New study concludes that selective serotonin reuptake inhibitors (SSRIs) used to treat PTSD likely do not help and may actually worsen their symptoms.

A newly published, DoD funded, study published in Biological Psychiatry is reviewed by Ann Trafton, a science writer from MIT, in an article posted by MedicalXpress titled 'Blocking a newly identified memory pathway could prevent PTSD'.

For reference, the article is found in PubMed as:
Stress Enables Reinforcement-Elicited Serotonergic Consolidation of Fear Memory.
Conclusion: Stress bolsters the consequences of aversive reinforcement, not by simply enhancing the neurobiological signals used to encode fear in unstressed animals, but rather by engaging distinct mechanistic pathways. These results reveal that predictions from classical associative learning models do not always hold for stressed animals and suggest that 5-HT2CR blockade may represent a promising therapeutic target for psychiatric disorders characterized by excessive fear responses such as that observed in PTSD.
Baratta MV, Kodandaramaiah SB, Monahan PE, Yao J, Weber MD, Lin PA, Gisabella B, Petrossian N, Amat J, Kim K, Yang A, Forest CR, Boyden ES, Goosens KA.
Biol Psychiatry. 2015 Jul 2. pii: S0006-3223(15)00533-8. doi: 10.1016/j.biopsych.2015.06.025. [Epub ahead of print]
PMID: 26248536
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As I am not a neuroscientist and this study is very complex, I can only provide a basic overview (mostly paraphrased) of the research then conclude by showing how psilocybin appears to play a promising role in treating PTSD by its effect on the amygdala.  Hopefully some "heroic investigators" will follow up on these new insights.

An animal subjected to chronic stress prior to experiencing a traumatic event engages a distinctive brain pathway that encodes traumatic memories in the amygdala (amygdala plays a key role in fear consolidation) more strongly than in unstressed animals. Serotonin promotes the process of memory consolidation in animals that go on to developed PTSD symptoms following chronic stress and a traumatic event. By blocking the amygdala cells' interactions with serotonin after trauma, the stressed animals did not develop PTSD symptoms.

Chronic stress causes cells in the amygdala to express many more 5-HT2C receptors, which bind to serotonin. Then, when a traumatic experience occurs, this heightened sensitivity to serotonin causes the memory to be encoded more strongly. It may be possible to weaken these memories by using serotonin-blocking drugs to interfere with the reconsolidation process (note: SSRIs do the opposite).

Ki Goosens, the senior author of the study, stated "there's no biological evidence to support the use of SSRIs for PTSD."  She continued, "The consolidation of traumatic memories requires this serotonergic cascade and we want to block it, not enhance it," she adds. "This study suggests we should rethink the use of SSRIs in PTSD and also be very careful about how they are used, particularly when somebody is recently traumatized and their memories are still being consolidated, or when a patient is undergoing cognitive behavior therapy where they're recalling the memory of the trauma and the memory is going through the process of reconsolidation."

So where does psilocybin fit in as a treatment for PTSD in light of this new information?

The dorsal raphe nucleus is the largest serotonergic nucleus and provides a substantial proportion of the serotonin innervation to the forebrain. Ten percent of the axons from the nucleus raphe dorsalis of the rat have been shown to project to the amygdala. Dorsal raphe serotonergic activity is required for the stress enhancement of fear in a stimulus-dependent manner. During this study inhibition of the serotonergic dorsal raphe during conditioning was sufficient to prevent stress related enhancement of fear by blocking memory consolidation in the amygdala.

Psilocybin reduces the dorsal raphe nucleus cell firing rate thus resulting in decreased serotonin release in terminal projection fields such as the amygdala. Further more, psilocybin decreases amygdala reactivity during emotion processing which is associated with an increase of positive mood in healthy volunteers. Psilocybin works on the 5HT2A receptors which are abundant in the amygdala. These findings may be relevant to the normalization of amygdala hyperactivity and negative mood states.

Since psilocybin is essentially non-addicting, has less toxicity than caffeine, and, as shown above, plays a key role in inhibiting the release of serotonin from the dorsal raphe nucleus as well as decreasing the reactivity of the amygdala to negative stimuli, it is a primary candidate for a Clinical Trial to treat PTSD.

