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Download references. You can also search for this author in PubMed Google Scholar. Correspondence to Gordon B. Reprints and Permissions. Feld, G. Neurochemical mechanisms for memory processing during sleep: basic findings in humans and neuropsychiatric implications.
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Download PDF. Subjects Circadian rhythms and sleep Consolidation Human behaviour. Abstract Sleep is essential for memory formation. You have full access to this article via your institution. Introduction Sleep benefits the long-term storage of memories [ 1 , 2 , 3 , 4 ]. Box 1: Memory domains: memory can be subdivided into different domains that rely on different brain structures On the first level, the differentiation between declarative and procedural memory is most common.
Theoretical frameworks The field of sleep and memory is in the fortunate position of having two strong theories that have been developed to accommodate its findings. Full size image. Glutamatergic neurotransmission Learning in the brain is thought to mainly rely on Hebbian plasticity where neurons that are active together get connected more tightly, so that activating one neuron will soon activate the other, i.
GABAergic neuromodulation GABA, the main inhibitory neurotransmitter of the brain, contributes to all of the major sleep EEG rhythms and GABAergic neurons, mainly in the ventrolateral preoptic area, that inhibit arousal centers in the brainstem, hypothalamus, and basal forebrain have been identified as crucial for sleep induction and maintenance [ 96 ]. Dopaminergic neuromodulation Dopamine plays a central role for reward-related memory processing [ , ], dopaminergic imbalances contribute to several neuropsychiatric disorders, including schizophrenia and depression [ ], and reward-related learning mechanisms are central in the pathogenesis of addiction [ ].
Acetylcholine Among the neurotransmitters of the brain, acetylcholine ACh plays an important and possibly the best-characterized role for active systems consolidation. Cortisol The adrenal gland hormone cortisol plays a similarly complex role for the different phases of memory formation.
Neuropsychiatric implications From a sleep research point of view, it is generally very interesting that neuropsychiatric disorders often come hand in hand with sleep disorders. Phobias Specific phobias that entail being afraid of and avoiding certain objects or places are among the most prevalent anxiety disorders [ , ]. Depression It has long been known that patients suffering major depression are biased towards remembering negative events [ ], and it has been suggested that a competition between negative and positive memories may lie at the root of this disorder, as well as its therapeutic improvement [ ].
Addiction Similar to anxiety, a two process theory of drug addiction has been developed [ , ], where the positive effects of the substance are connected to the context of consuming it through classical conditioning. Future directions and clinical implications While significant progress has been made in deciphering the neurochemical mechanisms of sleep-dependent memory processing, the sheer complexity and the vast difference to wake encoding machinery is only beginning to be appreciated.
Funding and disclosure G. References 1. Google Scholar 7. Google Scholar 8. Google Scholar 9. CAS Google Scholar PubMed Google Scholar Google Scholar PubMed Google Scholar Download references.
These neurotransmitters are then detected by postsynaptic receptors in the recipient cell. As information in the brain generally flows from the pre- to the postsynaptic neuron, it might seem unlikely to find any neurotransmitter receptors on the presynaptic, transmitting side Figure 1A.
A In the textbook view of central neurotransmission, the presynaptic spike lightning symbol elicits the release of a neurotransmitter e. B However, Lituma et al. Yet, early electron microscopy studies revealed that N-methyl-D-aspartate receptors NMDARs — which are glutamate receptors and ion channels — are present on both pre- and postsynaptic neurons e.
NMDARs on postsynaptic cells play an important role in memory formation and Hebbian plasticity — that is, the strengthening of the connections between presynaptic and postsynaptic neurons that are activated together.
However, their roles on the presynaptic side remain hotly debated Wong et al. Lituma et al. These axons help to encode contextual and spatial memory by forming the main information pathway from the dentate gyrus to the CA3 region of the hippocampus, where they contact both excitatory pyramidal neurons and inhibitory neurons Rebola et al. To identify the purpose of these preNMDARs, the researchers explored low-frequency facilitation, a form of short-term plasticity specific to mossy fiber synapses.
