VTA CRF Neuron Summary
In this paper, “VTA CRF neurons mediate the aversive effects of nicotine withdrawal and promote intake escalation” describes how the multiple researchers, such a Grieder, Herman...George, hypothesized that drug addiction is driven by two mechanisms. One of the mechanisms is the Ventral tegmental area (VTA), which is part of the brain that is rich in dopamine and serotonin neurotransmitter and is part of the two major reward pathway. The other mechanism is Corticotrophin-releasing hormone (CRF), which is a peptide hormone and a neurotransmitter involved in the stress response. However, it is revealed that the CRF neurons in the VTA, when receiving consistent nicotine exposure, it contributes negatively to the mesolimbic dopamine (DA) reward system when withdrawal. The researchers hypothesized that these two systems is the cause of nicotine dependence due to identifying a similar response in rodents in the same systems where addiction occurs.
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One of the methods that the scientist used to test their hypothesis was having different rodents being treated with different chemicals.
The researchers found that during increased CRF release, when drug withdrawal is happening there is a decreased immunodensity, meaning the density of the antibodies is lower when this chemical is released. With these findings, they used CRF immunohistochemistry to further examine the pVTA during withdrawal of chronic nicotine dependence. They decided to compare the results with the saline-treated mice in the pVTA and demonstrate the effects and compared them to the nicotine-dependent mice and the nicotine-withdrawn mice. The confounds that they found while conducting this experiment is CRF may also be released from other neurons, such as the CeA, and can also possibly decreased the
immunodensity.
The results section included different methods that had multiple major findings. The first one is being that nicotine dependence increases the chemical in CRH mRNA and this can be seen in the VTA. Another major finding is actually being able to identify the VTA CRF neurons in the different mice experiments. There are different types of viral vectors that make the downregulation of CRH mRNA in the VTA decrease nicotine points of self-administration and also prevents abstinence induced escalation of the chemical as well. Dual labeling of the CRF and DA neurons using CRH in situ hybridization and TH immunohistochemistry in mice and humans. Nicotine dependency is also link to dysregulation of the GABA-Da synapses which causes the opposite effects for the CRH mRNA. These results all point to the same thing that there are more chemicals put into play that are linked to nicotine dependence in the VTA.
One of the methods that the scientist used to test their hypothesis was having different rodents being treated with different chemicals.
The researchers found that during increased CRF release, when drug withdrawal is happening there is a decreased immunodensity, meaning the density of the antibodies is lower when this chemical is released. With these findings, they used CRF immunohistochemistry to further examine the pVTA during withdrawal of chronic nicotine dependence. They decided to compare the results with the saline-treated mice in the pVTA and demonstrate the effects and compared them to the nicotine-dependent mice and the nicotine-withdrawn mice. The confounds that they found while conducting this experiment is CRF may also be released from other neurons, such as the CeA, and can also possibly decreased the
immunodensity.
The results section included different methods that had multiple major findings. The first one is being that nicotine dependence increases the chemical in CRH mRNA and this can be seen in the VTA. Another major finding is actually being able to identify the VTA CRF neurons in the different mice experiments. There are different types of viral vectors that make the downregulation of CRH mRNA in the VTA decrease nicotine points of self-administration and also prevents abstinence induced escalation of the chemical as well. Dual labeling of the CRF and DA neurons using CRH in situ hybridization and TH immunohistochemistry in mice and humans. Nicotine dependency is also link to dysregulation of the GABA-Da synapses which causes the opposite effects for the CRH mRNA. These results all point to the same thing that there are more chemicals put into play that are linked to nicotine dependence in the VTA.