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ref: -0 tags: buszaki watson oscillations review gamma theta hippocampus cortex date: 09-30-2013 18:32 gmt revision:2 [1] [0] [head]

PMID-23393413 Brain rhythms and neural syntax: implications for efficient coding of cognitive content and neuropsychiatric disease.

  • His frequency band standards:
    • delta: 1.5 - 4Hz
    • theta: 4 - 10Hz
    • beta: 10 - 30 Hz
    • gamma: 30 - 80Hz
    • fast: 80 - 200 Hz
    • ultra fast: 200 - 600 Hz.
  • comodugram: power-power correlelogram
  • Reviews current understanding of important rhythms:
    • How gamma is preserved amongs mammals, owing to the same fundamental mechanisms (membrane time constant, GABA transmission, AMPA receptior latency) all around 25ms; suggests that this is a means of tieing neurons into meaningful groups. or symbols; (solves the binding problem?)
    • Theta rhythm, in comparison, varies between species, inversely based on the size of the hippocampus. Larger hippocampus -> greater axonal delay.
    • These and other the critical step is to break neurons into symbols (as part of a 'language' or sequenced computation), not arbitrarily long trains of spikes which are arbitrarily difficult to parse.
  • Reviews the potential role of oscillations in active sensing, though with a rather conjectorial voice: suggests that sensory systems
  • Suggests that neocortical slow-wave oscillations during sleep are critical for transferring information from the hippocampus to the cortex: the cortex become excitable at particular phases of SWS, which biases the fast ripples from the hippocampus. During wakefulness, the direction is reversed -- the hippocampus 'requests' information from the neocortex by gating gamma with theta rhythms.
  • "Typically, when oscillators of different freqencies are coupled, the network oscillation frequency is determined by the fastest one. (??)
  • I actually find figure 3 to be rather weak -- the couplings are not that obvious, espeically if this is the cherry-picked example.
  • Cross phasing-coupling, or n:m coupling: one observes m events associated with the “driven” cycle of one frequency occurring at n different times or phases in the “stimulus” cycle of the other.
    • The mechanism of cross-frequency coupling may for the backbone of neural syntax, which allows for both segmentation and linking of cell assemblies into assemblies (leters) and sequences (words). Hmm. this seems like a stretch, but I am ever cautious.
  • Brain oscillations for quantifiable phenotypes! e.g. you can mono-zygotic twins apart from di-zygotic twins.

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ref: -0 tags: hippocampus theta oscillations memory date: 03-18-2012 18:09 gmt revision:0 [head]

PMID-21696996 The hippocampus: hub of brain network communication for memory

  • Their hypothesis: memory encoding is dominated by theta oscillations 6-10 Hz; during inactivity, hippocampal neurons burst synchronously, creating sharp waves, theoretically supporting memory consolidation.
  • (They claim): to date there is no generally accepted theoretical view on memory consolidation.
  • Generally it seems to shift from hippocampus to neocortex, but still, evidence is equivocal. (Other than HM & other human evidence?)
  • Posit a theory based on excitation ramps of reverse-replay, which seems a bit fishy to me (figure 3).
  • Didn't know this: replay in visual and PFC can be so precise that it preserves detailed features of the crosscorrelograms between neurons. [58, 65, 81].

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ref: -0 tags: hippocampus theta oscillations date: 03-18-2012 17:34 gmt revision:2 [1] [0] [head]

