Serotonin and acetylcholine release response in the rat hippocampus during a spatial memory task

Stancampiano, Roberto; Cocco, Stefania; Cugusi, C; Sarais, L; Fadda, F

doi:10.1016/s0306-4522(98)00397-2

Cited by 114 publications

(67 citation statements)

References 71 publications

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“…These results are in part supported by other studies that demonstrate that stressful situations increase ACh levels in the hippocampus (eg . In addition, numerous other studies have implicated the hippocampus in memory formation and have attributed an increase in hippocampal ACh efflux to an enhancement of overall memory performance (see eg Fadda et al, 2000;Kopf et al, 2001;Stancampiano et al 1999). The increase in hippocampal ACh efflux observed during the training and retention sessions were abolished by a single systemic injection of fluoxetine 1 h prior to the training session, even though basal hippocampal ACh levels were not affected.…”

Section: Discussionmentioning

confidence: 97%

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

Degroot

Nomikos

2004

Neuropsychopharmacol

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Anxiety disorders may result from an overexpression of aversive memories. Evidence suggests that the hippocampal cholinergic system could be the point of convergence of anxiety and memory. We propose that clinically effective anxiolytics may exert their effect by interfering with this integration mechanism. To assess anxiety and aversive memory, we used the shock-probe burying test. A reduction in anxiety in this test is indicated by decreased burying, whereas impaired cognition is reflected by an increased number of probe-contacts and/or reduced retention latency. Both an aversive stimulus and the memory of that stimulus significantly increased hippocampal acetylcholine (ACh) levels (Experiment 1). In fact, the memory of the event seemed to be more important than the event itself since the aversive memory induced a greater increase in hippocampal ACh. Injections (i.p.) of fluoxetine (Prozac s ) reduced burying behavior, while not affecting probe contacts or retention latency (Experiment 2). Although injections of fluoxetine did not affect basal hippocampal ACh efflux (Experiment 3), fluoxetine abolished the increase in ACh induced by the aversive stimulus and the memory of that stimulus (Experiment 4), emphasizing the significance of aversive memories in anxiety disorders. These actions may be mediated by a decrease in the event-related enhancement in cholinergic neurotransmission through M1 cholinergic receptors (Experiment 5). Therefore, anxiety disorders may stem from an unopposed formation of aversive memories and clinically effective anxiolytics hinder the association between emotional and cognitive processing. This reduces the emotional impact of aversive memories, thereby opposing consequent anxiety.

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Section: Discussionmentioning

confidence: 97%

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

Degroot

Nomikos

2004

Neuropsychopharmacol

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“…There is a dramatic rise in hippocampal ACh while rats are transversing a T-maze or a radial arm maze-that in some instances is related to the degree of learning (Fadda, Cocco, & Stancampiano, 2000;Fadda, Melis, & Stancampiano, 1996). In addition to the hippocampus, ACh efflux in the striatum and amygdala can also be used to assess amount of neural activation during maze learning (Chang & Gold, 2003a;McIntyre, Marriott, & Gold, 2003;McIntyre, Pal, Marriott, & Gold, 2002;Stancampiano, Cocco, Cugusi, Sarais, & Fadda, 1999). ACh release in the hippocampus and striatum predicts which system and thus which strategy (place or response) a given rat will use to solve a T-maze discrimination task (Chang & Gold, 2003a;McIntyre et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Blunted hippocampal, but not striatal, acetylcholine efflux parallels learning impairment in diencephalic-lesioned rats

Roland

Savage

2007

Neurobiology of Learning and Memory

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A rodent model of diencephalic amnesia, pyrithiamine-induced thiamine deficiency (PTD), was used to investigate the dynamic role of hippocampal and striatal acetylcholine (ACh) efflux across acquisition of a nonmatching-to-position (NMTP) T-maze task. Changes in ACh efflux were measured in rats at different time points in the acquisition curve of the task (early= day 1, middle = day 5, and late = day 10). Overall, the control group had higher accuracy scores than the PTD group in the latter sessions of NMTP training. During the three microdialysis sampling points, all animals displayed significant increases in ACh efflux in both hippocampus and striatum, while performing the task. However, on day 10, the PTD group showed a significant behavioral impairment that paralleled their blunted hippocampal-but not striatal-ACh efflux during maze training. The results support selective diencephalic-hippocampal dysfunction in the PTD model. This diencephalichippocampal interaction appears to be critical for successful episodic and spatial learning/memory.

