Neuroscience
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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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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease preferentially affecting motoneurones. Transgenic mouse models have been used to investigate the role of abnormal motoneurone excitability in this disease. Whilst an increased excitability has repeatedly been demonstrated in vitro in neonatal and embryonic preparations from SOD1 mouse models, the results from the only studies to record in vivo from spinal motoneurones in adult SOD1 models have produced conflicting findings. ⋯ No reductions in repetitive firing were observed showing that this is not a common feature across all ALS models. Immunohistochemistry for the Na+ channel Nav1.6 showed that motoneurone AISs increase in length in G127X SOD1 mice at symptom onset. Consistent with this, the rate of rise of AIS components of antidromic action potentials were significantly faster confirming that this increase in length represents an increase in AIS Na+ channels occurring at symptom onset in this model.
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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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Pharmacological and optogenetic studies have demonstrated that the basolateral amygdala (BLA) plays a pivotal role in regulating fear-conditioned changes in sleep, in particular, rapid eye movement sleep (REM). However, the linkage between BLA and REM regulation has been minimally examined. In this study, we optogenetically activated or inhibited BLA selectively during spontaneous REM, and determined the effects on REM amounts and on hippocampus regulated EEG-theta (θ) activity. ⋯ IHC results showed that glutamatergic and GABAergic cells in CA3 of the hippocampus received inputs from BLAGlu projection neurons. Activation of BLAGlu reduced, and inhibition increased, REM-θ without otherwise altering sleep. Optogenetic stimulation of BLAGlu may be useful for systematically manipulating sleep-related amygdalo-hippocampal interactions.
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Since their discovery in the 1960s, the term paroxysmal depolarization shift (PDS) has been applied to a wide variety of reinforced neuronal discharge patterns. Occurrence of PDS as cellular correlates of electrographic spikes during latent phases of insult-induced rodent epilepsy models and their resemblance to giant depolarizing potentials (GDPs) nourished the idea that PDS may be involved in epileptogenesis. Both GDPs and - in analogy - PDS may lead to progressive changes of neuronal properties by generation of pulsatile intracellular Ca2+ elevations. ⋯ These PDS appear to be initiated in the dendritic sub-compartment. Their morphology critically depends on the position of recording electrodes and on their rate of occurrence. These results provide novel insight into induction mechanisms, origin, variability, and co-existence of PDS with other discharge patterns and thereby pave the way for future investigations regarding the role of PDS in epileptogenesis.