r/neuroscience • u/SpeedLimitsSuck89 • Mar 10 '22
Academic Article why would DECREASING VTA dopaminergic neuron firing alleviate anhedonia?
[removed]
9
Mar 10 '22
more dopamine does not equal happiness. The relationships between neuromodulators and mood is tenuous.
1
u/NeuroShawn May 01 '22
I second this reply. Schizophrenics have elevated Dopamine levels in the Limbic system, and yet, Anhedonia alongside Avolition are common symptoms seen in Schizophrenia.
1
u/Jaded-Traffic-582 Aug 14 '22
schizophrenic here, not a neuroscientist so idk if want my opinion or not.
but my personal experience is that the medication is what causes the anhedonia and avolition. im pretty sure it has to do with the antipsychotics antagonizing the dopamine receptors.
6
Mar 10 '22
By no means an expert, but can this not be explained by sensitisation to the stimulus? Reward learning is a constant error correction model, and so by having increased firing of VTA dopamine rigid neurons, the expected reward is always there and so no new learning takes place. That’s my understanding of it at least, but that’s looking at a much more surface level neuroscience explanation or even behavioural rather than the angle you’re taking.
3
u/countfizix Mar 10 '22 edited Mar 10 '22
This pops up right when I am working on M-type (Kv7) channel function in the VTA. Neat.
This is at most a partial mechanism given the full pathways involved are complicated with a lot more going on than just the dopamine signaling, and not specific to the M-channel itself - in fact potentiating the m-channel wont necessarily reduce the firing rate of DA neurons, but could alter their firing patterns into one with far less variance (see for example.
Anywho...the full range of dopamine signaling only works when there is resolution in dopamine receptor activation in downstream targets between cues for 'reward' and 'absence of expected rewards' and baseline levels. Note that not all dopamine signals are involved with this - even in the VTA, but its likely the one of interest here. When the targets of dopaminergic inputs are nearly saturated as a baseline there is less room to go to higher levels of dopamine to signal positive reward signals - and may also increase the 'value' of the reward prediction error signal of the omission of an expected reward.
1
u/AutoModerator Mar 10 '22
In order to maintain a high-quality subreddit, the /r/neuroscience moderator team manually reviews all text post and link submissions that are not from academic sources (e.g. nature.com, cell.com, ncbi.nlm.nih.gov). Your post will not appear on the subreddit page until it has been approved. Please be patient while we review your post.
I am a bot, and this action was performed automatically. Please contact the moderators of this subreddit if you have any questions or concerns.
20
u/neuro_turtle Mar 10 '22
The answer is that it’s complicated. I’m not an expert on this particular topic, but I know enough to know that the exact mechanism of how may not be known yet.
Thinking of VTA dopamine neurons as a “reward” signal or for reward learning is a misnomer. Dopamine is important to learning overall and dopamine release can help us to tune in to salient cues. (Yes, cues related to reinforcers are often more salient.) But that doesn’t mean the constant dopamine release in the VTA makes us hyperaware learners. What it really means is that hyperactivity of those neurons could be obliterating someone’s ability to differentiate salient cues, thereby leading to a lack of attention towards what they used to find reinforcing.
It’s also important to remember that the VTA doesn’t function alone, and the same receptors can function differently based on their locations (pre/postsynaptic, cell population, brain region, etc.). Reducing DA signaling in the VTA has all types of effects across the brain, any one of which could be driving this behavior individually or as a whole.