Synthesis And Secretion And Dendritic Spine Morphology

PURPOSE The main goal of experiment three was to test a rat’s ability to be conditioned to perform a behavior, and then relearn the same behavior after an extinction period. After ensuring that the rat was conditioned on a continuous reinforcement schedule (CRF), the next goal in the experiment was to extinct the previously learned behavior of lever pressing and receiving a food pellet. Once the behavior was extinct, the rat was reconditioned to lever press on a conditioned reinforcement schedule. The goal of the experiment was to demonstrate that a behavior could be learned, extinct, and then relearned.

It is therefore important to keep mentally engaged! When the child makes it to two years of age, billions of neuron connections are established, which only increases throughout the lifetime (Feldman 94). It was once alleged that the brain could not generate new neurons to replace old or damaged neurons, but this belief was found untruthful. Research from a part of the brain known as the hippocampus showed evidence of new cells and formation (Sprenger). This new research found that the brain loses cells on a daily basis while, at the same time, grows new neurons to replace the dead cells through a process known as neurogenesis (Coon and Mitterer 63). Another interesting fact is that most neurons are stored in columns in the neocortex part of brain and a chain of neurons are called the neural network. This all relates to the vital theory of Long-Term Potentiation (LTP), which states that every time a neuron sends information, the memory of the data sent is literally programmed to that cell. The information is learned multiple times while it is practiced and the signal has the potential to learn and go faster each time (Sprenger). Scientists must learn what these new cells do, but it is believed to be hugely involved in learning and memory processes (Coon and Mitterer 63). Dendrites are truly interesting and amazing cells!

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

Anterograde Amnesia does not have a specific age of onset, but can occur when one experiences damage to the hippocampus through viral or bacterial infections, seizures, strokes, or restricted blood flow. In a study by Clark, Broadbent, Zola, and Squire (2002), rats who had part of their hippocampus area removed experienced anterograde amnesia as opposed to the control group who did not when they were placed in a food judgement task. In this task, rats were given different food each day, but there was one piece of food that remained constant. Here, the lesion rats did not gain a preference or liking towards a specific food. Meanwhile, the control group gained a preference

C. APPROACH: Based on our preliminary data on lncRNA changes in specific regions of the brain associated with contextual fear, we hypothesize that specific lncRNAs mediate consolidation and extinction of fear memories. To test this hypothesis, the Puthanveettil and Stackman laboratories will bring together their strong expertise in genomics, bioinformatics, noncoding RNAs, genetics, behavioral models, non-coding RNAs, bioinformatics and functional, in vivo manipulations of novel molecular players. We will employ a research strategy that starts with an unbiased, genome-wide analysis of lncRNAs and funnel down to key players, at which point mechanisms of action will be identified. First, unbiased expression analysis of lncRNAs will be carried out with contextual fear conditioning following extinction of contextual fear memory. Second, we will then carry out in vivo manipulation of specific lncRNAs in specific regions of the brain to determine necessity of the expression of specific lncRNAs in consolidation and extinction of fear memory. We anticipate that our studies will establish the functional importance of candidate lncRNAs in consolidation and extinction and provide novel insights into the novel molecular regulators and mechanisms underlying development of PTSDs. All of the genomics, bioinformatics and rodent behavior analyses will be carried out locally, at Scripps Florida and FAU, with confocal imaging experiments being performed across the street at the Max Planck

During normal development of the mammalian central nervous system (CNS), neural stem cells (NSC) give rise to neurons via process of neurogenesis (Kempermann et al., 2004; Zhao et al., 2008). Neurogenesis normally occurs in dentate gyrus (DG) region of the hippocampus and lateral ventricle of sub-ventricular zone (SVZ) (Zhao et al., 2008). Hippocampal neurogenesis plays pivotal role in neurologic and psychiatric disorder like epilepsy, depression, schizophrenia and mood disorders (Antonova et al., 2004; Keller and Roberts, 2008; Lucassen et al., 2006; Zhao et al., 2008). Development of the nervous system is complex, and includes multistep dynamic processes such as proliferation, differentiation, migration, expansion of axons and dendrites, synapse formation, myelination and programmed cell death (Rice and Barone, 2000). These processes required the coordinated expression of cellular and molecular events in a spatial and temporal manner during the brain development (Rice and Barone, 2000; Rodier, 1994). Several growth factors and signal transduction cascades have been implicated in controlling NSC behavior in the developing brain (Faigle and Song, 2013). Among these, members of the Wnt family of secreted glycoprotein thought to be variably influence proliferation and lineage decisions of NSC and their progeny (Clevers et al., 2014).

