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Emotional enhancement of memory: how norepinephrine enables synaptic plasticity.

Tully K, Bolshakov VY - Mol Brain (2010)

Bottom Line: Changes in synaptic strength are believed to underlie learning and memory.Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes.We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Psychiatry, McLean Hospital, Harvard Medical School, 115 Mill Street, Belmont, Massachusetts 02478, USA. ktully@mclean.harvard.edu

ABSTRACT
Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.

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Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase in neurons of the locus coeruleus. Before the final β-oxidation, norepinephrine is transported into synaptic vesicles by a vesicual monoamine transporter. The vesicles are then transported along the axons comprising the noradrenergic bundle to release sites. At the synapse norepinephrine is released into the synaptic cleft where it binds to various pre- and post-synaptic adrenergic receptors which subsequently activate distinct G protein coupled signal cascades.
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Figure 1: Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase in neurons of the locus coeruleus. Before the final β-oxidation, norepinephrine is transported into synaptic vesicles by a vesicual monoamine transporter. The vesicles are then transported along the axons comprising the noradrenergic bundle to release sites. At the synapse norepinephrine is released into the synaptic cleft where it binds to various pre- and post-synaptic adrenergic receptors which subsequently activate distinct G protein coupled signal cascades.

Mentions: Norepinephrine, also called noradrenaline, is a catecholamine produced by dopamine β-hydroxylase [33] which is released either as a hormone from the adrenal medulla into the blood or as a neurotransmitter in the brain. Norepinephrine in the brain is synthesized primarily in neurons in the locus coeruleus and to a lesser extent in the lateral tegmental field [29]. Within these neurons norepinephrine is transported by vesicular monoamine transporters into synaptic vesicles and carried along the axons composing the noradrenergic bundle to the sites of release [34] (Figure 1). These neurons send projections throughout the brain where norepinephrine performs its action upon release and binding to the G protein-coupled adrenergic receptors. It is followed by degradation of norepinephrine and/or its reuptake. There are two classes of adrenergic receptors, α and β, with each of them divided into several subtypes [35]. The subtypes of α receptors include Gq-coupled α1receptors and Gi-coupled α2 receptors. Activation of three different subtypes of β-receptors (β1, β2, β3), linked to Gs proteins, results in a rise in the intracellular cyclic AMP concentration and subsequent PKA activation.


Emotional enhancement of memory: how norepinephrine enables synaptic plasticity.

Tully K, Bolshakov VY - Mol Brain (2010)

Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase in neurons of the locus coeruleus. Before the final β-oxidation, norepinephrine is transported into synaptic vesicles by a vesicual monoamine transporter. The vesicles are then transported along the axons comprising the noradrenergic bundle to release sites. At the synapse norepinephrine is released into the synaptic cleft where it binds to various pre- and post-synaptic adrenergic receptors which subsequently activate distinct G protein coupled signal cascades.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2877027&req=5

Figure 1: Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase in neurons of the locus coeruleus. Before the final β-oxidation, norepinephrine is transported into synaptic vesicles by a vesicual monoamine transporter. The vesicles are then transported along the axons comprising the noradrenergic bundle to release sites. At the synapse norepinephrine is released into the synaptic cleft where it binds to various pre- and post-synaptic adrenergic receptors which subsequently activate distinct G protein coupled signal cascades.
Mentions: Norepinephrine, also called noradrenaline, is a catecholamine produced by dopamine β-hydroxylase [33] which is released either as a hormone from the adrenal medulla into the blood or as a neurotransmitter in the brain. Norepinephrine in the brain is synthesized primarily in neurons in the locus coeruleus and to a lesser extent in the lateral tegmental field [29]. Within these neurons norepinephrine is transported by vesicular monoamine transporters into synaptic vesicles and carried along the axons composing the noradrenergic bundle to the sites of release [34] (Figure 1). These neurons send projections throughout the brain where norepinephrine performs its action upon release and binding to the G protein-coupled adrenergic receptors. It is followed by degradation of norepinephrine and/or its reuptake. There are two classes of adrenergic receptors, α and β, with each of them divided into several subtypes [35]. The subtypes of α receptors include Gq-coupled α1receptors and Gi-coupled α2 receptors. Activation of three different subtypes of β-receptors (β1, β2, β3), linked to Gs proteins, results in a rise in the intracellular cyclic AMP concentration and subsequent PKA activation.

Bottom Line: Changes in synaptic strength are believed to underlie learning and memory.Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes.We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Psychiatry, McLean Hospital, Harvard Medical School, 115 Mill Street, Belmont, Massachusetts 02478, USA. ktully@mclean.harvard.edu

ABSTRACT
Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.

Show MeSH
Related in: MedlinePlus