Sharp Tuning of Head Direction and Angular Head Velocity Cells in the Somatosensory Cortex.

Head direction (HD) cells form a fundamental component in the brain's spatial navigation system and are intricately linked to spatial memory and cognition. Although HD cells have been shown to act as an internal neuronal compass in various cortical and subcortical regions, the neural substrate of HD cells is incompletely understood. It is reported that HD cells in the somatosensory cortex comprise regular-spiking (RS, putative excitatory) and fast-spiking (FS, putative inhibitory) neurons. Surprisingly, somatosensory FS HD cells fire in bursts and display much sharper head-directionality than RS HD cells. These FS HD cells are nonconjunctive, rarely theta rhythmic, sparsely connected and enriched in layer 5. Moreover, sharply tuned FS HD cells, in contrast with RS HD cells, maintain stable tuning in darkness; FS HD cells' coexistence with RS HD cells and angular head velocity (AHV) cells in a layer-specific fashion through the somatosensory cortex presents a previously unreported configuration of spatial representation in the neocortex. Together, these findings challenge the notion that FS interneurons are weakly tuned to sensory stimuli, and offer a local circuit organization relevant to the generation and transmission of HD signaling in the brain.

[Relationship between excessive daytime sleepiness and oxygen saturation in obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To investigate polysomnographic determinants of excessive daytime sleepiness (EDS) and potential relationship in Chinese patients with obstructive sleep apnea-hypopnea syndrome (OSAS). METHODS: A total of 410 patients with obstructive sleep apnea-hypopnea syndrome were analyzed retrospectively who were obtained in Sleep medicine center of West China hospital from January to April in 2010. All of the patients with an apnea-hypopnea index (AHI) greater than 5 h(-1) were evaluated using the Epworth Sleepiness Scale (ESS) and sleep disorders questionnaire. The patients who ESS score was more than 10 were defined as EDS; otherwise, the other was considered to without EDS. RESULTS: A total of 176 patients with EDS (ESS: 15 ± 3) and 234 without EDS (ESS: 6 ± 3) were studied. Patients with EDS were slightly higher BMI (28 ± 4 vs 26 ± 4) and shorter REM sleep latency (99 ± 65 vs 125 ± 81) than patients without EDS. Furthermore, there were significant difference in awake SaO2, AHI, minimum SaO2, oxygen desaturation index and arousal index between EDS group were No-EDS group (P < 0.001). There was a significant difference in waking SaO2 of severe OSAS between both groups. CONCLUSION: Long-term chronic hypoxia already exists in severe OSAS patients with prominent sleepiness. Waking SaO2 may play a role as a predictor in evaluation and diagnosis in patients with OSAS.

Treatment with harmine ameliorates functional impairment and neuronal death following traumatic brain injury.

Traumatic brain injury (TBI) is a leading cause of mortality in young individuals, and results in motor and cognitive deficiency. Excitotoxicity is an important process during neuronal cell death, which is caused by excessive release of glutamate following TBI. Astrocytic glutamate transporters have a predominant role in maintaining extracellular glutamate concentrations below excitotoxic levels, and glutamate transporter 1 (GLT­1) may account for >90% of glutamate uptake in the brain. The ß­carboline alkaloid harmine has been demonstrated to exert neuroprotective actions in vivo, and the beneficial effects were specifically due to elevation of GLT­1. However, whether harmine provides neuroprotection following TBI remains to be elucidated. The present study performed intraperitoneal harmine injections in rats (30 mg/kg per day for up to 5 days), in order to investigate whether harmine treatment attenuates brain edema and improves functional recovery in a rat model of TBI. The neuronal survival ratio and the protein expression of apoptosis­associated caspase 3 were also assessed in the hippocampus of the rat brain. Furthermore, the expression levels of GLT­1 and inflammatory cytokines were detected, in order to determine the underlying mechanisms. The results of the present study demonstrated that administration of harmine significantly attenuated cerebral edema, and improved learning and memory ability. In addition, harmine significantly increased the protein expression of GLT­1, and markedly attenuated the expression levels of interleukin­1ß and tumor necrosis factor­α, thereby attenuating apoptotic neuronal death in the hippocampus. These results provided in vivo evidence that harmine may exert neuroprotective effects by synergistically reducing excitotoxicity and inflammation following TBI.

The acute effects of levetiracetam on nocturnal sleep and daytime sleepiness in patients with partial epilepsy.

This study investigated the effect of the novel antiepileptic drug levetiracetam (LEV) on sleep in eleven patients with partial epilepsy. At baseline and one week after therapy with LEV (1000 mg/day), patients underwent polysomnography (PSG) and the Multiple Sleep Latency Test (MSLT). Patients also rated their own degree of sleep disturbance and daytime sleepiness with the Athens Insomnia Scale (AIS) and the Epworth Sleepiness Scale (ESS). A group of 10 age- and gender-matched control participants were also included in the study. Patients had decreased total sleep time and increased daytime sleepiness compared to baseline, as evaluated by AIS subscales. Furthermore, LEV therapy significantly decreased the rapid eye movement sleep time and percentage as measured by PSG. Patients reported a significant increase in ESS score but did not exhibit changes in MSLT performance after LEV treatment. The study demonstrated that short-course LEV treatment can affect subjective sleep time and objective sleep architecture. Furthermore, LEV treatment affected subjective daytime sleepiness but did not influence objective mean daytime sleep latencies in patients with partial epilepsy.