Hippocampus Reactivation

Among these different processes are encoding, storage, consolidation, and retrieval. This study hypothesized that the hippocampus plays a different role in each of these. The method of this study is especially unique because it used temporary chemical inactivation of the hippocampus, which had not been done before. This temporary inactivation is unique because it lets the researchers selectively assess the role of the hippocampus during each of the processes discussed above. To test encoding, the inactivation occurred during learning of a maze task; to test retrieval, inactivation occurred during a retention task. Results indicate the temporary inactivation of the hippocampus impairs both encoding and retrieval. To test long-term consolidation, rats were trained and then separate groups received hippocampal treatment for different amounts of time between one and five days. Results showed that temporary inactivation during this time period disrupts memory for the already learned task. This study partially supports the result of the study by Eldridge et al. (2000) in that they both show the hippocampus is necessary for memory retrieval. However, it does not address the retrieval of different types of memory. This study also supports the idea from Wang et al. (2012) that the hippocampus may be involved in consolidation and storage of new memories but not necessarily of older

There is extensive evidence to prove that the hippocampus plays a vital role in memory retrieval. However the extent to what type of memories the hippocampus supports and the process in which retrieval occurs is an ongoing debate. The two theories that are dominant in this debate are the Standard Model of Systems Consolidation (SMSC) and the Multiple Trace Theory (MTT). This paper will provide a review on the evidence supporting these two composing theories, the research providing evidence against the models, and finally their limitations. Additionally, a novel theory coined the Competitive Trace Theory (CTT) will be reviewed in order to conclude whether or not this model can provide a more holistic and accurate representation of the role of the hippocampus in memory retrieval while simultaneously providing explanations for flaws in previously proposed models.

What is the hippocampus? The hippocampus is the formation of memories and a part of the cerebrum.Some people say if you damage the hippocampus you develop a disease called Antevograde amnesia which is the unibaily to form new memories.It also said there are regions that regulates the emotions.

Although the complete action of pathophysiological features AD is not fully well understood, it is generally characterized by a degeneration of nerve cells that produce acetylcholine (ACh), along with the presence of neurofibrillary tangles (NFTs) and senile plaques. Acetylcholine is an amine, serving as a neurotransmitter at all neuromuscular junctions, as well as in many other circuits of the central and peripheral nervous system. In order to prevent excessive build-up in the normal individual, the enzyme acetylcholinesterase (AChE) breaks down ACh into Acetyl CoA and Choline. In AD, the AChE breaks down what little ACh is left at the synapse. This reduction of ACh at the synapse results in a decreased amount of ACh available for synaptic

The hippocampus is important for learning and memory without it you cannot learn new facts or ideas. This acts as a gateway to learning new memories, all memories must pass through the hippocampus before they can become a permanent memory in the gray matter, also known as the cerebral cortex. Hippocampal damage results in the loss of new memories, if your hippocampus is destroyed your ability to learn new facts, learn new memories or ideas is then a lost necessity. The hippocampus is about declarative knowledge, that’s the knowledge that is learned by facts and memory.Glucocorticoids have the ability to damage neurons in the hippocampus. The hippocampus is about declarative knowledge, that’s the knowledge

Nishida, M., Pearsall, J., Buckner, R. L., & Walker, M. P. (2009). REM sleep, prefrontal theta, and the consolidation of human emotional memory. Cerebral Cortex, 19(5), 1158-1166.

The hippocampus was rapidly collected and homogenized in Cell lysis buffer (beyotime, P0013, China) containing protease and phosphatase inhibitors. The homogenate was centrifuge at 10,000rpm/min for 5min at 4 ̊C. The protein concentration of the supernatant was determined by SDS-PAGE with standard protein. Then the sample was run by 10% SDS-PAGE electrophoresis and transferred to polyvinylidene difluoride membrane. The membranes were incubated with blocked solution (5% nonfat milk in PBS) at room temperature for 1 h and probed with primary antibody against CaMkII (Cell signaling, #12716) and PSD95 (Abcam, ab192757) at 4 ̊C overnight, then the membranes were incubated with horse radish peroxidase conjugated secondary antibodies for 1 h at room

This essay is focusing on the current understanding of the neurobiology of memory reconsolidation and its implications for psychology. This paper will specifically focus on the molecular mechanisms of reconsolidation and research relating to fear memories and using propranolol and D-cycloserine as a treatment of post-traumatic stress disorder. Memory consolidation is the process by which memories are stabilised after being acquired. Consolidation studies have traditionally focused on the hippocampus and systems consolidation, where short term memories become long term memories and independent of the hippocampus over time (Pinel, 2011). The more recently discovered process of consolidation is synaptic consolidation, where memory is encoded within hours, and requires protein synthesis and gene transcription (Pinel, 2011). Long term memories were once considered to be stable, but within the last decade, the discovery of reconsolidation, the process in which stored memories can be retrieved and held in labile short-term memory, has changed theory and research on memory (Pinel, 2011). The potential ability to modify established emotional memories through the processes of reconsolidation has important implications for the treatment of many mental disorders, including anxiety disorders, such as post-traumatic stress disorder.

