Neurexins : Case Study

Glutamate-receptor-interacting protein (GRIP) is the interacting protein which is associated with AMPAR protein receptor in the postsynaptic cell. Amount of GRIP is associated with AMPAR receptors can lead to the prediction of activity in the presynaptic cell. AMPAR receptor change shape to be ready to receive neurotransmitter when GRIP bind. The presynaptic cell contains vesicle which neurotransmitters are accommodated. When calcium enters the presynaptic cell by calcium channel, vesicles dock to the presynaptic cell to become ready to release neurotransmitters to the synaptic gap. Neurotransmitters are released in a packet called quanta. AMPAR receptor has to change its shape by GRIP to receive the release of quanta in the synaptic

The University of Montréal conducted a study to further findings in the very under-researched field of neuroscience and to encourage proper diagnosis within their field. Scientists there postulated that the deregulation of the function of the synapse due to a severe genetic mutation of the SYN1 gene was the causal element of disorder in both ASD and epilepsy. This synapse gene focused on is known to be necessary in the formation and development of the synaptic vesicles, which carry out communication between the neurons. . A large Montréal family was used as a sample and microsatellite markers were evenly distributed throughout. To carry out their study, many elements were included to ensure proper level of statistical significance. This included genotyping, linkage analysis, screening of DNA for possible irregularities, and additional research conducted on lab-affected mice through hippocampal cultures and

NMDA Receptor is one of the crucial glutamate receptors present in the nerve cell. It gets activated when glutamate or Glycine binds to it. NMDA receptor is known for its role in synaptic plasticity and membrane function (learning and memory). Its activity is highly dependent on calcium influx. It is a tri heteromeric receptor with three different subunits NR1, NR2 and NR3. Each subunit has several other subunits, each of them having a unique function: NR1 has 8, NR2 has 4 (NR2A, NR2B, NR2C, NR2D), NR3 has 2 (NR3A, NR3B). Out of all the subunits, NR2A and NR2B have been extensively studied. NR2A, also known as GluN2A is believed to be involved in cell death pathways whereas NR2B, also known as GluN2B is believed to be involved in cell survival cascades (Bayer et al., 2006). Interestingly, GluN2B and GluN2A have differing roles, and both can affect either long-term potentiation (LTP) or long-term differentiation (LTD)

Life as a human is full of mystery and discovery. Throughout history, people have set out to learn more about the world and the people inhabiting it. In the process, they gained knowledge about a disorder that is now referred to as Autism Spectrum Disorder (ASD), or simply Autism. ASD is a developmental disorder that results in difficulty in social interactions, communication, and repetitive behaviors. Researchers have come a long way in gathering knowledge about the complex disorder since it was first discovered. Many of its aspects have been discovered and redefined to shape the disorder that is diagnosed and studied today. However, much like many other well-known psychological disorders, autism has yet to be fully understood; instead,

“A group of complex brain development disorders, which are characterised by difficulties in social interaction and communication and a restricted and repetitive repertoire of interests and activities”.

When an action potential races along the axon of a neuron, activating sodium and potassium channels in a wave, it eventually comes down to the presynaptic terminal, and activates the VGCC channels to release calcium into the neurons cytoplasm. This flow of positively-charged calcium ions causes the synaptic vesicles to fuse with the cell membrane and release their chemical messengers. It’s these neurotransmitters that act like couriers diffusing across the synaptic cleft and binding to receptor sites on the post synaptic

Social cognition is a complicated process that requires the integration of a wide variety of behaviors, including perception of social signals, reward-seeking, motivation, short-term recognition, and flexible adjustment in social groups. As crucial parts of social cognition, animals, including rodents and primates, have the desire to seek out contact and interaction with conspecifics. This is called social motivation. During this interaction, they need to recognize the behavior of other individuals or the group as a whole, and to respond to social signals appropriately. Social recognition/perception is required for forming long-term attachments, hierarchies, and other complex social strategies critical for survival

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?

Huntington’s Disease (HD) is a late-onset, chronic neurodegenerative disease characterized by impairments in motor, cognitive, and psychological functions. It is caused by a mutation in Exon 1 of the IT15 gene, which encodes the huntingtin (Htt) protein. Mutant huntingtin (mHtt) has an expanded CAG repeat in its N-terminal region, encoding a poly-glutamine (polyQ) track that can either form toxic aggregates in neurons or interact with various cellular proteins, leading to altered cellular processes and neuronal apoptosis. In HD, the loss of inhibitory medium spiny neurons within the striatum causes involuntary movements characteristic of the disease; These neurons are involved in refining the excitatory outputs of the cerebral cortex, which

Neurotransmitters are chemicals that are involved in transmitting the neural impulses from one brain cell to another. Neurotransmitters are packed together in small compartments called vesicles. Each vesicles holds a neurotransmitter, where it is serotonin or dopamine. When the neuron is ready to release a neurotransmitter, the vesicles fuse with the membrane of the particular neuron and lets go of its content in to the gap in the synapse. Every minute of every second of the day, neurons are sending signals to one another. All the brain disorders such as epilepsy, Alzheimer’s, autism and many more other disorders happen when there is a problem during the synapse. The synapse is when the neuron and the cell body of another neuron join together.

The previous study from mice model of Rett Syndrome suggests significant alterations in the expression of certain proteins in the brain. In our study, we assessed the state of several synaptic proteins in a MeCP2 knockout Rat model of Rett Syndrome (MeCP2 tm1sage) specifically in the Dorsal and Ventral Hippocampus by performing Western Blotting protocol. MeCP2 knockout, as well as wild-type rats, were euthanized at the age of 32-38 days (around the 5th week), brains were isolated and tissues were collected from the Dorsal and Ventral Hippocampus respectively. Protein extracts from these two regions of the brain were analyzed for different protein kinases, NMDA Receptor subunits and several other molecular targets (transcription factors). Rats

The objective of the experiment was to find the amount of bixin in plasma when given orally to dogs and to look at the stress and inflammatory biomarkers to measure the immunomodulatory and antioxidant effects of bixin. The authors believed that if bixin is taken orally it will be quickly absorbed by the plasma in dogs and eventually into the leukocytes which should increase immunomodulation. The blood constituent measure in this experiment is leukocytes. The significance of measuring the amount of white blood cells was to find how bixin is absorbed and how much ends up in the leukocytes. Also, the significance is because most of the bixin absorbed is in the mitochondria of leukocytes, which is one of the major organelles in the cell.

Brief background: In mice, the first DA neuron neurites appear at E11.5. These neurites extend towards the striatum, forming the medial forebrain bundle (MFB), the main neural tract connecting ventral tegmental area (VTA) and the substantia nigra (SNc) to the striatum. At E14.5 the DA neurites approach the border of ventrolateral ganglionic eminence (VM). These neurites then multiply without further

Synaptic transmission is trigger by calcium influx through voltage gated calcium channels (VGCCs). VGCCs open in response to membrane depolarization cause, in most cases, by action potentials propagating through a nerve ending. Once inside the terminal, calcium diffuses and binds to a calcium-sensing protein called synaptotagmin I, which acts as the trigger for vesicle fusion with the pre-synaptic active zone. The basic mechanisms of synaptic transmission have been extensively described in the past 70 years, but the finest details of how neurotransmitters are released in response to action potentials remain unclear. Recent work indicates that at Schaffer collateral synapses neurotransmitter release is triggered by opening of one single calcium

Previous study reported that the extracellular guidance cues, including UNC-6/Netrin and its receptor have role in determining the axon outgrowth