Intermediate-term memory (ITM) is a stage of memory distinct from sensory memory, working memory/short-term memory, and long-term memory. [1] [2] [3] While sensory memory persists for several milliseconds, working memory persists for up to thirty seconds, and long-term memory persists from thirty minutes to the end of an individual's life, intermediate-term memory persists for about two to three hours. [4] This overlap in the durations of these memory processes indicates that they occur simultaneously, rather than sequentially. Indeed, intermediate-term facilitation can be produced in the absence of long-term facilitation. [5] However, the boundaries between these forms of memory are not clear-cut, and they can vary depending on the task. [6] Intermediate-term memory is thought to be supported by the parahippocampal cortex. [7]
In 1993, Rosenzweig and colleagues demonstrated that, in chicks conditioned with an aversive stimulus, percent avoidance of the stimulus (and, by implication, memory of the aversive nature of the stimulus) reached relative minima at one minute, fifteen minutes, and sixty minutes. [8] These dips were theorized to correspond to the time points in which the chicks switched from working memory to intermediate-term memory, from intermediate-term memory to the early phase of long-term memory, and from the early phase of long-term memory to the late phase of long-term memory, respectively—thus demonstrating the presence of a form of memory that exists between working memory and long-term memory, which they referred to as "intermediate-term memory".
Though the idea of intermediate-term memory has existed since the 1990s, Sutton et al. introduced a novel theory for the neural correlates underlying intermediate-term memory in Aplysia in 2001, where they described it as the primary behavioral manifestation of intermediate-term facilitation. [9]
In 2001, Sutton and colleagues proposed that intermediate-term memory possesses the following 3 characteristics:
Because intermediate-term memory does not involve transcription, it likely involves the translation of mRNA transcripts already present in neurons. [4] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22]
Unlike short-term memory and working memory, intermediate-term memory requires changes in translation to occur in order to function.
While ITM requires only changes in translation, induction of long-term memory requires changes in transcription as well. [23] The change from short-term memory to long-term memory is thought to dependent on CREB, which regulates transcription, but because ITM does not involve a change in transcription, it is thought to be independent of CREB activity. [4] According to the definition of ITM proposed by Sutton et al. in 2001, it disappears completely before long-term memory is induced. [9]
Eric Richard Kandel is an Austrian-born American medical doctor who specialized in psychiatry, a neuroscientist and a professor of biochemistry and biophysics at the College of Physicians and Surgeons at Columbia University. He was a recipient of the 2000 Nobel Prize in Physiology or Medicine for his research on the physiological basis of memory storage in neurons. He shared the prize with Arvid Carlsson and Paul Greengard.
A dendritic spine is a small membranous protrusion from a neuron's dendrite that typically receives input from a single axon at the synapse. Dendritic spines serve as a storage site for synaptic strength and help transmit electrical signals to the neuron's cell body. Most spines have a bulbous head, and a thin neck that connects the head of the spine to the shaft of the dendrite. The dendrites of a single neuron can contain hundreds to thousands of spines. In addition to spines providing an anatomical substrate for memory storage and synaptic transmission, they may also serve to increase the number of possible contacts between neurons. It has also been suggested that changes in the activity of neurons have a positive effect on spine morphology.
In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.
The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor is an ionotropic transmembrane receptor for glutamate (iGluR) that mediates fast synaptic transmission in the central nervous system (CNS). It has been traditionally classified as a non-NMDA-type receptor, along with the kainate receptor. Its name is derived from its ability to be activated by the artificial glutamate analog AMPA. The receptor was first named the "quisqualate receptor" by Watkins and colleagues after a naturally occurring agonist quisqualate and was only later given the label "AMPA receptor" after the selective agonist developed by Tage Honore and colleagues at the Royal Danish School of Pharmacy in Copenhagen. The GRIA2-encoded AMPA receptor ligand binding core was the first glutamate receptor ion channel domain to be crystallized.
In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory.
In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.
The mushroom bodies or corpora pedunculata are a pair of structures in the brain of insects, other arthropods, and some annelids. They are known to play a role in olfactory learning and memory. In most insects, the mushroom bodies and the lateral horn are the two higher brain regions that receive olfactory information from the antennal lobe via projection neurons. They were first identified and described by French biologist Félix Dujardin in 1850.
Brain-derived neurotrophic factor (BDNF), or abrineurin, is a protein that, in humans, is encoded by the BDNF gene. BDNF is a member of the neurotrophin family of growth factors, which are related to the canonical nerve growth factor. Neurotrophic factors are found in the brain and the periphery. BDNF was first isolated from a pig brain in 1982 by Yves-Alain Barde and Hans Thoenen.
CREB-TF is a cellular transcription factor. It binds to certain DNA sequences called cAMP response elements (CRE), thereby increasing or decreasing the transcription of the genes. CREB was first described in 1987 as a cAMP-responsive transcription factor regulating the somatostatin gene.
