IntroductionEvidence has accumulated, which indicates that, in healthy individuals, sleep enhances procedural memory consolidation, and that sleep spindle activity modulates this process. However, whether sleep-dependent procedural memory consolidation occurs in patients medicated for major depressive disorder remains unclear, as are the pharmacological and physiological mechanisms that underlie this process.MethodsHealthy control participants (n=17) and patients medicated for major depressive disorder (n=11) were recruited and subjected to a finger-tapping motor sequence test (MST; nondominant hand) paradigm to compare the averaged scores of different learning phases (presleep, postsleep, and overnight improvement). Participants’ brain activity was recorded during sleep with 16 electroencephalography channels (between MSTs). Sleep scoring and frequency analyses were performed on the electroencephalography data. Additionally, we evaluated sleep spindle activity, which divided the spindles into fast-frequency spindle activity (12.5–16 Hz) and slow-frequency spindle activity (10.5–12.5 Hz).ResultSleep-dependent motor memory consolidation in patients with depression was impaired in comparison with that in control participants. In patients with depression, age correlated negatively with overnight improvement. The duration of slow-wave sleep correlated with the magnitude of motor memory consolidation in patients with depression, but not in healthy controls. Slow-frequency spindle activity was associated with reduction in the magnitude of motor memory consolidation in both groups.ConclusionBecause the changes in slow-frequency spindle activity affected the thalamocortical network dysfunction in patients medicated for depression, dysregulated spindle generation may impair sleep-dependent memory consolidation. Our findings may help to elucidate the cognitive deficits that occur in patients with major depression both in the waking state and during sleep.

The alteration in sleep spindles seen in medicated depressive subjects may reflect a pharmacological modulation of synaptic function involving the thalamic-reticular and thalamocortical mechanisms.

This contribution aims to integrate findings of our recently reported three brain imaging studies on young narcolepsy-cataplexy patients [1][2][3]. All brain images were acquired using 3.0 Tesla MRI. In our prior study of a voxel-based morphometry [1], narcoleptic patients showed gray matter (GM) deficits in the hypothalamus and fronto-limbic areas. Hypothalamic GM deficits correlated with severity of narcolepsy. In our diffusion tensor imaging study that assessed global white matter (WM) integrity [2], narcoleptic patients had decreased WM integrity especially in fronto-limbic areas, which were associated with sleepiness and attention deficit. Prefrontal metabolite concentration was measured in a proton magnetic resonance spectroscopy [3]. Narcoleptic patients had higher GABA levels in the medial prefrontal areas. This is potentially related to the compensation of nocturnal sleep disturbance. Hypothalamus seems to be a key structure in narcoleptic symptoms. However, both GM and WM abnormalities of fronto-limbic areas were also related to narcolepsy and its symptoms. Compensatory alteration of GABA was also found in the areas. Taken together, our reports suggest that fronto-limbic area, as well as hypothalamus, may be implicated in narcolepsy. References[1] Gray matter deficits in young adults with narcolepsy. Acta Neurol Scand 2009;119:61-7. [2] Decreased fractional anisotropy values in brains of young narcoleptic patients. 2009; presented in APSS. [3] Increased GABA levels in medial prefrontal cortex of young adults with narcolepsy.Two types of monoamine oxidase (MAO), type A (MAO-A) and type B (MAO-B), have been identified. Generally, MAO-A is highly expressed in noradrenergic/adrenergic neurons such as the locus coeruleus, whereas MAO-B is highly expressed in serotonergic and histaminergic neurons and distinct populations of glia such as tanicytes. On the other hand, it has been reported that non-catecholaminergic neurons also express MAOs in an adult rat brain. Extracellular serotonin (5-HT), norepinephrine / epinephrine (NE/E), and dopamine (DA) appear to be removed by a reuptake mechanism; subsequently, they are metabolized by intracellular MAO activity. In the hypothalamus, 5-HT and DBHpositive varicosities densely distribute around hypothalamic nucleus, likely MAO activity affecting the neuronal functions. In the present study, we investigated the distribution of MAOs and the anatomical relation to the neuropeptide-expressing neurons in the rat hypothalamus. We performed enzyme histochemistry for MAO-A or MAO-B, and use specific antibodies for MAO-A and MAO-B. In the result, we found moderate MAO-A enzyme activities in the distinct neuronal populations, and strong MAO-B activity in some glial cells including tanicytes. MAO-A-immunoreactivities (IR) were found in the varicosities of noradrenergic/adrenergic neurons and in the cell bodies of some neuropeptides-expressing neurons in the lateral hypothalamus. Especially, orexin neurons robustly express MAO-A, but not MAO-B. Objective:We have elucidated the p...

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