Cram notes: Memory

We have different kinds of memory. These can be called declarative and non-declarative.
Declarative memory is divided into semantic and episodic memory so that you can recall facts and contextual information. These can be accessed consciously: EXPLICIT.

Non-declarative memory is more to do with skills, habits and behaviours. IMPLICIT.

Learning is the acquisition of new information or knowledge; memory is the storage and retrieval of that information.

Memory has often traditionally been considered 'long term' or 'short term'. The concepts of sensory memory and the working memory have also been explored. The sensory memory is of things that just happened. The working memory is said to retain 7+/- 2. This can be improved by rehearsal. If not, material is forgotten quickly. The working memory can be trained to store a lot more than this.

Though forgetting is a natural process, if it occurs secondary to a disease it is termed amnesia. Amnesia can be caused by concussion, encephalitis or CNS resection. It can either manifest as retrograde or anterograde.

Rats have been used to explore 'where' memory is stored in the brain. It has been shown that more cortical lesions make a poorer memory. However, the location of the lesion was not linked with specific memory loss. Therefore, the memory could be seen to be quite diffuse. Hippocampal lesioning did have a profound effect on the rat's ability to remember.

Results on looking at human brain activity indicate that medial temporal lobe lesions were indicated in the loss of episodic memory. This involved the hippocampus, entorhinal and perirhinal cortices. There is also a link with the limbic system or emotion.

This picture is not one of my own, but it shows this episodic memory. 

In amnesia the more recent memories are more likely to be lost than distant ones. This is called Ribot's Law.

Semantic memory has been shown to be stored differently to episodic memory. It is located in the inferolateral temporal lobes. These are particularly affected in Alzheimer's disease and normal social inhibition is lost.

Procedural memory is spared in patients with medial temporal lobe lesions so may be stored in the supplementary motor area (area 6), basal ganglia and the cerebellum. Patients with Parkinson's disease particularly struggle with learning procedural skills.

The long term potentiation of memory has been investigated by causing a brief electrical stimulus over them, and then passing another brief high frequency burst which then leads to a higher response which lasts for longer. It improves the ability of the synapses to communicate.

Glutamate receptors in the hippocampus (AMPA) cause Na+ influx and NMDA receptors which are Mg2+ bound are activated so that Ca2+ can pass into the cell. This activates kinases and calcium-calmodulin dependent protein kinase II which can sometimes become persistantly active, being permenantly on.

If tetany is at low frequency the AMPA receptors may be internalised.

In ketamine abuse declarative episodic memories can be lost. Anterograde amnesia results from taking ketamine. This occurs via ketamine blocking the NMDA receptor, which prevents long term potentiation. There is no flow of calcium into the neurone.