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“…More recently, in vivo microdialysis has allowed for the ability to examine changes in hippocampal extracellular ACh levels in conscious, freely moving rats during behavioral tests of learning and memory. With few exceptions (e.g., Hironaka et al 2001), the findings of such studies show that hippocampal-dependent learning and memory is associated with an increase in hippocampal extracellular ACh levels (Yamamuro et al 1995;Fadda et al 1996Fadda et al , 2000Orsetti et al 1996;Ragozzino et al 1996Ragozzino et al , 1998Stancampiano et al 1999;Nail-Boucherie et al 2000;Stefani and Gold 2001;McIntyre et al 2002McIntyre et al , 2003Chang and Gold 2003). Combined, the findings of these studies show that hippocampal extracellular ACh is elevated by learning and memory processes, that the elevation is often correlated with the type of learning and memory or its time course, and that these increases cannot be accounted for solely by locomotor activity or by handling.…”

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confidence: 99%

Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

Parent¹,

Baxter²

2004

Learn. Mem.

175

132

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The neurotransmitter acetylcholine (ACh) has been accorded an important role in supporting learning and memory processes in the hippocampus. Cholinergic activity in the hippocampus is correlated with memory, and restoration of ACh in the hippocampus after disruption of the septohippocampal pathway is sufficient to rescue memory. However, selective ablation of cholinergic septohippocampal projections is largely without effect on hippocampal-dependent learning and memory processes. We consider the evidence underlying each of these statements, and the contradictions they pose for understanding the functional role of hippocampal ACh in memory. We suggest that although hippocampal ACh is involved in memory in the intact brain, it is not necessary for many aspects of hippocampal memory function.The goal of this review is to consider the role of septohippocampal acetylcholine (ACh) in learning and memory processes. The evidence in this regard falls broadly into two different classes. On the one hand, considerable data implicate septohippocampal ACh in memory function. This system is engaged during memory processing, indexed by ACh release or by modification of cholinergic markers, and manipulations that affect memory produce parallel changes in hippocampal cholinergic activity. Furthermore, agents that increase hippocampal cholinergic function are sufficient to reverse memory impairments caused by disruption of the septohippocampal system. However, data from studies of selective lesions of septohippocampal cholinergic neurons with the immunotoxin 192 IgG-saporin call into question the essential role of this system in learning and memory, because these studies generally failed to find severe impairments in memory function. Our goal in this article is to review the data underlying each of these lines of evidence, and to attempt to reconcile these apparently disparate observations.The discrepancy between these lines of evidence might imply that septohippocampal ACh is involved in memory processing, but is not necessary for it to occur. This viewpoint would allow for correlated changes in ACh release and memory, and for the ability of cholinergic agents to reverse memory impairments caused by disruption of septohippocampal function. However, it also would permit memory to proceed relatively normally in the absence of septohippocampal cholinergic input. By describing this viewpoint and its implications for the functional role of hippocampal ACh in memory, we seek to promote the idea that data from lesions are compatible with data from other experimental approaches. Furthermore, we suggest that a convergent approach that incorporates observations from different experimental methods will reveal functional characteristics of hippocampal ACh that would not be apparent from studies using a single strategy.Before discussing the role of this system in cognition, a brief review of its anatomical and neurochemical organization is warranted. The septum is connected to the hippocampus via the fimbria-fornix, which carries projections ...

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Serotonin and acetylcholine release response in the rat hippocampus during a spatial memory task

Cited by 114 publications

References 71 publications

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

Blunted hippocampal, but not striatal, acetylcholine efflux parallels learning impairment in diencephalic-lesioned rats

Septohippocampal Acetylcholine: Involved in but not Necessary for Learning and Memory?

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