Skip to main content

Final Paper Topic

By
I am going to be writing my paper of on dual glutamatergic-GABAergic neurons and propose how these neurons might affect different depressive behavioral phenotypes based on their distribution in the brain. It is more widely accepted the neurons only release one type of neurotransmitter. However, recent studies have shown that this might not be true; that neurons can co-release neurotransmitters. One of the first papers to propose the neurons could co-release neurotransmitters was Corelease of Two Fast Neurotransmitters at a Central Synapse by Jonas et al. (1998), which used paired recording from synaptically connected neurons in spinal cord slices to determine that spinal interneurons were releasing both glycine and GABA. Since this time, several papers have come out in support of the concept of  neurons co-releasing neurotransmitter including Ottem et al. (2004) which explored the role of the neurotransmitters I am more specifically interested in, dual glutamatergic-GABAergic neurons, in the adult preoptic area and Gutiérrez (2005) which noted that the dual glutamatergic-GABAergic neuron hypothesis needed further testing with paired recordings. A laboratory that has done really interesting work in studying dual glutamatergic-GABAergic neurons is the Root Laboratory located at Colorado University, Boulder. The Root Lab published a paper back in 2018 entitled  Selective Brain Distribution and Distinctive Synaptic Architecture of Dual Glutamatergic-GABAergic Neurons that confirms that glutamatergic-GABAergic neurons are found in the ventral tegmental area (VTA), entopeduncular (EPN), and supramammillary (SUM) nuclei.

These are just some of the papers I am going to use to establish a background for my topic. I am going to incorporate articles that also talk about how it can to be believed that one neuron can only release one type of neurotransmitter (Mosier 2010) and might also include a paper about the monoamine transporters. I want to mainly focus on VTA when honing in on depressive phenotypes but I want to make sure I can find enough information to support this.


Gutiérrez, R. (2005). The dual glutamatergic–GABAergic phenotype of hippocampal granule cells. Trends in Neurosciences, 28(6), 297–303. doi: 10.1016/j.tins.2005.04.005

Jonas, P. (1998). Corelease of Two Fast Neurotransmitters at a Central Synapse. Science, 281(5375), 419–424. doi: 10.1126/science.281.5375.419

Mosier, D. R. (2010). Clinical Neuroscience. Neurology Secrets, 7–17. doi: 10.1016/b978-0-323-05712-7.00001-5.

Ottem, E. N. (2004). Dual-Phenotype GABA/Glutamate Neurons in Adult Preoptic Area: Sexual Dimorphism and Function. Journal of Neuroscience, 24(37), 8097–8105. doi: 10.1523/jneurosci.2267-04.2004

Root, D. H., Zhang, S., Barker, D. J., Miranda-Barrientos, J., Liu, B., Wang, H.-L., & Morales, M. (2018). Selective Brain Distribution and Distinctive Synaptic Architecture of Dual Glutamatergic-GABAergic Neurons. Cell Reports, 23(12), 3465–3479. doi: 10.1016/j.celrep.2018.05.063

Comments

Post a Comment

Popular posts from this blog

Gut-Brain Interactions: Buffington et al, Reber et al 2016

By
April 13 Papers (Buffington et. al, Reber et. al) I found this week’s papers to be quite novel in that they both proposed potential treatments for neurodevelopmental or psychiatric disorders that target bacterial or microbial abnormalities and how these give rise to certain behavioral and physical symptoms associated with the disorders. I thought this was a very unusual yet interesting approach, and as I have not previously studied the gut-brain axis, these papers offered me a fresh perspective on researching psychiatric and neurodevelopmental disorders. They were also unconventional in their focus of the physical symptoms that often accompany mental disorders, as this is not something that I have seen many other papers touch upon very much. Particularly, I was surprised by the Reber et al paper’s focus on the link between psychiatric disorders and inflammation in organs other than the brain, such as the colon, and the Buffington et al paper’s description of a relationship between ...
Post a Comment
Read more

Gut-brain axis

By
This weeks papers Reber et al. 2016 and Buffington et al. 2016 present a super interesting look into the gut-brain axis. Regarding both of these papers, it was amazing to see how potent favorable or unfavorable gut microbiome compositions are in affecting neuronal signaling and overall behavior. Reber et al. shows how immunoregulatory immunization with specifically heat killed M.vaccae can serve as a protective factor against chronic subordinate stress induce colotis as well as behavioral symptoms due to chronic stress as such. Interestringly, this paper depleted regulatory T cell activity via the anti CD25 antibody in order to show that the antiinflammatory mechanism induced by m vaccae immunization is depented on the secondary regulatory mechanisms offered by Treg proliferation and signaling. But, when T reg signaling was removed, this did not seem to cause a significant change in behavior . Therefore, this begs the consideration of what othe rmechanisms may be at play in order ...
Post a Comment
Read more

Ramirez et al.: 2013 and 2015 Papers

By
In these papers, Ramirez et al. strive to understand how memory encoding via optogenetic manipulation of engram-bearing cells in the hippocampus, specifically the dentate gyrus, can affect an animal’s response to a stressful context.  The first paper, published in 2013, was crucial to the field as it introduced this very exciting technique; in this paper, Ramirez et al. use tet-tag to manipulate brain circuity and establish associations between two contexts. Throughout the paper, this is referred to as “false memories.” Using these artificial memories, the investigators are able to manipulate the animal’s fear response in a specific context. Specifically, after the animals are conditioned to a repeated fearful stimulus (a foot shock, in context B), activation of the involved DG cells in a different context (context A’) will also initiate a fear response (in absence of any foot shock). In this experiment, the false memory is used to create an unnatural fear association in a given...
Post a Comment
Read more