The hippocampal formation is rich in mineralocorticoid (MRs) and glucocorticoid receptors (GRs). The receptors work to maintain basal HPA tone and regulate the negative feedback of glucocorticoid release during a stress response. Therefore it is not a surprise that the hippocampus is vulnerable to influences of stress and depression. Depressed patients have a decreased hippocampal volume which differs with the amount of incidences and duration of the illness. Similarly, post-mortem studies of hippocampal tissue gathered from individuals with depression reveal changes in grey matter density, decreased neuropil, and reduced hippocampal neurogenesis. Animal models of depression exposed to chronic stress exhibit similar changes in hippocampal structure

The hippocampus is a part of the brain involved in memory and emotion. It’s known that someone with schizophrenia, the hippocampus tends to reduce in size. With this being said, a team at the University of Texas Health Science Center at Houston is running a research on whether or not this may be true with someone who has bipolar disorder. They’ve taken MRIs of three different groups of patients: bipolar, major depressive, and those without mood disorders. The results have shown that certain parts of the hippocampus in people with bipolar disorder are smaller than they are in both people with major depressive disorder and without mood disorders.

Optogenetics has been used to show that activating a specific ensemble of hippocampal neurons that contribute to a memory engram can erase or even alter a memory. The purpose of the study was to use optogenetics and the addition of an external stimuli to try and create a false memory. Neurons of mice were labeled with a light-sensitive channel during the exploration of a safe room. Mice were then placed in a new room and given foot shocks while simultaneously using light pulses to activate the neurons that had been previously labeled in the safe room. After being placed back into the safe room, mice exhibited freezing responses. A false memory of fear was created in these mice as they demonstrated freezing behavior in the room in which they had not been shocked. Multiple methods have been used to manipulate neuronal pathways, and the fact that so many different methods already exist suggest a bright future for the discovery of a method that can be beneficial to humans. Understanding how the hippocampus functions is essential to understanding how psychological diseases affect memory, and this procedure has the potential to be a type of treatment. This study demonstrates how unreliable memories are, and how the complete manipulation of one can be accomplished simply by activating a specific neuronal population.

This paper examines five different sources of information that addresses information pertaining to wakeful resting or sleeping and the effects it has on memory garnered by experiments performed on humans and animals. Wakeful resting is defined as an individual that has not fallen asleep but has engaged in a period of rest that cuts them off from the distractions of the outside world. Sleep is the bodies natural cycle of rest that suspends the consciousness and allows both the body and the mind to take a break from any stressful activities and recover. By either taking a short wakeful rest or going to sleep after learning new material, memory consolidation in both humans and animals will be improved, and it is not limited to humans that

The following experiment was preformed by Marieke Soeter and Merel Kindt. Their research tested if the disruption of reconsolidation of memories also lowers fear in an individual who has an ongoing fear of spiders in their everyday life. Studies over the past years have found that retrieving previously consolidated memories may signal a process known as reconsolidation (restabilization due to proteins). In the lab setting, a process known as Pavlovian fear conditioning can be used to train the mind to fear a stimulus. This conditioned fear can then easily be used to test the neurobiology of associative fear learning and memory. Fear conditioning is also a great method to be used in studying new treatments for anxiety disorders focused around

Lots of research had been accomplished by those researchers, and they eventually proved that healthy students are the better learners. According to a 2010 essay penned by Charles Basch of Colombia University, physical activities not only increased oxygen to flow to the brain, but also, students became responsible for learning, memory and higher thinking.

Retrieving memories, in contrast, increases hippocampal activity12 and often facilitates later recall13. Thus, hippocampal activity can be modulated according to task goals, though practice at suppressing retrieval is often necessary to achieve hippocampal reductions6. A key assumption of the present work is that this modulation does not target particular memories, which may be a person’s goal, but rather reflects a broadly targeted suppression (hereinafter, ‘systemic suppression’) of regional activity in the hippocampus that generally disrupts other memory functions supported by this region. For instance, beyond simply disrupting episodic retrieval, systemically suppressing hippocampal activity may also prevent freshly encoded stimulus input from generating new hippocampal traces