PubMed Health⌕ Search

Biomedical subjects

Marcos G Frank

Publications and source records attributed to Marcos G Frank.

9 recordsLinked to original sources
PubMed2006

Blockade of postsynaptic activity in sleep inhibits developmental plasticity in visual cortex.

Ocular dominance plasticity is enhanced by sleep and reduced by sleep deprivation or when all neural activity in the sleeping visual cortex is reversibly inhibited. These latter findings demonstrate that the mechanisms responsible for the effects of sleep on cortical plasticity are activity dependent. To better isolate this activity dependent mechanism, we investigated the role of postsynaptic activity by inactivating the sleeping visual cortex after a period of monocular deprivation with the gamma-amino-n-butyric acid agonist muscimol. Microelectrode recordings showed that ocular dominance plasticity was significantly reduced in cortices reversibly silenced during sleep compared with cortices infused with vehicle only. These findings demonstrate that postsynaptic activity during sleep is required for the consolidation of experience-dependent cortical plasticity.

Action Potentials↗
PubMed2006

Sleep and sleep regulation in the ferret (Mustela putorius furo).

We investigated sleep-wake (S-W) architecture and sleep regulation in the ferret: a phylogenetically primitive mammal increasingly used in neurobiological studies. Twenty-four hour S-W baseline data were collected in eight adult ferrets. Seven ferrets were then sleep deprived for 6h at the beginning of the light period. Like other placental mammals, ferrets exhibited the main vigilance states of wakefulness, rapid-eye-movement (REM) sleep and non-REM (NREM) sleep. Interestingly, the amount of REM sleep in the ferret was considerably higher (24.01+/-1.61% of total recording time) than typically reported in placental mammals. Ferret sleep was homeostatically regulated as sleep deprivation produced a significant increase in NREM EEG delta power during the recovery period. Therefore, ferret sleep in most respects is comparable to sleep in other placental mammals. However, the large amount of REM sleep in this phylogenetically more ancient species suggests that REM sleep may have been present in greater amounts in early stages of mammalian evolution.

Animals↗
PubMed2006

The role of sleep in memory consolidation and brain plasticity: dream or reality?

The notion that a good night of sleep improves memory is widely accepted by the general public. Among sleep scientists, however, the idea has been hotly debated for decades. In this review, the authors consider current evidence for and against the hypothesis that sleep facilitates memory consolidation and promotes plastic changes in the brain. They find that despite a steady accumulation of positive findings over the past decade, the precise role of sleep in memory and brain plasticity remains elusive. This impasse may be resolved by more integrated approaches that combine behavioral and neurophysiological measurements in well-described in vivo models of synaptic plasticity.

Brain↗
PubMed2006

The mystery of sleep function: current perspectives and future directions.

The function of sleep is one of the most persistent and perplexing mysteries in biology. Many theories have been proposed to explain why we sleep, but most account for only a portion of sleep behavior and very few enjoy strong experimental support. A critical review of current findings leads to the following conclusions. Sleep is for the brain rather than the body, and the neural process most impacted by sleep is cognition. Sleep may influence cognition in many ways, including the removal of a toxic byproduct of wakefulness, or the restoration of neural substrates needed for mental processes. The evidence for these possibilities, however, is weak or equivocal. On the other hand, converging lines of evidence support the hypothesis that sleep promotes brain plasticity.

Animals↗
PubMed2005

Sleep-dependent plasticity requires cortical activity.

Recent findings in humans and animals suggest that sleep promotes synaptic plasticity, but the underlying mechanisms have not been identified. We have demonstrated recently an important role for sleep in ocular dominance (OD) plasticity, a classic form of in vivo cortical remodeling triggered by monocular deprivation (MD) during a critical period of development. The mechanisms responsible for the effects of sleep on OD plasticity are unknown but may depend on neuronal activity in the sleeping brain. We investigated the role of cortical activity in sleep-dependent plasticity by reversibly inactivating the sleeping visual cortex (V1) after a period of MD. Critical period cats were bilaterally implanted with cannulas in V1 and standard EEG/EMG electrodes for polysomnographic recording. After a period of MD, visual cortices were infused with the sodium channel blocker lidocaine in vehicle or vehicle only during sleep. A third group of cats served as sham controls and were infused with lidocaine outside of V1 (into the CSF). Both optical imaging of intrinsic cortical signals and microelectrode recordings showed that OD plasticity was significantly reduced in cats whose visual cortices were reversibly silenced during sleep. These findings demonstrate that the mechanisms governing this form of sleep-dependent plasticity require cortical activity. They provide an important insight into how sleep modifies synaptic circuitry by narrowing the range of possible candidate mechanisms to those that are activity dependent.

Action Potentials↗
PubMed2003

Cellular and molecular connections between sleep and synaptic plasticity.

The hypothesis that sleep promotes learning and memory has long been a subject of active investigation. This hypothesis implies that sleep must facilitate synaptic plasticity in some way, and recent studies have provided evidence for such a function. Our knowledge of both the cellular neurophysiology of sleep states and of the cellular and molecular mechanisms underlying synaptic plasticity has expanded considerably in recent years. In this article, we review findings in these areas and discuss possible mechanisms whereby the neurophysiological processes characteristic of sleep states may serve to facilitate synaptic plasticity. We address this issue first on the cellular level, considering how activation of T-type Ca(2+) channels in nonREM sleep may promote either long-term depression or long-term potentiation, as well as how cellular events of REM sleep may influence these processes. We then consider how synchronization of neuronal activity in thalamocortical and hippocampal-neocortical networks in nonREM sleep and REM sleep could promote differential strengthening of synapses according to the degree to which activity in one neuron is synchronized with activity in other neurons in the network. Rather than advocating one specific cellular hypothesis, we have intentionally taken a broad approach, describing a range of possible mechanisms whereby sleep may facilitate synaptic plasticity on the cellular and/or network levels. We have also provided a general review of evidence for and against the hypothesis that sleep does indeed facilitate learning, memory, and synaptic plasticity.

Animals↗
PubMed2003

The ontogeny of mammalian sleep: a reappraisal of alternative hypotheses.

Newborn mammals spend as much as 90% or more of their time in a sleep state characterized by frequent twitches, rapid eye movements (REMs), and irregular respiratory cycles. These motor and respiratory patterns resemble the phasic motor/respiratory components of adult REM sleep, and as a consequence, this sleep state is traditionally viewed as an immature form of REM sleep. An alternative view is that a significant portion of what has been called REM sleep in these species is a form of spontaneous activity typical of the immature nervous system. In this review, we compare and contrast these two opposing views about the ontogenetic origins of REM sleep, and review the evidence most often cited to support the idea that REM sleep is present in newborn altricial mammals. Critical review of this evidence indicates that REM sleep may not be present at birth in these species; rather, it appears that all mammals early in development exhibit spontaneous, dissociated activity that progressively becomes organized into the distinct states of REM and non-rapid eye movement sleep.

Acetylcholine↗
PubMed2002

Sleep and sleep homeostasis in mice lacking the 5-HT2c receptor.

Studies in humans and rats indicate that serotonin (5-hydroxytryptamine, 5-HT) receptors are involved in mammalian sleep expression. We investigated the contribution of the 5-HT2c receptor to sleep expression by examining sleep patterns in mice bearing a targeted null mutation of this receptor. 5-HT2c receptor knock-out mice had more wakefulness, several abnormalities in rapid eye movement sleep expression and an enhanced response to sleep deprivation compared with wild-type control mice. These findings suggest that 5HT2c receptors may mediate several effects on sleep that have been ascribed to serotonin.

Animals↗