Acetylcholine and associative memory in the piriform cortex

Barkai, Edi; Hasselmo, Michael

doi:10.1007/bf02740613

Cited by 39 publications

(20 citation statements)

References 36 publications

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“…For example, Hasselmo and colleagues have been concerned with the differential effects of high and low levels of acetylcholine on the processing of information in the piriform cortex (Barkai & Hasselmo, 1997;Hasselmo, Anderson, & Bower, 1992), entorhinal cortex (Hasselmo, Fransen, Dickson, & Alonso, 2000), and hippocampus (Giocomo & Hasselmo, 2005); see also (McGaughy, Koene, Eichenbaum, & Hasselmo, 2005). Most relevant to the present findings is the hypothesis that high levels of ACh promote the encoding of memory by facilitating sensory transmission while at the same time suppressing recurrent excitation and intracortical processing.…”

Section: The Cholinergic Nucleus Basalis and The Encoding And Storagementioning

confidence: 81%

The level of cholinergic nucleus basalis activation controls the specificity of auditory associative memory

Weinberger

Miasnikov

Chen

2006

Neurobiology of Learning and Memory

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Learning involves not only the establishment of memory per se, but also the specific details of its contents. In classical conditioning, the former concerns whether an association was learned while the latter discloses what was learned. The neural bases of associativity have been studied extensively while neural mechanisms of memory specificity have been neglected. Stimulation of the cholinergic nucleus basalis (NBs) paired with a preceding tone induces CS-specific associative memory. As different levels of acetylcholine may be released naturally during different learning situations, we asked whether the level of activation of the cholinergic neuromodulatory system can control the degree of detail that is encoded and retrieved. Adult male rats were tested pre-and post-training for behavioral responses (interruption of ongoing respiration) to tones of various frequencies (1-15 kHz, 70 dB, 2 s). Training consisted of 200 trials/day of tone (8.0 kHz, 70 dB, 2 s) either paired or unpaired with NBs (CS-NBs = 1.8 s) at moderate (65.7 ± 9.0 μA, one day) or weak (46.7 ± 12.1 μA, three training days) levels of stimulation, under conditions of controlled behavioral state (pre-trial stable respiration rate). Post-training (24 h) responses to tones revealed that moderate activation induced both associative and CS-specific behavioral memory, whereas weak activation produced associative memory lacking frequency specificity. The degree of memory specificity 24 h after training was positively correlated with the magnitude of CS-elicited increase in γ activity within the EEG during training, but only in the moderate NBs group. Thus, a low level of acetylcholine released by the nucleus basalis during learning is sufficient to induce associativity whereas a higher level of release enables the storage of greater experiential detail. γ waves, which are thought to reflect the coordinated activity of cortical cells, appear to index the encoding of CS detail. The findings demonstrate that the amount of detail in memory can be directly controlled by neural intervention.

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Section: The Cholinergic Nucleus Basalis and The Encoding And Storagementioning

confidence: 81%

The level of cholinergic nucleus basalis activation controls the specificity of auditory associative memory

Weinberger

Miasnikov

Chen

2006

Neurobiology of Learning and Memory

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“…Acetylcholine plays a major role in odor processing and plasticity throughout the olfactory pathway from the OB [9, 23], to PCX [4, 26] to the EC [6]. In the piriform cortex, muscarinic receptor agonists suppress association fiber synaptic efficacy through a reduction in pre-synaptic glutamate release, with minimal effect on afferent fiber synapses from mitral cells [18, 25] and enhance long-term potentiation of association fiber synapses [17].…”

Section: Discussionmentioning

confidence: 99%

Cholinergic modulation of olfactory pattern separation

Chapuis

Wilson

2013

Neuroscience Letters

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Pattern separation plays an important role in perception and memory. In olfaction, pattern separation is critical component of piriform cortical odor processing contributing to behavioral perception of overlapping odor mixtures. Previous work has demonstrated that odor discrimination ability is modulated by acetylcholine. Here, we extended this previous work by using a distinct, well characterized complex odor stimulus set that has been shown to differentially involve pattern separation processes within piriform cortex. We find that the cholinergic muscarinic receptor agonist oxotremorine facilitates the acquisition of odor discrimination. Furthermore, the muscarinic receptor antagonist scopolamine impairs acquisition of odor discrimination even if the antagonist is limited to the piriform cortex. Finally, acetylcholine effects are most robust during discrimination acquisition, with minimal effects during expression.

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“…Deterioration of cholinergic neurons in the medial septal nucleus that project to the hippocampus, amygdale, and cortex (e.g., critical memory areas) was demonstrated in rat models of epilepsy [172]. In support, acetylcholine esterase inhibitors are shown to improve memory functioning in diverse neurological conditions [173]. The hippocampus, a cerebral structure highly involved in learning and memory, is a target for abundant cholinergic innervation and hippocampal nicotinic acetylcholine receptors that modulate synaptic plasticity via mechanisms involved in LTP [174].…”

Section: Cognitive States With Antiepileptic Medicationsmentioning

confidence: 99%

The Aspects and Mechanisms of Cognitive Alterations in Epilepsy: The Role of Antiepileptic Medications

Hamed

2009

CNS Neuroscience & Therapeutics

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Epilepsy is a major health problem. Several studies suggest a significant influence of epilepsy and its treatment on dynamic and functional properties of brain activity. Epilepsy can adversely affect mental development, cognition, and behavior. Epileptic patients may experience reduced intelligence, attention, and problems in memory, language, and frontal executive functions. Neuropsychological, functional, and quantitative neuroimaging studies revealed that epilepsy affect the brain as a whole. Mechanisms of epilepsy-related cognitive dysfunction are poorly delineated. Cognitive deficits with epilepsy may be transient, persistent, or progressive. Transient disruption of cognitive encoding processes may occur with paroxysmal focal or generalized epileptic discharges, whereas epileptogenesis-related neuronal plasticity, reorganization, sprouting, and impairment of cellular metabolism are fundamental determinants for progressive cognitive deterioration. Also antiepileptic drugs (AEDs) have differential, reversible, and sometimes cumulative cognitive adverse consequences. AEDs not only reduce neuronal irritability but also may impair neuronal excitability, neurotransmitter release, enzymes, and factors critical for information processing and memory. The present article serves as an overview of recent studies in adult and childhood epilepsy literatures present in PubMed that highlighted cognitive evaluation in epilepsy field (publications till 2008 were checked). We also checked the reference lists of the retrieved studies for additional reports of relevant studies, in addition to our experience in this field. Our search revealed that although the aspects of cognitive dysfunction, risk factors, and consequences have been explored in many studies; however, the mechanisms of contribution of epilepsy-related variables, including AEDs, to patients' cognition are largely unexplored. In this review, we discussed the differential effect of AEDs in mature and immature brains and the known mechanisms underlying epilepsy and AEDs adverse effects on cognition. The nature, timing, course, and mechanisms of cognitive alteration with epilepsy and its medications are of considerable clinical and research implications.

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Acetylcholine and associative memory in the piriform cortex

Cited by 39 publications

References 36 publications

The level of cholinergic nucleus basalis activation controls the specificity of auditory associative memory

The level of cholinergic nucleus basalis activation controls the specificity of auditory associative memory

Cholinergic modulation of olfactory pattern separation

The Aspects and Mechanisms of Cognitive Alterations in Epilepsy: The Role of Antiepileptic Medications

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