Brain damage can cause anterograde amnesia in which there is a loss of complex relational learning. At a glance it seems as though there is an inability to learn all new information, but the basic abilities of perceptual learning, sensory-response learning, and motor learning are intact.
A person with anterograde amnesia can remember events in the past, events that occurred before the brain damage, but cannot retain any information he or she encountered after the brain damage.
Korsakoff's syndrome is a severe form of anterograde amnesia that is usually a result of chronic alcoholism. This is due to the severe malnutrition that can occur from years of drinking. Alcohol is a very high calorie drink, and alcoholics often substitute regular healthy meals with a drink. Without the essential vitamine B-1 (thiamine) the end products from glycolysis (the process by which carbohydrates, fats, and proteins are broken down) cannot be further metabolized in the Kreb's cycle. It is likely that the build up of these end products (namely pyruvate) are the cause of the brain damage. Furthermore, alcohol also interferes with intestinal absorption of thiamine. For this reason, the standard medical practice is to administer thiamine along with glucose for those patients being treated for severe malnutrition. Otherwise glucose would only be partially metabolized and pyruvate would still build up in the patient.
Anterograde amnesia can also be caused by bilateral damage to the temporal lobes. In an attempt to alleviate some psychotic disturbances in patients, nurosurgeons were lesioning the hippocampal formation. This worked reasonably well (I think) until they lesioned one patient and didn't know that he had damage to the other hippocampal formation. So at the end of the operation he had bilateral destruction, and he was all messed up with memory problems. Man, I'd be so pissed. Now they do a pre-surgical test in order to determine if either temporal lobe is damaged.
Short term memory is an immediate memory for stimuli that have just been perceived. Long term memories consist of relatively permanent biochemical or structural changes in neurons (called long term potentiation). A way to store short-term memory is repetition until it becomes ingrained in long-term.
Three very basic and simple conclusions about memory function are as follows:
1. The hippocampus is not the location of long-term memories; nor is it necessary for the retrival of long-term memory. Otherwise, people with anterograde amnesia would not be able to remember pre-brain damage events.
2. The hippocampus is not the location of immediate (short-term) memories. If it were, patients wouldn't even be able to hold a conversation with their doctors. People with retrograde amnesia can remember what they are presently thinking about, but as soon as they look away, or become distracted, the conversation, image, whatever is gone forever.
3. The hippocampus is involved in converting immediate (short-term) memories into long-term memories.
The conversion of short-term memory into long-term memory is called consolidation, memories are made solid.
Damage to the hippocampus, or regions that supply its inputs and receive its outputs, causes anterograde amnesia.
Certain learning abilities are spared with retrograde amnesia. These abilities include perceptual learning, sensory-response learning, and motor learning. An example of perceptual learning would be a series of drawings that are disconnected and broken, and become more connected as the series progresses until the final drawing presents a full comprehensive image. Patients that do the exercise over and over can learn to recognize the images sooner and sooner - even though they don't remember they have ever seen them before. Sensory-response learning is basically classical conditioning. A patient with retrograde amnesia can be classically conditioned to eyeblink with a stimulus before a puff of air. An example of motor learning is learning to draw images while looking at an object in the mirrow, which is really difficult but patients that do it over become really good at it, even though they say that they have never done it before.
So learning can take place after retrograde amnesia occurs, but the patient doesn't know it, isn't conciously aware of it. Patients can learn to perform these tasks, they do not remember anyting abou having learned them.
Declarative memories are defined as those that are explicity available to conscious recollection as facts, events, or specific stimuli (you remember that George Washington is the first president of the US). Non-declarative memories include instances of perceptual, stimulus-response, and motor learning that we aren't conscious of. They appear to opperate automatically (you remeber how to ride a bike, without thinking of every individual action necessary to do so).
Episodic memories consist of collections of perceptions of events organized in time and identified by a particular context. This is a type of relational learning, which is lost to people with bilateral temporal damage.
The most important input into the hippocampus is the entorhinal cortex. Neurons there have axons that terminate in the dentate gyrus, CA1 and CA3. The entorhinal cortex receives inputs from the cingulate cortex (hey, hey, part of the limbic system!!) both directly and via two different regions of the limbic cortex: the perirhinal and parahippocampal cortex.
The hippocampal functions are controlled by dopaminergic input, noradrenergic input, serotonergic input, and acetylcholiinergic input from different areas of the brain.
The CA1 field of the hippocampal formation is very sensitive to anoxia and even short periods of time wihout oxygen can destruct this region, more so than other regions. This region is especially rich in NMDA (so that long term potentiate can occur here) receptors which are very sensitive to oxygen. Animals that are pretreated with drugs that block NMDA receptors are much less affected by periods of anoxia.
Lesions to the amygdala do not seem to affect relational learning, but lesioning the surrounding cortex of this structure does.
Once again, damage to the hippocampal system or its major inputs and outputs causes anterograde amnesia. The anterior thalamus seems to be a major input, so....
Working memory consists of information about things that have just happened, erasable memory that is repalced on a regular basis. Reference memory is permanent, long-term memory, produced by consistent conditions.
Hippocampal formations play a part in land-mark recognition. This was demonstrated by lesioned homing-pigeons, and by rats in the lab, and by certain species of birds and rodents that store food and come back for it later.
Place cells are located in the hippocampus and are only active when the animal is in a specific location. That is, different neurons have different spatial receptive fields. Place cells respond to places defined in relation to objects in the environment.