Neuroscience
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Face recognition is one of the most important cognitive functions for humans in social activities. The ability will be negatively affected when the face images deteriorate. However, the neural process of extracting facial information under challenging conditions is still poorly understood. ⋯ For each subject, the behavioral performance and magnitudes of the HGP for the face-specific sites significantly both fit a sigmoid function and showed similar changes. Additionally, the curve profile of the average HGP magnitude across the face-specific sites was almost equal to the average behavior curve; the former could precisely track the behavioral performance. In general, these results suggest that the HGP in the FG is closely related to the performance of face image recognition.
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Evidence is mounting that emotional conflict is mainly resolved by the rostral anterior cingulate inhibiting the processing of emotional distractors. However, this theory has not been verified from the perspective of memory retrieval. This experiment aimed to explore the offline effect of emotional conflict processing on memory retrieval. ⋯ Besides, for LPN (700-900 ms), the old/new effects of the incongruent condition are greater than the congruent condition. The results prove that the encoding phase's emotional congruency factor has a regulatory effect on the retrieval phase's early familiarity processing and evaluation of retrieval outcomes. Our data confirm the inhibitory effect of emotional conflict control on memory retrieval and support the emotional conflict control mechanism found in previous studies.
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Localization of sound sources in the environment requires neurons that extract interaural timing differences (ITD) in low-frequency hearing animals from fast and precisely timed converging inputs from both ears. In mammals, this is accomplished by neurons in the medial superior olive (MSO). MSO neurons receive converging excitatory input from both the ipsilateral and contralateral cochlear nuclei and glycinergic, inhibitory input by way of interneurons in the medial and lateral nuclei of the trapezoid body (MNTB and LNTB, respectively). ⋯ Herein, we utilized neuron reconstructions and immunohistochemistry to investigate the distribution of glutamatergic and glycinergic inputs onto human MSO neurons. Our results indicate that human MSO neurons have simple, symmetric dendrites and that glycinergic inputs outnumber glutamatergic inputs on MSO cell bodies and proximal dendrites. Together these results suggest that the human MSO utilizes similar circuitry to other mammals with excellent low-frequency hearing.
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Sensory disturbance in the orofacial region owing to trigeminal nerve injury is caused by dental treatment or accident. Commercially available therapeutics are ineffective for the treatment of sensory disturbance. Additionally, the therapeutic effects of rapamycin, an allosteric inhibitor of mammalian target of rapamycin (mTOR), which negatively regulates autophagy, on the sensory disturbance are not fully investigated. ⋯ Rapamycin administration facilitated axon regeneration after IANX and increased the number of brain-derived neurotrophic factor positive neurons in the trigeminal ganglion. Thus, recovery from sensory disturbance in the lower lip caused by IANX was markedly facilitated by rapamycin. These findings suggest that rapamycin administration is a promising treatment for the sensory disturbance caused by IANX.
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Although ionotropic glutamate receptors and nicotinic receptors for acetylcholine (ACh) have usually been studied separately, they are often co-localized and functionally inter-dependent. The objective of this review is to survey the evidence for interactions between the two receptor families and the mechanisms underlying them. These include the mutual regulation of subunit expression, which change the NMDA:AMPA response balance, and the existence of multi-functional receptor complexes which make it difficult to distinguish between individual receptor sites, especially in vivo. ⋯ In addition, ACh and glutamate are released as CNS co-transmitters, including 'cholinergic' synapses onto spinal Renshaw cells. It is concluded that ACh should be viewed primarily as a modulator of glutamatergic neurotransmission by regulating the release of glutamate presynaptically, and the location, subunit composition, subtype balance and sensitivity of glutamate receptors, and not primarily as a classical fast neurotransmitter. These conclusions and caveats should aid clarification of the sites of action of glutamate and nicotinic receptor ligands in the search for new centrally-acting drugs.