in seizure generation and maintenance. ⋯ Our results indicate that THDOC can modulate epileptiform synchronization in the piriform cortex presumably by potentiating GABAA receptor-mediated signaling. This evidence supports the view that neurosteroids regulate neuronal excitability and thus control the occurrence of seizures.
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We investigated in this study the pharmacological properties of AC-3933 (5-(3-methoxyphenyl)-3-(5-methyl-1,2,4-oxadiazol-3-yl)-1,6-naphthyridin-2(1H)-one), a novel benzodiazepine receptor (BzR) partial inverse agonist. AC-3933 potently inhibited [3H]-flumazenil binding to rat whole brain membrane with a Ki value of 5.15 ± 0.39 nM and a GABA ratio of 0.84 ± 0.03. AC-3933 exhibited almost no affinity for the other receptors, transporters and ion channels used in this study. ⋯ AC-3933 (0.1-10 μM) significantly enhanced KCl-evoked acetylcholine (ACh) release from rat hippocampal slices in a concentration-dependent manner. Moreover, in vivo brain microdialysis showed that intragastric administration of AC-3933 at the dose of 10 mg/kg significantly increased extracellular ACh levels in the hippocampus of freely moving rats (area under the curve (AUC₀₋₂ h) of ACh level; 288.3% of baseline). These results indicate that AC-3933, a potent and selective BzR inverse agonist with low intrinsic activity, might be useful in the treatment of cognitive disorders associated with degeneration of the cholinergic system.
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One of the major consequences of stroke is brain injury caused by glutamate-mediated excitotoxicity. Glutamate-mediated excitatory activities are partially driven by β2-containing nicotinic acetylcholine receptors (β2-nAChRs). In examining the role of β2-nAChRs in cerebral ischemic injury, excitotoxicity and stroke outcome, we found that deficiency of β2-nAChRs attenuated brain infarction and neurological deficit at 24 and 72 h after transient middle cerebral artery occlusion (MCAO). ⋯ Pharmacologic pretreatment with a selective β2-nAChRs antagonist reduced brain infarction, neurological deficit, and MCAO-induced glutamate release. These findings suggest that deficiency of β2-nAChRs, also achievable by pharmacological blockade, can decrease brain infarction and improve the neurological status in ischemic stroke. The improved outcome is associated with reduced extracellular glutamate level and lower excitatory inputs into ischemic neurons, suggesting a reduction of glutamate-mediated excitotoxicity in the mechanisms of neuroprotection.