As expected, stimulation at 1 Hz temporarily strengthened the mossy fiber connections onto CA3 neurons in mouse brain tissue. However, pharmacologically blocking the receptors, or selectively deleting them through genetic engineering, reduced low-frequency facilitation, indicating an involvement of preNMDARs. Next, Lituma et al. Therefore they stimulated mossy fibers using optogenetics and electrophysiological methods to mimic the brief bursts of action potentials seen in granule cells of the intact brain.
Indeed, connections between mossy fibers and CA3 neurons were strengthened during these brief bursts. The purpose of the present study was to investigate this issue. The investigation was carried out by reviewing relevant studies of neurochemistry and cognition. Inclusion criteria were set for selection of behavioral tasks to be elucidated and for studies employing acceptable tasks. We chose to use a one-trial step-down inhibitory passive avoidance task in rats for several reasons.
Second, it depends on the integrated activity of a well-studied neural circuit, i. Fourth, years of work have established that using a 0. Finally, it has been reliably shown to depend on the actual inhibition of one particular response stepping down with the four paws on the grid and not of others rearing, exploration, sticking the head out, placing just the forepaws on the grid. Our methodology consisted in testing animals twice: first at 1.
One concern was whether testing the animals twice might alter LTM either by extinction or by a reminder effect. This was ruled out by two facts: First, there were no significant differences in control groups between STM and LTM performance in any of our studies Figures Second, it was recently shown that repeated testing over the first 6 h after training does not lead to extinction, whereas repeated testing between 9 and 96 h does Medina et al.
The whole data is published elsewhere Izquierdo et al. Results shown in Figure 1 demonstrate the involvement of the different glutamatergic receptor subtypes, and of the , colinergic muscarinic, dopaminergic D1 and of the serotonergic hippocampal receptors on the early events of STM and LTM processsing. The subsequent data Figures demonstrate the selective contribution of different signal transduction cascades to the prolonged postraining period of STM and LTM simultaneous processing.
Interestingly, some treatments selectively affected one but not the other memory type. These results, specially those obtained with the infusion of and receptor agonists, clearly demonstrates the independence of both memory types. The two compounds given 10 min before, or 50 or min after training canceled LTM.
As shown in figure 4 , STM was cancelled when PD was given immediatelly after training whereas LTM was sensitive to the inhibitor only when administration occurred three hours later.
As shown in Figures , we were indeed able to replicate and considerably extend the separation of short- and long-term plastic events demonstrated by Emptage and Carew Our results clearly demonstrate that STM and LTM are in a great degree independent phenomena, recruiting cellular and molecular events in a separate manner.
Several of the neurotransmitter systems and signal transduction cascades studied were demonstrated to be selectively involved in STM and LTM processing, contributing at diferent time-windows of the posttraining period. Moreover, the abolishment of STM without interference on LTM retention by several drugs definitively points to the independence of both memory types.
Of course, in addition, there are links between the mechanisms of STM and of LTM at the receptor and at the post-receptor level. Frey and Morris have suggested various possible mechanisms of 'synaptic tagging' in order to explain the links between STP and LTP, or between the very early 0 min and the much later h molecular events that determine persistence of the plastic change over long periods of time. PKA clearly has separate influences on the two memory types.
It is in charge of STM between 0 and 90 min after training, and it is in charge of LTM at 0 and again at min after training, but not in the period between these two peaks Vianna et al.
Whereas LTM apparently does not discriminate among the PKC isoforms, depending on their activity during almost two hours after training, STM selectively recruits the and I isoforms in a more restricted time-window Figure 3. This also correlates with the report by Paratcha et al. The findings on STM may also agree with those of Bourtchouladze et al. It is tempting to suggest that some substrate of the studied kinases may be involved in the tagging of synapses during the early phase of memory formation in CA1, during which STM runs its full course Vianna et al.
The relative importance or intervention of one or other link, or one or other modulatory mechanism, would be expected to vary with the nature of the task, and with the relation of each task to others Izquierdo , Medina et al. Therefore, it might be judicious at this stage to refrain from postulating theoretical connections or disconnections among memory types.
Further research will no doubt contribute to this, and will eventually find out the extent to which some or all of the many hypothetical constructs on cognition Gold , McGaugh , Squire are right or wrong. At this stage it is safe to say that STM and LTM pertain to and are regulated by separate subsystems of the brain, which belong in some cases to the same and in others to different brain structures see Izquierdo et al.
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