Nature reveals how dopamine, which governs love, regulates the brain's forgetting mechanisms

In a recent study published in Nature, researchers from the Scripps Institute in the United States, entitled Dopamine-based mechanism for transient forgetting, found that the brain uses the neurotransmitter dopamine to cause short-term forgetfulness through the PPL1-alpha2 alpha-2-DAMB path, and that memory recovers spontaneously over time.
To explore the neurobiological mechanisms that lead to short-term oblivion, the researchers performed periodic intervals of aversion olfactory condition reflex stimulation on the model bio-fruit fly, caused it to have long-term memory (LTM), and then used airflow, electric shock, or blue light to stimulate the fruit fly briefly, finding that part of the memory expression decreased as the intensity of the stimulus increased.
but the expression of LTM reappears at a significant level after 1 h.
The back and outer frontal brain region 1 (PPL1) of the brain hemisphere contains 12 dopamine neurons (DAN), of which the MBN can mediat long-term brain oblivion by receiving DAN information from PPL1, so the researchers speculate that DAN in the brain hemisphere PPL1 may also be involved in mediating short-term forgetting.
In further experiments, the researchers performed a powerful and prolonged heat stimulation on the 12 DANs, and found that the expression of LTM was similarly significantly reduced when dans were physically stimulated, and observed that synthesical output from PPL1 DAN was suppressed.
Single DAN in PPL1 corresponding to the individual stimulation of alpha-2 alpha'2 mushroom body neurons (unlike the region involved in active forgetting of gamma-2-alpha'1), the researchers found that PPL1-alpha2 alpha'2 neurons were specifically responsible for this short-term amnesia.
interruption of memory caused by PPL1-alpha2 alpha'2 indicates the presence of dopamine liposes that transmit short-term forgotten signals.
Previous studies have found that DAMB subjects are involved in transducting the neuron-DAN signals associated with active forgetting, so the researchers speculate that DAMB distributed on the axons protruding by neurons may be the primary subject for short-term forgetting caused by DAN in PPL1-alpha2 alpha'2.
researchers looked at the expression levels of LTM in fruit flies after mutations in DAMB, and found that LTM showed significant elevated levels at all points in the test, consistent with expectations of the disappearance of short-term amnesia.
, the researchers used cross-genetic methods to further identify DAMB as a recipient of dopamine signals from PPL1-alpha2 alpha'2 and a key component of the short-term forgetting path.
, is the short forgetfulness that followed the previous airflow, electric shock, or blue light-stimulating fruit flies also occurring through the PPL1-alpha2 alpha-2-DAMB route? By suppressing the synhapus output of PPL1-alpha2 alpha'2 and stimulating fruit flies with airflow or blue light at the same time, the researchers found that inhibition of dopamine signal output also eliminated the short-term forgetting effects of external stimulation of fruit flies, no different from undestrulating control fruit flies.
also suggests that external interference stimulation does trigger the PPL1-alpha2 alpha-2-DAMB path, causing short-term oblivion.
. Davis, who co-authored the study, said: "We now know that there is a specific recipient in memory that receives a signal of short-term forgetting from dopamine.
but we don't yet know what will happen after that, and how this dopamine receptor activation causes this memory block, which is our next goal.
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