Ltp Quotes

Moderate, transient stress (i.e., the good, stimulatory stress) promotes hippocampal LTP, while prolonged stress disrupts it and promotes LTD—one reason why cognition tanks at such times. This is the inverted-U concept of stress writ synaptic.4

Moreover, sustained stress and glucocorticoid exposure enhance LTP and suppress LTD in the amygdala, boosting fear conditioning, and suppress LTP in the frontal cortex. Combining these effects—more excitable synapses in the amygdala, fewer ones in the frontal cortex—helps explain stress-induced impulsivity and poor emotional regulation.

How does stress influence the midbrain pleasure circuit (or the feeding control circuits)? The short answer is that we don't really know. However, there are some tantalizing initial clues. Recall that twenty-four hours after a single exposure to cocaine, the excitatory glutamate-using synapses recived by VTA dopamine neurons express LTP. This change, which will result in greater dopamine release in VTA target areas, could also be produced by nicotine, mophine, amphetamines, or alcohol. Amazingly, even breif exposure to stress (a rat's five-minute-long forced swim in cold water) also produced LTP of the VTA synapses that was indistinguishable from that evoked by drugs. What's more, the stress-induced LTP could be prevented by pretreatment with a corticosterone receptor blocker. This suggests that drugs and stress rewire the pleasure circuit in overlapping ways and that the stress response to trigger LTP in the VTA requires a stress hormone signaling loop from the brain to the body and back.

As the stories of BDNF and exercise developed in parallel, it became clear that BDNF was important not merely for the survival of neurons but also for their growth (sprouting new branches) and thus for learning. Eero Castrén, as well as Susan Patterson from Kandel’s lab at Columbia, found that if you stimulate LTP in mice by making them learn, BDNF levels increase. Looking inside their brains, researchers determined that mice without BDNF lose their capacity for LTP; conversely, injecting BDNF directly into the brains of rats encouraged LTP.