Single neuron burst firing in the human hippocampus during sleep.

Department of Neurobiology, UCLA School of Medicine, Los Angeles, California 90095, USA.
Hippocampus (Impact Factor: 4.3). 01/2002; 12(6):724-34. DOI: 10.1002/hipo.10026
Source: PubMed

ABSTRACT Although there are numerous non-primate studies of the single neuron correlates of sleep-related hippocampal EEG patterns, very limited hippocampal neuronal data are available for correlation with human sleep. We recorded human hippocampal single neuron activity in subjects implanted with depth electrodes required for medical diagnosis and quantitatively evaluated discharge activity from each neuron during episodes of wakefulness (Aw), combined stage 3 and 4 slow-wave sleep (SWS), and rapid eye movement (REM) sleep. The mean firing rate of the population of single neurons was significantly higher during SWS and Aw compared with REM sleep (p = 0.002; p < 0.0001). In addition, burst firing was significantly greater during SWS compared with Aw (p = 0.001) and REM sleep (p < 0.0001). The synchronized state of SWS and associated high-frequency burst discharge found in human hippocampus may subserve functions similar to those reported in non-primate hippocampus that require burst firing to induce synaptic modifications in hippocampal circuitry and in hippocampal projections to neocortical targets that participate in memory consolidation.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The hypothalamic-pituitary-adrenal axis (also called the HPA or stress axis) exhibits distinct circadian and ultradian rhythms in cortisol release that cannot be explained solely by the feedback loops from cortisol to the control systems in the paraventricular nucleus (PVN) and pituitary gland. The HPA axis is intimately connected with other brain functions. In particular, it is strongly aff ected by the sleep-wake cycles via direct and indirect eff ects of the circadian and homeostatic mechanisms. For example, the HPA axis has direct inputs from the master circadian clock in the suprachiasmatic nuclei (SCN), and from the various sleep-wake related neuronal populations, which themselves are under the eff ects of the circadian and homeostatic processes. In this paper a first step towards a physiologically based mathematical model of the HPA-axis under eff ects of the sleep-wake cycles is presented. This model accounts for 3 major characteristics of daily cortisol profi le in the blood: i) abrupt increase of cortisol concentration in response to awakening, the so-called cortisol-awakening response (CAR); ii) reduced cortisol levels during daytime with underlying ultradian oscillations; and iii) suppression of cortisol release during sleep.
    Pharmacopsychiatry 05/2013; 46(S 01). DOI:10.1055/s-0033-1333763 · 2.17 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The establishment of memories involves reactivation of waking neuronal activity patterns and strengthening of associated neural circuits during slow-wave sleep (SWS), a process known as "cellular consolidation" (Dudai and Morris, 2013). Reactivation of neural activity patterns during waking behaviors that occurs on a timescale of seconds to minutes is thought to constitute memory recall (O'Keefe and Nadel, 1978), whereas consolidation of memory traces may be revealed and served by correlated firing (reactivation) that appears during sleep under conditions suitable for synaptic modification (Buhry et al., 2011). Although reactivation has been observed in human neuronal recordings (Gelbard-Sagiv et al., 2008; Miller et al., 2013), reactivation during sleep has not, likely because data are difficult to obtain and the effect is subtle. Seizures, however, provide intense and synchronous, yet sparse activation (Bower et al., 2012) that could produce a stronger consolidation effect if seizures activate learning-related mechanisms similar to those activated by learned tasks. Continuous wide-bandwidth recordings from patients undergoing intracranial monitoring for drug-resistant epilepsy revealed reactivation of seizure-related neuronal activity during subsequent SWS, but not wakefulness. Those neuronal assemblies that were most strongly activated during seizures showed the largest correlation changes, suggesting that consolidation selectively strengthened neuronal circuits activated by seizures. These results suggest that seizures "hijack" physiological learning mechanisms and also suggest a novel epilepsy therapy targeting neuronal dynamics during post-seizure sleep. Copyright © 2015 the authors 0270-6474/15/350999-12$15.00/0.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Investigations of interictal epileptiform spikes and seizures have played a central role in the study of epilepsy. The background EEG activity, however, has received less attention. In this chapter we discuss the characteristic features of the background activity of the brain when individuals are at rest and awake (resting wake) and during sleep. The characteristic rhythms of the background EEG are presented, and the presence of 1/f (β) behavior of the EEG power spectral density is discussed and its possible origin and functional significance. The interictal EEG findings of focal epilepsy and the impact of interictal epileptiform spikes on cognition are also discussed.
    Advances in Experimental Medicine and Biology 01/2014; 813:43-54. DOI:10.1007/978-94-017-8914-1_3 · 2.01 Impact Factor

Full-text (2 Sources)

Available from
Jun 5, 2014