Abstract
Neurobiological oscillations are regarded as essential to normal information processing, including coordination and timing of cells and assemblies within structures as well as in long feedback loops of distributed neural systems. The hippocampal theta rhythm is a 3–12 Hz oscillatory potential observed during cognitive processes ranging from spatial navigation to associative learning. The lower range, 3–7 Hz, can occur during immobility and depends upon the integrity of cholinergic forebrain systems. Several studies have shown that the amount of pre-training theta in the rabbit strongly predicts the acquisition rate of classical eyeblink conditioning and that impairment of this system substantially slows the rate of learning. Our lab has used a brain-computer interface (BCI) that delivers eyeblink conditioning trials contingent upon the explicit presence or absence of hippocampal theta. A behavioral benefit of theta-contingent training has been demonstrated in both delay and trace forms of the paradigm with a two- to four-fold increase in learning speed. This behavioral effect is accompanied by enhanced amplitude and synchrony of hippocampal local field potential (LFP)s, multi-unit excitation, and single-unit response patterns that depend on theta state. Additionally, training in the presence of hippocampal theta has led to increases in the salience of tone-induced unit firing patterns in the medial prefrontal cortex, followed by persistent multi-unit activity during the trace interval. In cerebellum, rhythmicity and precise synchrony of stimulus time-locked LFPs with those of hippocampus occur preferentially under the theta condition. Here we review these findings, integrate them into current models of hippocampal-dependent learning and suggest how improvement in our understanding of neurobiological oscillations is critical for theories of medial temporal lobe processes underlying intact and pathological learning.
Highlights
Septohippocampal ThetaReports have identified a 3–7 Hz frequency band as atropine-sensitive, or Type II, theta due to its disruption by the competitive cholinergic inhibitor, atropine, and have distinguished it from a higher, 8–12 Hz frequency band, deemed atropine-resistant, non-cholinergic, or Type I, theta despite technically falling within the alpha bandwidth in most literatures including those classically defined by human scalp EEG (Kramis et al, 1975)
SD (2015) Harnessing the power of theta: natural manipulations of cognitive performance during hippocampal theta-contingent eyeblink conditioning
Our findings suggest that the presence of pre-trial hippocampal theta may optimize the magnitude and proportion of excitatory and inhibitory pyramidal cell/interneuron response profiles in a manner that coordinates the neural responses throughout the distributed network supporting trace Eyeblink conditioning (EBC)
Summary
Reports have identified a 3–7 Hz frequency band as atropine-sensitive, or Type II, theta due to its disruption by the competitive cholinergic inhibitor, atropine, and have distinguished it from a higher, 8–12 Hz frequency band, deemed atropine-resistant, non-cholinergic, or Type I, theta despite technically falling within the alpha bandwidth in most literatures including those classically defined by human scalp EEG (Kramis et al, 1975). These GABAergic and other neuron populations (cholinergic and glutamatergic projections) send pacing inputs to hippocampus via the fimbria-fornix (Amaral and Kurz, 1985; Hajszan et al, 2003; Sotty et al, 2003) which, when transected, results in abolition of hippocampal theta (M’HarziandMonmaur,1985) Both in vitro (Konopacki and Gołebiewski, 1992; Konopacki et al, 1997) and in vivo studies (Colom et al, 1991; Smythe et al, 1992; Vinogradova et al, 1998) provide evidence that the GABAergic and cholinergic systems interact to produce the amplitude and frequency components of hippocampal theta rhythm. This oscillator does not require external timing inputs, it does require a permissive MS-vDBB cholinergic activation since, the theta remaining in the absence of entorhinal input is abolished by anticholinergics (Kramis et al, 1975; Vanderwolf and Leung, 1983; Amaral and Witter, 1989; Kocsis et al, 1999)
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