Essay On Long-Term Potentiation

The cerebral cortex directs functions like speech, behavior, reactions, movement, thinking, and learning. In fact, some research suggests that bipolar disorder originates with problems with the thalamus, which links sensory input to good and bad feelings. The hippocampus also affects depression. It, like the amygdala, is part of the limbic system. It is vital in processing long-term memory. This section of the brain registers recurring fear. In people with clinical depression, the hippocampus is much smaller. Research suggests, even, that ongoing exposure to stress impairs the growth of nerve cells in this part of the brain. One of the most important jobs of the brain is to process senses, through neurons. Neurotransmitters are specific substances that help relay information to the brain. Scientists have identified many neurotransmitters that affect depression. A lack or excess of the neurotransmitters acetylcholine, serotonin, norepinephrine, dopamine, glutamate, lithium carbonate and gamma-aminobutyric acid are thought to contribute to depression. Acetylcholine is involved in learning and enhances memory. Serotonin helps regulate sleep, appetite, and mood, and inhibits pain. Research shows the idea that many depressed people have reduced levels of serotonin. Low levels of a byproduct of serotonin have been linked to a high risk for suicide. Norepinephrine is a neurotransmitter which constricts blood vessels and raises blood pressure. An excess in

Many scientists hypothesize that protein dysfunction plays a role in the progressive damage and death of nerve cells. The nerve cells may be blocked from communication

Whether aging impair learning related long-term plasticity at LESN-L7MN synapses? (Aim 1). Though several studies have brought insights into the aging associated behavioral, cellular and electrophysiological changes, none of these studies have examined learning related long-term synaptic plasticity at LE SN-L7MN synapses connections of GWR during aging. First, using the semi-intact preparation [6,34], we will measure basal electrophysiological

Furthermore, the protective properties of APP are often correlated with its functions of synaptic formation and repair and iron transport and

c. Ca2+ dependent protease, calpains, is a key player and responsible in the degeneration of the axon and synapse during Wallerian degeneration (Ma, M., Ferguson, T. A., Schoch, K. M., Li, J., Qian, Y., Shofer, F. S., . . . Neumar, R. W., 2013).

Introduction. Dysregulation of β-cat causes abnormal brain development (121-123) and defective dendritic morphogenesis (124, 125). By interacting with N-cadherin, β-cat shapes synaptic structure (83, 84) and regulates excitatory postsynaptic strength (126, 127). In addition, the axonal localization and translation of β-cat modulate presynaptic vesicle release (128-130). As a consequence, abnormal levels of β-cat in different brain regions or circuits lead to impaired memory (12, 131, 132), and a depression-like phenotype (91). However, the circuitry mechanisms for how β-cat dysfunction leads to the pathogenesis of ASDs are largely unknown. An imbalance of excitatory and inhibitory signals has been implicated in the pathophysiology of

Levodopa does begin to become less effective as time goes on but another drug Dopamine Agonists takes Levodopa’s place in slowing the loss of neurons.

The neurobiological process of synaptic memory consolidation is thought to be long-term potentiation (LTP), which is the prolonged strengthening of the

Although there are many factors that influence an individual’s ability to learn, the most biological support for the process of learning involves the strengthening and weakening of synaptic connections in the brain. These processes, termed long-term potentiation (LTP)

Short Term Memory Loss. Ironically most of us don’t even think about memory that often, much less Short Term Memory. Because of that, this psychological disorder often tends to get overlooked for a small problem that no one wants to take serious. Most people would recognize this disorder from the popular movie, Finding Nemo. In which one of the main characters suffers from short term memory loss. In the film it’s taken as a lovable flaw, instead of the serious disorder that it is. But Short Term Memory is a lot more than one disorder found in a character in a movie. It is a somber disorder that could happen to any of us. This paper will be going through the gravity of this disorder and the causes to its victims.

Disruption of hippocampal function, including the capacity for neuroplasticity, could contribute to a range of aspects of major depression. In addition to the role in declarative memory, the hippocampus is the primary regulator of prefrontal cortical function; hippocampus and DLPFC function together to regulate explicit memory. Disruption of hippocampal function in major depression may therefore add to observed deficits in concentration. Hippocampal afferents are important regulators of both the nucleus accumbens and the ventral tegmental area (VTA). It has been suggested that an indirect excitatory projection from hippocampus to VTA is critical for coordinating the firing of VTA cells in response to novelty; impairment of this hippocampal

The human brain is capable of storing a massive amount of data utilizing short and long term memory. Recent discoveries in the field of neuroscience allow us to at least partially understand the mechanism behind the cellular basis of information storage and retrieval. Currently, several medications, regulating activities of chemical balance of neurohormones, are approved by FDA for the treatment of mild to severe memory loss associated with Alzheimer's dementia. With a rapid progression of medical technologies, the discovery and production of medications designed to enhance brain performance and memory

In the cord preparations with TTX treatment, 5-HT application reintroduced the negative slope conductance in the I-V curve of healthy motoneurons failing to show the negative slope conductance in the presence of NMDA alone (Schmidt and Jordan, 2000). Moreover, in other motoneurons showing the negative slope conductance in the presence of NMDA alone, 5-HT caused the negative slope conductance to shift toward the hyperpolarizing direction, which could be reversed by 5-HT antagonist mianserin (Schmidt and Jordan, 2000). Reducing the bath concentration of Mg2+ also mimicked the hyperpolarizing shift of the negative slope conductance by 5-HT (Schmidt and Jordan, 2000). Via 5-HT2 receptor activation, protein kinase C (PKC) can enhance the hyperpolarizing shift of the negative slope conductance in the I-V curve of NMDA receptors and also reduce Mg2+ blockade of the receptor channels (Blank et al., 1996; Chen and Huang, 1992). Therefore, the effect of 5-HT on the negative slope conductance of NMDA receptors may result from reduction of Mg2+ blockade of the receptor channels. Even more interestingly, Li and Zhuo (1998) discovered that 5-HT can induce the transformation of silent glutamatergic synapses into functional ones in some rat superficial dorsal horn neurons (Li and Zhuo, 1998). They detected silent synapses, which are excitatory postsynaptic currents mediated by NMDA receptors, by depolarizing the cells from -70 mV to +40 mV (Li and Zhuo, 1998). However, 5-HT

The members of the D2 subfamily (D2, D3, and D4 receptors) are reported to be involved with inhibitory neurotransmission, which is achieved via inhibiting the enzyme adenylate cyclasea, thus resulting in decreasing the signaling molecule cyclic AMP levels.

Memory formation occurs through LTP. This is due to the fact that LTP is synapse-specific. Synapse specificity is the process of when a synapse is stimulated, only that synapse is affected; neighboring synapses that lie close by remain unaffected.1 Extending into this topic, CaMKII, an enzyme, was found to play a major role in synapse specificity. The increase of intracellular calcium from the unblocking of the NMDA-type glutamate receptors resulting in the activation of CaMKII triggers LTP. The broad question that is then addressed in Lee et al’s article, “Activation of CaMKII in Single Dendritic Spines during Long-Term Potentiation” is what makes up the foundation of synapse specificity of LTP and how does CaMKII affect synapse specificity?