known as the memory enhancement effect. patients with amygdala damage, however, do not show a memory enhancement effect. hebb distinguished between short-term and long-term memory. he postulated that any memory that stayed in short-term storage for a long enough time would be consolidated into a long-term memory. later research showed this to be false. research has shown that direct injections of cortisol or epinephrine help the storage of recent experiences. this is also true for stimulation of the amygdala. this proves that excitement enhances memory by the stimulation of hormones that affect the amygdala. excessive or prolonged stress (with prolonged cortisol) may hurt memory storage. patients with amygdalar damage are no more likely to remember emotionally charged words than nonemotionally charged ones. the hippocampus is important for explicit memory. the hippocampus is also important for memory consolidation. the hippocampus receives input from different parts of the cortex and sends its output out to different parts of the brain also. the input comes from secondary and tertiary sensory areas that have processed the information a lot already. hippocampal damage may also cause memory loss and problems with memory storage. this memory loss includes retrograde amnesia which is the loss of memory for events that occurred shortly before the time of brain damage. cognitive neuroscience cognitive neuroscientists consider memory as the retention, reactivation, and reconstruction of the experience-independent internal representation. the term of internal representation implies that such a definition of memory contains two components: the expression of memory at the behavioral or conscious level, and the underpinning physical neural changes (dudai 2007). the latter component is also called engram or memory traces (semon 1904). some neuroscientists and psychologists mistakenly equate the concept of engram and memory, broadly conceiving all persisting after-effects of experiences as memory; others argue against this notion that memory does not exist until it is revealed in behavior or thought (moscovitch 2007). one question that is crucial in cognitive neuroscience is how information and mental experiences are coded and represented in the brain. scientists have gained much knowledge about the neuronal codes from the studies of plasticity, but most of such research has been focused on simple learning in simple neuronal circuits; it is considerably less clear about the neuronal changes involved in more complex examples of memory, particularly declarative memory that requires the storage of facts and events (byrne 2007). convergence-divergence zones might be the neural networks where memories are stored and retrieved. considering that there are several kinds of memory, depending on types of represented knowledge, underlying mechanisms, processes functions and modes of acquisition, it is likely that different brain areas support different memory systems and that they are in mutual relationships in neuronal networks: "components of memory representation are distributed widely across different parts of the brain as mediated by multiple neocortical circuits". encoding. encoding of working memory involves the spiking of individual neurons induced by sensory input, which persists even after the sensory input disappears (jensen and lisman 2005; fransen et al. 2002). encoding of episodic memory involves persistent changes in molecular structures that alter synaptic transmission between neurons. examples of such structural changes include long-term potentiation (ltp) or spike-timing-dependent plasticity (stdp). the persistent spiking in working memory can enhance the synaptic and cellular changes in the encoding of episodic memory (jensen and lisman 2005). working memory. recent functional imaging studies detected working memory signals in both medial temporal lobe (mtl), a brain area strongly associated with long-term memory, and prefrontal cortex (ranganath et al. 2005), suggesting a strong relationship between working memory and long-term memory. however, the substantially more working memory signals seen in the prefrontal lobe suggest that this area plays a more important role in working memory than mtl (suzuki 2007). consolidation and reconsolidation. short-term memory (stm) is temporary and subject to disruption, while long-term memory (ltm), once consolidated, is persistent and stable. consolidation of stm into ltm at the molecular level presumably involves two processes: synaptic consolidation and system consolidation. the former involves a protein synthesis process in the medial temporal lobe (mtl), whereas the latter transforms the mtl-dependent memory into an mtl-independent memory over months to years (ledoux 2007). in recent years, such traditional consolidation dogma has been re-evaluated as a result of the studies on reconsolidation. these studies showed that prevention after retrieval affects subsequent retrieval of the memory (sara 2000). new studies have shown that post-retrieval treatment with protein synthesis inhibitors and many other compounds can lead to an amnestic state (nadel et al. 2000b; alberini 2005; dudai 2006). these findings on reconsolidation fit with the behavioral evidence that retrieved memory is not a carbon copy of the initial experiences, and memories are updated during retrieval. genetics