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You don?t have to be a combat vet to know that your response to stress?whether a loud noise, dying relative or looming deadline?changes over time. After the first exposure, we are somehow primed for the next, even weeks or years later. And when something in that process goes wrong, the consequences can be tragic.
Neuroscientists don?t understand much about how the brain encodes such a versatile stress response. It?s part of a complicated mess of hormonal, chemical and electrical signals in a brain system called the hypothalamic-pituitary-adrenal (HPA) axis. A new rat study has made the picture slightly less muddled, opening the door a tiny bit to new treatments for PTSD and other types of chronic stress.
Re: Stress Factors - Possible New Treatments for Post Trauma Stress Disorder
Re: Stress Factors - Possible New Treatments for Post Trauma Stress Disorder
Stress-induced priming of glutamate synapses unmasks associative short-term plasticity
J Brent Kuzmiski<sup>1,</sup><sup>3</sup>, Vincent Marty<sup>1,</sup><sup>2,</sup><sup>3</sup>, Dinara V Baimoukhametova<sup>1</sup> & Jaideep S Bains<sup>1</sup>
<hr class="separator"> Abstract
Exposure to a stressor sensitizes or 'primes' the hypothalamic-pituitary-adrenal axis to a subsequent novel stressor. The synaptic mechanisms underlying this priming, however, are not known. We found that exposing a rat to a single stressor primed glutamate synapses in the paraventricular nucleus of the hypothalamus and allowed them to undergo a short-term potentiation (STP) following a burst of high-frequency afferent activity. This transient potentiation requires a corticotrophin-releasing hormone–dependent depression of postsynaptic NMDA receptors (NMDARs).
The long-term depression of NMDAR function after stress prevented the vesicular release of an inhibitory retrograde messenger that, in control conditions, arrests STP.
Following stress, STP manifested as an increase in the release probability of glutamate that was sufficient to induce multivesicular release.
Our findings indicate that the priming of synapses to express STP is a synaptic correlate to stress-induced behavioral and neuroendocrine sensitization.
