Cellular bases of hippocampal EEG in the behaving rat

Buzsáki, György; Leung, L.-W.S.; Vanderwolf, C.H.

doi:10.1016/0165-0173(83)90037-1

Cited by 1,270 publications

(1,067 citation statements)

References 108 publications

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“…The septal and intrahippocampal pathways produce a current source in the CA1 pyramidal layer and a sink in the stratum radiatum of CA1. Indeed, these current generators are abolished by atropine (acetylcholine antagonist), but remain intact after lesions of the entorhinal cortex (Buzsáki et al, 1983;Vanderwolf and Leung, 1983;Ylinen et al, 1995b). In addition to the MSDB, the hippocampus receives rhythmic subcortical modulatory inputs from several sources (Kocsis and Vertes, 1994;Vertes and Kocsis, 1997).…”

Section: Slow (<1 Hz) Rhythms-mirceamentioning

confidence: 99%

“…Perforant path input to distal dendrites of the CA1 and CA3 pyramidal cells and dentate granule cells is believed to produce current dipoles that are responsible for the large amplitude of theta at around the hippocampal fissure (Buzsáki et al, 1983). This latter oscillator is atropine-resistant, but is abolished by urethane anesthesia and lesions of the entorhinal cortex and originates mainly in layers 2/3 of the entorhinal cortex Ylinen et al, 1995b;Kamondi et al, 1998).…”

Section: Slow (<1 Hz) Rhythms-mirceamentioning

confidence: 99%

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Interaction between neocortical and hippocampal networks via slow oscillations

Sirota

Buzsáki

2005

THL

Self Cite

230

219

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Both the thalamocortical and limbic systems generate a variety of brain state-dependent rhythms but the relationship between the oscillatory families is not well understood. Transfer of information across structures can be controlled by the offset oscillations. We suggest that slow oscillation of the neocortex, which was discovered by Mircea Steriade, temporally coordinates the self-organized oscillations in the neocortex, entorhinal cortex, subiculum and hippocampus. Transient coupling between rhythms can guide bidirectional information transfer among these structures and might serve to consolidate memory traces.

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Section: Slow (<1 Hz) Rhythms-mirceamentioning

confidence: 99%

Section: Slow (<1 Hz) Rhythms-mirceamentioning

confidence: 99%

Interaction between neocortical and hippocampal networks via slow oscillations

Sirota

Buzsáki

2005

THL

Self Cite

230

219

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“…During theta, cellular activity tends to be smooth; a relatively constant proportion of hippocampal pyramidal cells fire spikes, with each cell firing on the order of a second or two [94,150,169]. The other state, called LIA (large-amplitude irregular activity) shows a noisier EEG punctuated by occasional 100 ms sharp-wa6es with a 200 Hz rhythm riding on them [25,150,229,249]. Cellular activity in LIA is usually quiet, with strong bursts of activity during the sharp-waves [25,94,150,169].…”

Section: A1 Hippocampal Representational Replaymentioning

confidence: 99%

“…The other state, called LIA (large-amplitude irregular activity) shows a noisier EEG punctuated by occasional 100 ms sharp-wa6es with a 200 Hz rhythm riding on them [25,150,229,249]. Cellular activity in LIA is usually quiet, with strong bursts of activity during the sharp-waves [25,94,150,169]. Place fields are only seen during theta states; during LIA states, cells fire during sharp-waves, independent of the location of the animal [94,150].…”

Section: A1 Hippocampal Representational Replaymentioning

confidence: 99%

The hippocampal debate: are we asking the right questions?

Redish

2001

Behavioural Brain Research

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For years, the debate has been: 'Is the hippocampus the cognitive map?' or 'Is the hippocampus the core of memory?' These two hypotheses derived their original power from two key experiments-the cognitive map theory from the remarkable spatial correlates seen in recordings of hippocampal pyramidal cells and the memory theory from the profound amnesias seen in the patient H.M. Both of these key experiments have been reinterpreted over the years: hippocampal cells are correlated with much more than place and H.M. is missing much more than just his hippocampus. However, both theories are still debated today. The hippocampus clearly plays a role in both navigation and memory processing. The question that must be addressed is rather: 'What is the role played by the hippocampus in the navigation and memory systems?' By looking at the navigation system as a whole, one can identify the major role played by the hippocampus as correcting for accumulation errors that occur within idiothetic navigation systems. This is most clearly experimentally evident as reorientation when an animal is lost. Carrying this over to a more general process, this becomes a role of recalling a context, bridging a contextual gap, or, in other words, it becomes a form of recognition memory. I will review recent experimental data which seems to support this theory over the more general spatial or memory theories traditionally applied to hippocampus.

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“…Administration of cholinergic antagonists or excitotoxic lesions of cholinergic neurons in the basal forebrain increase slow-wave power and decrease high-frequency power (Buzsáki et al 1983(Buzsáki et al , 1988Stewart et al 1984;Riekkinen et al 1990;Ray and Jackson 1991;Vanderwolf 1992;Holschneider et al 1997), whereas cholinergic agonists result in a reversal of this phenomenon (Vanderwolf 1992). Furthermore, indirect cholinergic agonists such as physostigmine or eserine enhance the synchronization of theta activity, whereas cholinergic antagonists or excitotoxic lesions of the basal forebrain diminish it (Dickson et al 1994;Leung et al 1994;Holschneider et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Changes in electrocortical power and coherence in response to the selective cholinergic immunotoxin 192 IgG-saporin

Holschneider

Waite

Leuchter

et al. 1999

Experimental Brain Research

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Changes in brain electrical activity in response to cholinergic agonists, antagonists, or excitotoxic lesions of the basal forebrain may not be reflective entirely of changes in cholinergic tone, in so far as these interventions also involve noncholinergic neurons. We examined electrocortical activity in rats following bilateral intracerebroventricular administration of 192 IgG-saporin (1.8 μg/ventricle), a selective cholinergic immunotoxin directed to the low-affinity nerve growth factor receptor p75. The immunotoxin resulted in extensive loss of choline acetyl transferase (ChAT) activity in neocortex (80%-84%) and hippocampus (93%), with relative sparing of entorhinalpiriform cortex (42%) and amygdala (28%). Electrocortical activity demonstrated modest increases in 1-to 4-Hz power, decreases in 20-to 44-Hz power, and decreases in 4-to 8-Hz intraand interhemispheric coherence. Rhythmic slow activity (RSA) occurred robustly in toxin-treated animals during voluntary movement and in response to physostigmine, with no significant differences seen in power and peak frequency in comparison with controls. Physostigmine significantly increased intrahemispheric coherence in lesioned and intact animals, with minor increases seen in interhemispheric coherence. Our study suggests that: (1) electrocortical changes in response to selective cholinergic deafferentation are more modest than those previously reported following excitotoxic lesions; (2) changes in cholinergic tone affect primarily brain electrical transmission within, in contrast to between hemispheres; and (3) a substantial

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Cellular bases of hippocampal EEG in the behaving rat

Cited by 1,270 publications

References 108 publications

Interaction between neocortical and hippocampal networks via slow oscillations

Interaction between neocortical and hippocampal networks via slow oscillations

The hippocampal debate: are we asking the right questions?

Changes in electrocortical power and coherence in response to the selective cholinergic immunotoxin 192 IgG-saporin

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