The hippocampal control of neuronal discharges in the septum of the rat

McLennan, H.; Miller, J. F. A. P.

doi:10.1113/jphysiol.1974.sp010500

Cited by 189 publications

(73 citation statements)

References 19 publications

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“…This is consistent with experimental evidence suggesting that activity in region CA1 and region CA3 can inhibit activity in the medial septum, and thereby downregulate cholinergic modulation [105]. This allowed the network to respond initially to patterns with dynamics set by strong cholinergic modulation, suppressing the autoassociative and hetero-associative function of excitatory connections.…”

Section: Feedback Regulation Of Cholinergic Modulationsupporting

confidence: 74%

Free recall and recognition in a network model of the hippocampus: simulating effects of scopolamine on human memory function

Hasselmo

Wyble

1997

Behavioural Brain Research

311

263

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Section: Feedback Regulation Of Cholinergic Modulationsupporting

confidence: 74%

Free recall and recognition in a network model of the hippocampus: simulating effects of scopolamine on human memory function

Hasselmo

Wyble

1997

Behavioural Brain Research

311

263

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“…This node controlled the release of acetylcholine (ACh) in all modelled layers. The node itself received input from the septal y oscillator, and from hippocampal interneurons (Dragoi et al, 1999;McLennan and Miller, 1974; Tóth et al, 1993). The latter connections were inhibitory; in essence, the cholinergic node was disinhibited only when entorhinal input did not elicit any recall in the hippocampus; that is, when the input was new.…”

Section: Modelmentioning

confidence: 99%

Effects of 5-HT on Memory and the Hippocampus: Model and Data

Meeter

Talamini

Schmitt

et al. 2005

Neuropsychopharmacol

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5-Hydroxytryptamine (5-HT) transmission has been implicated in memory and in depression. Both 5-HT depletion and specific 5-HT agonists lower memory performance, while depression is also associated with memory deficits. The precise neuropharmacology and neural mechanisms underlying these effects are unknown. We used neural network simulations to elucidate the neuropharmacology and network mechanisms underlying 5-HT effects on memory. The model predicts that these effects are largely dependent on transmission over the 5-HT 1A and 5-HT 3 receptors, which regulate the selectivity of retrieval. It also predicts differential memory deficit profiles for 5-HT depletion and overactivation. The latter predictions were confirmed in studies with healthy and depressed participants undergoing acute tryptophan depletion or ipsipirone challenge. The results suggest that the memory impairments in depressed subjects may be related to 5-HT undertransmission, and support the notion that 5-HT 1A agonists ameliorate memory deficits in depression. INTRODUCTIONHypofunction of the 5-hydroxytryptamine (5-HT) system has emerged as a leading candidate cause for depression (Naughton et al, 2000;Middlemiss et al, 2002). At the same time, several lines of evidence point to a role for 5-HT in memory (Buhot et al, 2000). Most prominently, depletion of tryptophan (TRP), a precursor of 5-HT, is associated with lower performance on episodic memory retention tests in humans (Riedel et al, 1999). This mirrors findings in depression, which is accompanied by moderate to severe memory deficits (Johnson and Magaro, 1987;Schaub et al, 2003). However, manipulations that increase 5-HT concentration or 5-HT receptor activation also lower memory performance, as indicated by receptor agonist studies in both humans (Riedel et al, 2002) and animals (Altman and Normile, 1988). Up to now, it is not known why both increased and decreased 5-HT activation have adverse effects on memory.5-HT binds to a large and disparate family of CNS receptors, which have effects that are sometimes opposite. Thus, many effects of different receptors seem to cancel each other out. In a review (see Supplementary Information on internet), we identify two robust effects of 5-HT in the hippocampus. First, 5-HT exerts a hyperpolarizing influence on principal cells; directly, via 5-HT 1A receptors, and indirectly, via facilitation of GABA release from local interneurons through 5-HT 3 receptors (Burnet et al, 1995;Piguet and Galvan, 1994). Activation of 5-HT 2A and 5-HT 2C receptors has been suggested to induce depolarization in principal cells (Piguet and Galvan, 1994;Barnes and Sharp, 1999), but these effects appear to be dominated by the depolarizing effects of 5-HT, as bath application of 5-HT will hyperpolarize principal cells in slice preparations of the dentate gyrus (Piguet and Galvan, 1994). In addition, through 5-HT 2C , 5-HT 4 , and 5-HT 7 receptors, afterhyperpolarizing (AHP) currents are downregulated, leading to reduced adaptation in principal cells (Torres et al, 1996;Bac...

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“…These hippocampo-septal projection cells receive convergent input from large numbers of hippocampal principal cells (Tóth et al, 1993). Hippocampal activity may thus inhibit the septum; indeed, both fimbria stimulation (McLennan and Miller, 1974) and hippocampal sharp waves (Dragoi et al, 1999) were shown to inhibit neuronal activity in the medial septum.…”

Section: Acetylcholine and Learning Dynamicsmentioning

confidence: 99%

“…In this respect it is noteworthy that the few studies addressing the function of the hippocampo-medioseptal pathway were performed in anaesthetized rats, and did not characterize the neurons responding to hippocampal input (McLennan and Miller, 1974;Dragoi et al, 1999). Moreover, the clearest effects of hippocampal influence on septal activity were observed during hippocampal sharp waves, rather than REM-associated theta (Dragoi et al, 1999).…”

mentioning

confidence: 99%

Mode shifting between storage and recall based on novelty detection in oscillating hippocampal circuits

2004

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ABSTRACT:It has been suggested that hippocampal mode shifting between a storage and a retrieval state might be under the control of acetylcholine (ACh) levels, as set by an autoregulatory hippocampo-septohippocampal loop. The present study investigates how such a mechanism might operate in a large-scale connectionist model of this circuitry that takes into account the major hippocampal subdivisions, oscillatory population dynamics and the time scale on which ACh exerts its effects in the hippocampus. The model assumes that hippocampal mode shifting is regulated by a novelty signal generated in the hippocampus. The simulations suggest that this signal originates in the dentate. Novel patterns presented to this structure lead to brief periods of depressed firing in the hippocampal circuitry. During these periods, an inhibitory influence of the hippocampus on the septum is lifted, leading to increased firing of cholinergic neurons. The resulting increase in ACh release in the hippocampus produces network dynamics that favor learning over retrieval. Resumption of activity in the hippocampus leads to the reinstatement of inhibition. Despite theta-locked rhythmic firing of ACh neurons in the septum, ACh modulation in the model fluctuates smoothly on a time scale of seconds. It is shown that this is compatible with the time scale on which memory processes take place. A number of strong predictions regarding memory function are derived from the model.

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The hippocampal control of neuronal discharges in the septum of the rat

Cited by 189 publications

References 19 publications

Free recall and recognition in a network model of the hippocampus: simulating effects of scopolamine on human memory function

Free recall and recognition in a network model of the hippocampus: simulating effects of scopolamine on human memory function

Effects of 5-HT on Memory and the Hippocampus: Model and Data

Mode shifting between storage and recall based on novelty detection in oscillating hippocampal circuits

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