or if they are filtered out after the brain examines their significance. Mapping Activity Positron emission tomography (PET) demonstrates a consistent functional anatomical blueprint of hippocampal activation during episodic encoding and retrieval. Activation in the hippocampal region associated with episodic memory encoding has been shown to occur in the rostral portion of the region whereas activation associated with episodic memory retrieval occurs in the caudal portions. This is referred to as the Hippocampal memory encoding and retrieval model or HIPER model. One study used PET to measure cerebral blood flow during encoding and recognition of faces in both young and older participants. Young people displayed increased cerebral blood flow in the right hippocampus and the left prefrontal and temporal cortices during encoding and in the right prefrontal and parietal cortex during recognition. Elderly people showed no significant activation in areas activated in young people during encoding, however they did show right prefrontal activation during recognition. Thus it may be concluded that as we grow old, failing memories may be the consequence of a failure to adequately encode stimuli as demonstrated in the lack of cortical and hippocampal activation during the encoding process. Recent findings in studies focusing on patients with post traumatic stress disorder demonstrate that amino acid transmitters, glutamate and GABA, are intimately implicated in the process of factual memory registration, and suggest that amine neurotransmitters, norepinephrine-epinephrine and serotonin, are involved in encoding emotional memory. Molecular Perspective The process of encoding is not yet well understood, however key advances have shed light on the nature of these mechanisms. Encoding begins with any novel situation, as the brain will interact and draw conclusions from the results of this interaction. These learning experiences have been known to trigger a cascade of molecular events leading to the formation of memories. These changes include the modification of neural synapses, modification of proteins, creation of new synapses, activation of gene expression and new protein synthesis. One study found that high central nervous system levels of acetylcholine during wakefulness aided in new memory encoding, while low levels of acetylcholine during slow-wave sleep aided in consolidation of memories. However, encoding can occur on different levels. The first step is short-term memory formation, followed by the conversion to a long-term memory, and then a long-term memory consolidation process. Synaptic Plasticity Synaptic plasticity is the ability of the brain to strengthen, weaken, destroy and create neural synapses and