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Here's the only one that's easy to find in google scholar, but there might be more:
Page, F., Coleman, G., & Conduit, R. (2006). The effect of transdermal nicotine patches on sleep and dreams. Physiology & Behavior, 88(4), 425-432.
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Quoting my thesis:
CNS Dopamine/DA projections primarily emerge from two subcortical basal ganglia nuclei in the brain stem, travelling along three major pathways (Purves et al., 2004).
The nigrostriatal pathway, connecting the substantia nigra and the striatum, is mainly implicated in higher motor control. The mesolimbic pathway contains DA projections ...
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Allow me to extend a more empathetic answer; stack exchange is great, but the rigid responses are sometimes hard to stomach.
Dopamine is a neurotransmitter that basically works as a messenger between nerve cells. It tells you when you do something good by releasing a chemical that tells the brain “this is nice, this is good”. It’s closely associated with ...
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The way that you are describing dopamine fundamentally misunderstands how neurotransmitters work.
It makes sense to talk about hormones as elevated or reduced above a baseline level. This does not work for neurotransmitters such as dopamine, serotonin and oxytocin. This is because hormones are usually synthesised and released within specific systems, and ...
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Disclaimer: I do not work with receptor bindings very often.
First point binding sites...
Both Atropine and Nicotine bind to Cholinergic receptors. However receptor binding is not competitive as the rector sites for each neurotransmitter is different (NT): Atropine is a direct-antagonist of Muscarine binding with AChRm (muscarinic receptors) while nicotine ...
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Parts of the brain affected by dopamine
Dopamine exerts different effects in different regions and pathways throughout the brain. In the mesolimbic pathway, dopamine is believed to be involved in motivation and addiction due to the feelings of reward and pleasure associated with dopamine release here. In the mesocortical pathway, dopamine is linked to ...
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A bit of context
In mammalian brains, a main neurotransmiter linked with reward is Dopamine. This molecule is produced in the Ventral Tegmental Area (VTA) and in the Substantia Nigra (SN).
In a very famous study, Schultz recorded neurons in this two regions (at the time, we didn't really make the difference between them), and realised that the activity of ...
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The effect of dopamine signaling is one of the areas where computational neuroscience has provided insight into brain mechanisms, specifically via Reinforcement Learning (RL) models.
Based off this paper and PHD thesis from Dan Rasmussen, this first began with this publication from Schultz showing that dopamine acts as a reward signaler. From the abstract:
...
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I am not from a pure field of neuroscience so I did a bit of research. (Part put in bold by me is the bit which pertains to Bipolar Disorder (BPD))
Simon N Young of McGill University in Montréal, Quebec, Canada said in ResearchGate:
While catecholamines and serotonin in the blood and urine are not derived from the brain sometimes, for reasons that are ...
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Short answer
I cannot give an exclusive answer, but if you are talking about a schoolbook neuron with different neurons synapsing onto it, then excitation is indeed generally mediated by another neurotransmitter than inhibition. Why?...
Background
First and foremost. While recognizing that neurotransmitters in themselves are not excitatory or inhibitory, ...
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I'd say it is a low-impact theory. The original (2004) paper in which this was proposed has around 60 citations in Google Scholar. That's pretty low for a paper like this (if the theory were influential). For contrast a 2000 paper on the monoamine hypothesis for depression (which is far from being the first paper proposing it) has around 460 citations and ...
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I think you're confused about proteins that are GPCRs versus having homology. GABA-B is another that is a GPCR (it is not particularly related to GABA-A). These are also called metabotropic receptors.
Ionotropic receptors are from separate families, many from the Cys-loop family (see Sine & Engel, 2006) with a characteristic 5-subunit composition, or ...
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I have what is mostly a frame-challenge to your question as an answer: the simple "neurotransmitter imbalance" hypothesis is a bit outdated, and it hasn't been strongly influential in a research context for a very long time.
Rather, it is an extremely oversimplified way to try to explain that there are brain differences involved in depression: that it's a ...
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Wikipedia has a comprehensive list of neurotransmitters, categorized as (a short list):
Amino acids: glutamate, aspartate, D-serine, γ-aminobutyric acid (GABA), glycine
Gasotransmitters: nitric oxide (NO), carbon monoxide (CO), hydrogen sulfide (H2S)
Monoamines: dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine, ...
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triptans could help boost the efficacy of SSRIs
There is minimal evidence for this Chris. One of the reasons for that is that there is a limit to how much serotonin is released for the nerve cell. So more of the same isn't going to make much difference.
edit: So in terms of reuptake inhibitors, triptans are agonists. So increased agonism seems unlikely to ...
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Haha, yep. We don't know how depression or SSRIs work. We have hypotheses for both schizophrenia and depression - the dopamine hypothesis and the serotonin hypothesis.
While I was conducting my research, I too was faced with this conundrum. And Dr. David Healy is one of the trailblazers of the side which says that it's all clever pharma marketing.
As in ...
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Question: Does neural repair result in firing neurons?
This is a difficult question. Because a repair occurs when and where there is a damage. If there are abnormal firings of neurons, it will be difficult to sort out which one is the cause. It is also possible that both cause the firings.
However, there is no evidence that the majority of repairs, which ...
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There's a recent negative study: Bergwerff et al. (2016) "No Tryptophan, Tyrosine and Phenylalanine Abnormalities in Children with Attention-Deficit/Hyperactivity Disorder":
This study is the first to explore AAA metabolism in children with ADHD using a well-defined and relatively large sample. We found that AAA deficiencies are not related to ADHD. The ...
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No, unlike norepinephrine and serotonin, dopamine's pathway is limited.actually it affects two part of cognition, reward and motor functions.
As part of the reward pathway, dopamine is manufactured in nerve cell bodies located within the ventral tegmental area (VTA) and is released in the nucleus accumbens and the prefrontal cortex. The motor functions of ...
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Actually it's a bit complicated but in simple terms :
Neurotransmitters are stored in a synapse in synaptic vesicles, clustered beneath the membrane in the axon terminal located at the presynaptic side of the synapse. Neurotransmitters are released into and diffused across the synaptic cleft, where they bind to specific receptors in the membrane on the ...
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No. For example, the neurotransmitter at the first stage of auditory processing (the inner hair cell VII cranial nerve synapse) and visual processing (rod and cone synapses with a bipolar cells) is glutamate.
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There are neurotransmitters that are associated with specific functions within a neural circuit, but I would not associate a specific neurotransmitter with a specific sensation. There is also more complexity to this, because there is a plenty of receptors for each neurotransmitter. These receptors have slightly different properties, which may influence the ...
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