Describe the animal models of memory.

Animal Models of Memory.

An invaluable contribution in the field of developing animal models of human memory and amnesia has been made by studies on monkeys. In knowing the role played by the medial temporal lobe to primate memory systems, monkeys with lesions to the hippocampus and surrounding cortex have been very helpful. The relations between specific memory and brain structures are being revealed with such models.

A variety of animal species have been studied to help understand human memory but owing to similarity among primate brains, monkeys may be more applicable to human processes.

However, human brain has organization and functional capabilities which differs in a major way from monkeys. Therefore, studies in humans, too have to be linked with animal models. The extent of the role of hippocampus causing memory deficits of patients like H.M has been a preoccupation of research. Its role has been as compared with surrounding structures in the medial temporal lobe to their involvement in episodic memory.

For instance, it has been found that amygdala plays a role in emotion and emotional memories but not in episodic memory system. To verify this, surgical lesions were created in the medial temporal lobe.

Mortimer Mishkin once concluded in his studies on the monkey that memory was impaired only if the lesion included the hippocampus and amygdala. This meant that the amygdala was a key structure in memory. However, R.B.s (R.B.s another patient) case of anterograde amnesia showed that it was caused by a lesion restricted to neurons of the hippocampus. He had no damage in the amygdala.

Thus, to know the exact part, Stuart Zola and colleagues (1993) surgically created lesions of the amygdala, the entorhinal cortex, or the surrounding neocortex of the parahippocampal gyrus and the perirhipal cortex (Brodmann’s areas 35 and 36) on monkey models.

Their research showed that only if lesions were in the cortex surrounding the hippocampus and amygdala, severe memory deficits occurred but this was not the case surrounding cortex was left without lesions. This means amygdala could not be in the , system which supported the acquisition of long-term memory.

Later, Zola and his colleagues showed that lesions of only the parahippocampal and perirhinal cortices also produced significant memory deficit. This again puts us in dilemma as in the case of R.B. damage was limited to the hippocampus and did not include the surrounding parahippocampal or perirhinal cortex. It is explained by the fact that the parahippocampal and perirhinal areas send inputs to the hippocampus and hence if these vital connections are damaged, the hippocampus is unable to function properly.

Since these regions are involved in much processing themselves, damage restricted to the hippocampus does not produce .a severe form of amnesia.

Thus, tests regarding long term memories on animals are highly consistent with studies on human amnesic patients like R.B. and H.M. Apart from this, test on preservation of short-term memory in the animals having damage in the medial temporal lobe, also show similarity with humans suggesting that, medial temporal lobe is not necessary for processes of short-term or working memory.

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