PMID-11832222 Theta Oscillations in the Hippocampus

  • Theta-alpha oscillations have been found in 'all mammals to-date, including humans. (Hence conserved, hence possibly essential).
    • Prevalent in REM sleep.
    • Present in slices bathed in carbachol, too.
    • As well as locomotor activities; but not usually when the animal is resting.
  • Other reviews: Bland 1986, VAnderwolf 1988, Lopes da Silva et al 1990, Buzaki et al 1994 Stewart and Fox 1990, Vinogradova 1995, Vertex and Kocsis 1997.
    • Modeling reviews used passive cable properties; actually, it seems neurons, and their dendrites are have active conductances & active oscillatory features.
  • Theta oscillations most strongly present in CA1
  • Along similar lamina, oscillations are similar.
  • Osc. visible in cortical structures ...
    • subicular complex, entorhinal cortex, perirhinal cortex, cingulate cortex, amygdala -- though none of these structures are capable of generating theta oscillations intrinsically.
  • Also apparent in subcortical structures,
    • Dorsal raphe nucleus, ventral tegmental nucleus, and anterior thalamic nuclei. None of these seem required for oscillation, however:
  • Oscillations may emanate from the medial-septum-diagonal band of Broca (MS-DBB); lesion inactivates theta oscillations in all cortical areas, but the relative role is uncertain, as MS-DBB oscillations may require hippocampal and entorhinal afferents.
    • EPSPs brought about by the MS-DBB cholinergic neurons on hippocampal pyramidal cells cannot be responsible for the atrophine-sensitive form of theta.
    • That said, even though atrophine treatment only modestrly affects theta, it is reduced several-fold after selective neurotoxin elminiation of MS-DBB cholinergic cells -- maybe it's nicotinic synapses?
  • Drugs:
    • Theta can be blocked by GABA antagonist (picrotoxin, induces epilepsy) or agonist (pentoparbital anesthesia).
    • Many other drugs affect oscillations.
    • Broken down into atrophine-sensitive and atrophine-resistant oscillations.
      • (Atrophine blocks muscarinic Ach receptors).
    • Amplitude and frequency of theta does not appreciably change even after large doses of systematic muscarinic blockers.
      • Same drugs abolish theta under anesthesia.
    • The neurotransmitter and receptor causative in theta have never been clearly determined.
  • Theta in CA3 is much smaller than in CA3:
    • Distal dendritic arbor of CA3 pyramidal cells is considerably smaller than that of CA1 pyramidal neurons.
    • CA3 pyramidal neurons receive perisomatic exitation near their somata from the large mossy terminals of granule cells.
      • Regarding this, size of mossy fiber projection correlates well with spatial ability in mice, possibly causative. link (note: used the dryland radial maze, more appropriate for non-swimming mice!)
    • Intrahippocampal oscillator (CA3?) can change its frequency and phase relatively independently from the extrahippocampal (entorhinal) theta inputs.
  • CA1 interneurons discharge on the descenting phase of theta in the pyramidal cell layer, and are assumed to be responsible for the increased gamma of this phase.
  • CA1 pyramidal cells discharge on the negative phase (makes sense) of theta as recorded from the CA1 pyramidal cell layer.
    • Phase fluctuation of spikesis not random and correlates with behavioral varaibles.
      • Stronger excitation = more spikes earlier in the theta negative phase.
    • Firing of place cells varies systematically with animal position and theta phase -- there is a phase precession.
      • Seems as though place is encoded in both which cell is firing as well as when in theta.
      • alternately, this may be an effect of the CA3 oscillator running slightly faster than the extrinsic oscillator.

Original model for theta oscillation creation (figure 2):

  • Note that all oscillations require a dipole which periodically inverts along it's axis, as is required in a conductive solution.
    • And yet there is no 'null' zone in theta oscillation, as dipole would imply. Rather, there is a gradual shift, more like a traveling wave.
  • Dendrites are passive cables, LFP generated by summed activity of IPSP and EPSP on soma and dendrites.
    • Excitation from perforant path,
    • Inhibition from septum to feed-forward inhibitory neuron inputs.
  • That said, the model is not completely consistent with experimental evidence:
    • The highest probability of discharge in the behaving rat occurs around the positive peak of theta recorded at the level of the distal dendrites, corresponding to the negative phase in the pyramidal level. (Remember, spiking corresponds to sodium influx, hence decreased extracellular +)
    • Cells may oscillate by themselves, without input.
    • The cell connections within the hippocampus matter a lot, too.


  • Induction is present / optimal when the spacing between pulses is 200ms.
    • Priming can be only one pulse!
    • Not clear how this works - endogenous cannabanoids?
  • Theta oscillation may provide a mechanism for bringing together time afferent inducing depolarization and dendritic invasion of fast spikes.


  • A theta cycle may be considered an information quantum, allowing the exchange of information among the linked members in a phase-locked manner. ...
  • This discontinuous mode of operation may be a unique solution to temporally segregate and link neuronal assemblies to perform various operations.
  • Notable support of this hypothesis:
    • Theta cycle phase resets upon sensory stimulation
    • Motor activity can become theta locked.


  • Ketamine blocks NMDA receptors.
  • Granule cells can be eliminated by neonatal X-ray exposure. (why?)

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ref: BuzsAki-1996.04 tags: hippocampus neocortex theta gamma consolidation sleep Buzsaki review learning memory date: 12-07-2011 02:31 gmt revision:6 [5] [4] [3] [2] [1] [0] [head]

PMID-8670641[0] The hippocampo-neocortical dialogue.

  • the entorhinal ctx is bidirectionally conneted to nearly all areas of the neocortical mantle.
  • Buzsaki correctly predicts that information gathered during exploration is played back at a faster scale during synchronous population busts during (comnsummatory) behaviors.
  • looks like a good review of the hippocampus, but don't have time to read it now.
  • excellent explanation of the anatomy (with some omissions, click through to read the caption):
  • SPW = sharp waves, 40-120ms in duration. caused by synchronous firing in much of the cortex ; occur 0.02 - 3 times/sec in daily activity & during slow wave sleep.
    • BUzsaki thinks that this may be related to memory consolidation.
  • check the cited-by articles : http://cercor.oxfordjournals.org/cgi/content/abstract/6/2/8
[0] Buzsaiki G, The hippocampo-neocortical dialogue.Cereb Cortex 6:2, 81-92 (1996 Mar-Apr)