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If there were a competition to determine the current biological “wonder molecule,” brain-derived neurotrophic factor, or BDNF, would have to be among the finalists. Found in the central nervous system, BDNF is important for neuronal growth and differentiation, and has been shown to stave off neurodegeneration in animal models of Alzheimers [1]. Additionally, BDNF appears to play a vital role in LTP and memory.
Back in 2007, Bekinschtein et al published an article in Neuron showing that maintenance of a recently acquired associative-learning task required BDNF synthesis 12 hours after learning [2]. That is, BDNF appeared to be necessary for consolidation of the memory, though not for its initial formation. But as the title of this post would indicate, this story can't all be about our hot little BDNF molecule. Dopamine has got to enter the picture somewhere, right?
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Fast forward to the present. Following up on these earlier findings, Rossato and colleagues now report that dopaminergic signaling in CA1 may underlie the delayed upregulation of BDNF necessary for long-term memory (LTM) formation [3]. In this impressive study – wherein everything seemed to fall nicely into place (why can’t it work that way for the rest of us?) – the authors show that administration of a D1 dopamine receptor antagonist faithfully blocked LTM of a fearful association when given 12 hours following learning. Interestingly, this antagonist had no effect on LTM if given immediately or 9 hours after learning, indicating that D1 signaling may underlie the increased expression of BDNF previously reported. In a series of follow-ups, the authors drilled into the D1 signaling pathway to flesh out the processes involved, ultimately supporting the conclusion that dopamine regulates expression of BDNF. A cool little addition to this study is that, normally, weak training only causes a memory to persist for a couple days (short-term memory), whereas strong training will trigger LTM (>14 days). Both short-term and long-term memory require dopaminergic signaling during initial learning. However, only strong conditioning produces the 12-hour delayed D1/BDNF signaling that leads to prolonged memory. What if weakly trained animals had D1 signaling artificially induced 12 hours later??? The memory is preserved for the long haul, that’s what. Or, to put it another way, Rossato et al were able to take a weak memory and artificially boost its strength (unfortunately for the rats, the memory was a fearful one). So why dopamine? As you may have read in previous posts on The Axon, dopamine is believed to denote stimuli or events of high motivational value. Thus, it makes sense that stimuli eliciting strong dopamine release would support formation of lasting memories for said stimuli. How early and delayed dopamine signaling are linked remains an open question. Leave a Comment |
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Aug 30 2009 11:18 am
dopamine is dope
Nov 20 2009 1:13 am
"both short-term and long-term memory require dopaminergic signaling during initial learning"
My question is, how early does that occur during our stages of development? Do we make the conclusion that the stronger release of dopamine, the less chances to develop alzheimer's plaques? I am just trying to draw the links somewhere....
BCNov 04 2010 2:55 am
Isn't BDNF released any time there is an increase in cytosolic cAMP?
cAMP increase = PKA = CREB activation = Gene transcription = cFos BDNF increase
Did they block cAMP [checking...]
Yep
My point is, dopamine is cool, but acetylcholine has been doing the same thing for years. No respect!Dec 15 2011 10:05 am
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