Emotion, memory and small conductance channels

Our deepest and most vivid memories are usually triggered by traumatic events provoking strong emotions such as fear, love or rage.

It is known that this effect is precipitated by the release of stress hormones like adrenaline and corticosterone and the activation of adrenergic receptors in the amygdala, which plays a major role in emotional learning.

The actual cellular mechanisms are only partially understood. Now, researchers from the Queensland Brain Institute (QBI) led by Dr Louise Faber have described a new mechanism by which emotional memories are formed.

The QBI researchers have found that the activation of beta adrenergic receptors – or adrenoceptors – regulates certain channels in neurons in the amygdala. These small conductance (SK) channels are present in neuronal synapses in the amygdala and the hippocampus and work to limit synaptic transmission and plasticity.

In a paper published in the Journal of Neuroscience, the team has found that activation of beta adrenoceptors removes these channels from excitatory synapses, resulting in enhanced synaptic transmission and plasticity. The mechanism is mediated by protein kinase A.

Functionally, the researchers say, the modulation of SK channels by beta adrenoceptor activation enhances long-term potentiation – the increase in communication between neurons that is the basis of learning and memory.

“Modulation of SK channel trafficking by beta adrenoceptors enhances excitatory synaptic transmission and plasticity in the amygdala” by Louise Faber et al is published in the Journal of Neuroscience [doi: 10.1523/jneruosci.1796-08.2008].