Retrograde signaling in biology is the process where a signal travels backwards from a target source to its original source. For example, the nucleus of a cell is the original source for creating signaling proteins. During retrograde signaling, instead of signals leaving the nucleus, they are sent to the nucleus. In cell biology, this type of signaling typically occurs between the mitochondria or chloroplast and the nucleus. Signaling molecules from the mitochondria or chloroplast act on the nucleus to affect nuclear gene expression. In this regard, the chloroplast or mitochondria act as a sensor for internal external stimuli which activate a signaling pathway.
Neuromodulation is the physiological process by which a given neuron uses one or more chemicals to regulate diverse populations of neurons. Neuromodulators typically bind to metabotropic, G-protein coupled receptors (GPCRs) to initiate a second messenger signaling cascade that induces a broad, long-lasting signal. This modulation can last for hundreds of milliseconds to several minutes. Some of the effects of neuromodulators include: alter intrinsic firing activity, increase or decrease voltage-dependent currents, alter synaptic efficacy, increase bursting activity and reconfiguration of synaptic connectivity.
Neurturin (NRTN) is a protein that is encoded in humans by the NRTN gene. Neurturin belongs to the glial cell line-derived neurotrophic factor (GDNF) family of neurotrophic factors, which regulate the survival and function of neurons. Neurturin’s role as a growth factor places it in the transforming growth factor beta (TGF-beta) subfamily along with its homologs persephin, artemin, and GDNF. It shares a 42% similarity in amino acid sequence with mature GDNF. It is also considered a trophic factor and critical in the development and growth of neurons in the brain. Neurotrophic factors like neurturin have been tested in several clinical trial settings for the potential treatment of neurodegenerative diseases, specifically Parkinson's disease.
Ca2+
/calmodulin-dependent protein kinase II is a serine/threonine-specific protein kinase that is regulated by the Ca2+
/calmodulin complex. CaMKII is involved in many signaling cascades and is thought to be an important mediator of learning and memory. CaMKII is also necessary for Ca2+
homeostasis and reuptake in cardiomyocytes, chloride transport in epithelia, positive T-cell selection, and CD8 T-cell activation.
Kalirin, also known as Huntingtin-associated protein-interacting protein (HAPIP), protein duo (DUO), or serine/threonine-protein kinase with Dbl- and pleckstrin homology domain, is a protein that in humans is encoded by the KALRN gene. Kalirin was first identified in 1997 as a protein interacting with huntingtin-associated protein 1. Is also known to play an important role in nerve growth and axonal development.
Activity-regulated cytoskeleton-associated protein is a plasticity protein that in humans is encoded by the ARC gene. It was first characterized in 1995. ARC is a member of the immediate-early gene (IEG) family, a rapidly activated class of genes functionally defined by their ability to be transcribed in the presence of protein synthesis inhibitors. ARC mRNA is localized to activated synaptic sites in an NMDA receptor-dependent manner, where the newly translated protein is believed to play a critical role in learning and memory-related molecular processes. Arc protein is widely considered to be important in neurobiology because of its activity regulation, localization, and utility as a marker for plastic changes in the brain. Dysfunction in the production of Arc protein has been implicated as an important factor in understanding various neurological conditions, including amnesia, Alzheimer's disease, Autism spectrum disorders, and Fragile X syndrome. Along with other IEGs such as ZNF268 and HOMER1, ARC is also a significant tool for systems neuroscience as illustrated by the development of the cellular compartment analysis of temporal activity by fluorescence in situ hybridization, or catFISH technique.
The cellular transcription factor CREB helps learning and the stabilization and retrieval of fear-based, long-term memories. This is done mainly through its expression in the hippocampus and the amygdala. Studies supporting the role of CREB in cognition include those that knock out the gene, reduce its expression, or overexpress it.
Kaang Bong-Kiun was born in Jeju-do, South Korea, on November 21, 1961. He is a professor of neuroscience in the Department of Biological Sciences of Seoul National University. He is a Fellow of the Korean Academy of Science and Technology.
Thomas Carew, Dean of the Faculty of Arts and Sciences at New York University, is an American neuroscientist whose interests center on the behavioral, cellular, and molecular analyses of learning and memory. His work provides provide empirical support for the idea that different temporal phases of memory consolidation can be best identified not by their different temporal domains, but by their molecular signatures.
Marina Rachel Picciotto is an American neuroscientist known for her work on the role of nicotine in addiction, memory, and reward behaviors. She is the Charles B. G. Murphy Professor of Psychiatry and professor in the Child Study Center and the Departments of Neuroscience and of Pharmacology at the Yale University School of Medicine. Since 2015, she has been editor-in-chief of the Journal of Neuroscience.
TLQP-62 (amino acid 556-617) is a VGF-derived C-terminal peptide that was first discovered by Trani et al. TLQP-62 is derived from VGF precursor protein via proteolytic cleavage by prohormone convertases PC1/3 at the RPR555 site. TLQP-62 is named after its first four N-terminal amino acids and its peptide length.