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

Week 2- Dopamine Modulation of Depressive-like Behaviors

By
The Chaudhury et al paper explored the neural circuit mechanisms involved in the dopamine modulation of certain symptoms of depression. In this study, the researchers looked at social interaction and sucrose preference as part of their social-defeat paradigm, which has been shown in the past to be indicative of depressive-like behaviors. Although I initially did not completely see the connection between the social-defeat stress model of depression and the tonic vs phasic firing of dopamine neurons, it seemed that susceptibility and resilience to stress played a role in the functional/behavioral effects of dopamine firing. It was interesting to see how chronic mild stress with phasic firing of VTA dopamine neurons converted even resilient mice into susceptible mice.  The Tye et al paper similarly looked at the dopamine modulation of depressive-like behaviors, focusing on motivation with the forced swim tests and open field tests, followed by measurement of anhedonia by quantifyi...
Post a Comment
Read more

Sial & Allsop

By
Sial et al. derived a novel approach for studying what they deem vicarious defeat stress (VSDS) as a model for MDD, PTSD, and other mood-related disorders as an alternative to the classical CSDS paradigm. Using adult male mice, they demonstrate that their model induces a robust and measurable social avoidant phenotype as well as other stress and anxiety related behavioral outputs. Their subsequent rescue study with chronic fluoxetine treatment shows reversal of the behavioral phenotypes and emphasizes the predictive validity of the model. Allsop et al. found that BLA-projecting ACC neurons preferentially encode socially derived aversive cue information by encoding the demonstrator’s distress response during observational learning, hence enabling acquisition of negative valence of cue by BLA neurons and behavioral output. In order to test their hypothesis, Allsop et al. used an observational fear conditional paradigm to create association between a conditioned stimulu...
Post a Comment
Read more

Buffington and Reber

By
Buffington et al. explore a mechanism by which maternal obesity can induce neuronal and subsequent behavioral disorders. Using a model of high-fat diet (MHFD)-induced obesity, the authors showcase the strong connection between the brain and the gut, and its impact on behavior. The findings are provocative; by exposing these offspring to the microbiome of control offspring, there was evidence of a rescued observed behavioral phenotype. Furthermore, a phylogenetic profiling of the gut microbiome revealed a decrease in L. reuteri within MHFD offspring, and introduction of live L. reuteri into the drinking water shows successful rescue of the behavioral issues in the MHFD offspring. L. reuteri-induced expression of oxytocin within the paraventricular nuclei of the hypothalamus provides a potential mechanistic explanation for the behavioral changes. I thought this paper provided robust support for the hypothesized interaction between the gut biome and the developing CNS, with tremendous po...
Post a Comment
Read more