We have discovered that contextual fear memories, reliant on synaptic plasticity, altered the expression of specific lncRNAs in two regions of the mouse brain implicated in PTSD, the medial prefrontal cortex (mPFC), and CA1 sub-region of hippocampus. Among the nine lncRNAs we measured, one (GM11549) was upregulated in mPFC and two lncRNAs are regulated in CA1. Our working hypothesis is that the consolidation of contextual fear memory is dependent upon a subset of lncRNAs within the circuit governing fear memories. To test this hypothesis, we will focus on the CA1 region of hippocampus that is critically involved in memory consolidation. We will employ two relevant behavioral model, contextual fear conditioning to achieve the following: (1) Identify specific changes in lncRNAs transcriptome profiles in the CA1 by RNAseq analyses at 30 min, 1 and 6 hrs after training and validate specific changes in lncRNAs by quantitative PCR and confocal imaging. (2) Assess the ability of in vivo intra-CA1 manipulations of specific lncRNAs identified by RNAseq to interfere with the consolidation of fear memory. For these functional studies, we will select the top five lncRNAs based on a fold change of >1.5 (p<0.05) and their sequence homology to humans. (3) Elucidate the mechanism(s) of action of the lncRNAs in the consolidation of fear memory. We anticipate that these studies

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

Steve Ramirez, Xu Liu, Pei-Ann Lin, Junghyup Suh, Michele Pignatelli, Roger L. Redondo, Tomás J. Ryan, Susumu Tonegawa

Since hippocampus plays an important function in the brain, it has become a great topic for many conducted research not only on human but also animals, specifically primates and rodents. In primate model of amnesia, the experiment is performed through three main tasks – delayed nonmatch to sample, object discrimination paradigm and motor skill learning across multiple trials (Eichenbaum et al, 1992). In delayed non-matching test, both amnesic and intact monkey show nearly same performance rate in remembering objects across delayed in short period of time (Eichenbaum et al, 1992). In contrast, amnesic monkeys show a great impairment for longer delayed conditions, hours, in picking the right non-matched samples (Eichenbaum et al, 1992). Likewise, in object discrimination task, amnesic monkeys are unable to recognize objects, as compared to control monkeys (Eichenbaum et al, 1992).These tests suggest the importance of hippocampus in acquisition of new information and recollection old events from episodic memory. Additionally, hippocampus also contributes largely to relational representation, as a characteristic of declarative memory (Eichenbaum et al, 1992). This can be shown through odor discrimination and place

While dendritic spines help the brain communicate with neurons, synaptic plasticity enables people to learn and remember things. Secondly, the scientists discovered that the old mice who were exposed to blood from young mice had higher levels of long-term potentiation (LTP) for a longer period of time compared to the old mice who were exposed to blood from other old mice. Since it is general knowledge in the scientific community that LTP is correlated with learning and memory, Villeda and his colleagues inferred that exposure to blood from young mice improves these cognitive abilities. Thirdly, the scientists found that the old mice who were exposed to blood from young mice performed better on certain fear conditioning tasks. They excelled in fear conditioning tasks that involved environmental context rather than cues. Since environmental fear conditioning tasks are used to test hippocampal involvement, this experiment demonstrated that changes due to young blood occurred in the

Learning is a very important aspect of humans and creatures alike. Not only is it essential to the survival and adaption into this world but it also defines who we are as individuals (Schiller et al, 2010; Tronson & Taylor, 2007). Memories from past experiences shape the people that we are today. A crucial element to learning is memory, without it we would not be able to retain information. The process of memory is very distinct and consists of several different stages: acquisition of memory, consolidation, retrieval and then either reconsolidation or extinction (Debiec & Ledoux, 2004; Diergaarde, Schoffelmeer & De Vries, 2008). As memory is such a critical aspect of learning, it is no wonder that its distinct process has become the topic of much research in the neurobiological universe (Hupbach et al, 2007; Nader & Hardt, 2009).

It has been considered that neural mechanisms involving memories undergo synaptic plasticity modification such as LTP and LTD. Indicating the association between memories and synaptic mechanisms has been elusive, until now. Robert Malinow and his colleagues were able to demonstrate this modification of synaptic plasticity by fear conditioning mice. Malinow and his group used optogenetics to focus on a specific fear circuitry. They then induced LTD and LTP in the memory circuitry to reinstate or remove the fear memory. Optogenetics is slightly different from the original tone fear conditioning. To observe the connection between memory and plasticity they induce cued fear conditioning in mice with a tone and shock. There are some main components in conditioning. First, there is a neutral

for the Neurobiology of Learning and Memory at UC Irvine, California. They conducted a study where a