Hi everyone! I'm a bit confused with this dotpoint 'interactions between specific regions of the brain (cerebral cortex, hippocampus, amygdala and cerebellum) in the storage of long-term memories, including implicit and explicit memories.' What else would I need to know besides what kind of memories each region specialises in? And I don't really understand what they mean by the interactions. Thank you!
I think it is trying to highlight interactions such as that between the amygdalae and hippocampi in the encoding of emotionally-arousing memories. (Quite similar to the question above yours!)
From Jacaranda: "Through its interaction with the amygdala, then hippocampus also plays a role in the formation of emotional memories, particularly the explicit memory component of an emotional event."
It may also be referring to processes - like the transfer of LTM from hippocampi to cerebral cortex, and the way they are stored there. For example, memories aren't stored in one separate cortical area, but rather are spread over many areas of the brain and are 'combined' into a fluid, whole reconstruction when recalled.
The Jacaranda textbook gives this example: "...the name of the band will be stored in a cortical area involved with language (frontal lobe), images in visual cortex (occipital lobe) and sounds in auditory cortex (temporal lobe). Furthermore, the different components are linked to ensure they do not remain a collection of separate memories. When required, the separate parts are gathered together and reconstructed as a single, integrated memory for retrieval into our conscious awareness. This can be likened to pieces of a jigsaw coming together to create a vivid recollection. The cortex has a crucial role in this process, particularly for explicit memories (Bergland, 2015)."
Need clarification specifically on adrenaline's role on consolidation of emotionally arousing memories as I felt a bit hesitant about my response to a question that involved this concept.
During a stressful situation adrenaline is released which in turn stimulates release of noradrenaline neurotransmitters which signals the amygdala that a particular experience needs to be strengthened and reinforced in the long term memory. The amygdala then communicates this message to the hippo campus and encodes the emotional response of an experience which is then stored in the cerebral cortex.
Is this correct or am I saying something wrong? Not too sure on how the amygdala interacts with the hippo campus and whether this is important or not.
Cheers in advance
It looks pretty good to me! You have included the neuronal/physiological basis of emotional memory encoding (including the roles of the amygdala and hippocampus) and then the storage afterwards.
This is from the Jacaranda textbook: "...adrenaline induces the release of noradrenaline in the amygdala. The presence of noradrenaline is believed to stimulate the amygdala to attach more emotional significance to the experience and signal the hippocampus to encode..."
I found an interesting Wikipedia page that also might make sense of the whole 'signalling to the hippocampus':
https://en.wikipedia.org/wiki/Fear_processing_in_the_brain#Molecular_basisI'm going to try and explain it here, but please take it with a grain of salt because I'm not confident I understand it wholly myself.
Essentially, in the amygdala, there are beta-adrenergic receptors that bond with noradrenaline (and others, but for the sake of simplicity). The receptors (especially beta2 ones) are activated during flight-or-fight (lending into our ideas of emotional arousal). Research has found when these receptors are blockaded (when noradrenaline cannot bond to them)
acquisition of fear learning is prevented, but not the retrieval of fear memories. On the other hand, when noradrenaline interacts with these beta-adrenergic receptors, it also affects GABAergic interneurons by inhibiting their effect. GABA, if you remember, has an inhibitory effect and doesn't help with LTP. Therefore, the inhibiting effect of GABA is reduced, and instead the effect of glutamate is heightened. This activates Hebbian synaptic plasticity (think LTP and Hebb's Law: neurons that fire together, wire together). Therefore, the fear learning is strengthened as a result of noradrenaline interaction with the amygdala, which triggers all of these effects which will affect encoding in the hippocampus.
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