Note: there is an article citing the article above by Baratta et al. that  demonstrates how a 5-HT2CR blockade (put another way, serotonin 2C receptor antagonism) improves fear discrimination and subsequent safety signal recall that would be helpful for those with PTSD since their capacity to discriminate between safety and danger, which is fundamental for survival, is disrupted. The article as found in PubMed:

Serotonin 2C receptor antagonist improves fear discrimination and subsequent safety signal recall.
Foilb AR, Christianson JP.
Prog Neuropsychopharmacol Biol Psychiatry. 2015 Sep 4;65:78-84. doi: 10.1016/j.pnpbp.2015.08.017. [Epub ahead of print]
PMID: 26344640
(PDF)

Psilocybin use results in an increase in positive mood by decreasing activation of the amygdala

Psilocybin-Induced Decrease in Amygdala Reactivity Correlates with Enhanced Positive Mood in Healthy Volunteers 
Conclusion:  These results demonstrate that acute treatment with psilocybin decreased amygdala reactivity during emotion processing, and that this was associated with an increase of positive mood in healthy volunteers. These findings may be relevant to the normalization of amygdala hyperactivity and negative mood states in patients with major depression.
Kraehenmann R, Preller KH, Scheidegger M, Pokorny T, Bosch OG, Seifritz E, Vollenweider FX. 
Biol Psychiatry. 2014 Apr 26. pii: S0006-3223(14)00275-3. 
PMID: 24882567 
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This research was conducted by the Department of Psychiatry, Psychotherapy and Psychosomatics, Psychiatric Hospital, University of Zurich, Switzerland.  Among the well know academics associated with this institution is Carl Jung.

Do individuals with PTSD experience depression or negative thoughts?  Might psilocybin, given therapeutically with the proper mindset and in a supportive environment, assist in their recovery? Research in this area needs to be furthered by those who have a responsibility for treatment of individuals with PTSD.

The amygdala is hyperactive in those with PTSD.  "The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus in particular during extinction. This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability." (Wikipedia: PTSD)

So how does the amygdala relate to mindfulness?  The passage below may shed some light on this matter.

"Mindfulness mediation is designed to alter peoples’ perception of the world by making them disengage from ruminations and attention to negative thoughts and become aware of and accept thoughts non-judgmentally without trying to change them. An 8-week course of mindfulness meditation increased grey matter in brain regions involved in learning and memory, emotion regulation, self-referential processing and perspective taking in healthy people. In stressed individuals, the decrease in perceived stress after an 8-week course of mindfulness meditation was associated with a decrease in the right basolateral amygdala grey matter density. If the changed perception of the world brought about by mindfulness meditation over a period of 8 weeks can cause changes in the brain, this raises the possibility that the change in perception due to psilocybin may result in changes in the brain over a matter of weeks. How such brain changes may interact with the changes in psychology is not known. There is need for more work on the long-term psychological changes associated with psilocybin, as well as research on the long-term brain changes and their possible association with the psychological changes." (From: Young SN. J Psychiatry Neurosci. 2013 Mar;38(2):78-83. Review.)

Psilocybin appears to be uniquely structured (structure determines function) to calm those areas of the brain that are overactive in those suffering from PTSD, plus its effects are long lasting.  If there is another substance or therapy that has similar or better potential, I'd sure like to read about it.

Psilocybin reduces threat-induced modulation of amygdala connectivity

Researchers from Psychiatric Hospital, University of Zurich, led by Rainer Kraehenmann found that psilocybin substantially reduced the modulatory effect of threat on the top-down connection from the amygdala to the primary visual cortex in normal human subjects. These findings may have important implications for the treatment of mood and anxiety disorders as well as inhibiting the fear-responses during exposure-based psychotherapy, which may facilitate therapeutic progress during the treatment of post-traumatic stress disorder.

The August 2015 article from NeuroImage: Clinical titled 'The mixed serotonin receptor agonist psilocybin reduces threat-induced modulation of amygdala connectivity' (PDF) stems from previous research (2014) from the journal Biological Psychiatry titled 'Psilocybin-Induced Decrease in Amygdala Reactivity Correlates with Enhanced Positive Mood in Healthy Volunteers' (PDF) (Cited by - Google Scholar). The 2014 research demonstrated that "acute treatment with psilocybin decreased amygdala reactivity during emotion processing and that this was associated with an increase of positive mood in healthy volunteers. These findings may be relevant to the normalization of amygdala hyperactivity and negative mood states in patients with major depression." It should be noted that amygdala hyperactivity plays a role in PTSD pathology and the amygdala abundantly expresses 5-HT2a receptors.

Recent research/news keeps trickling in

Publication source: Journal of Psychopharmacology (August 2016)
Survey study of challenging experiences after ingesting psilocybin mushrooms: Acute and enduring positive and negative consequences.  (PDF)
Basically concludes a 'bad trip' may not be so bad in the long run and may even be positive.  Still, be advised to only ingest for the right reason in a supportive environment.

Publication source: Journal of Toxicological Sciences (2015):
Ecstasy (MDMA) Alters Cardiac Gene Expression and DNA Methylation: Implications for Circadian Rhythm Dysfunction in the Heart.
Another reason why MDMA should NOT be used to treat PTSD.  Psilocybin does not have the high degree of toxicity that MDMS has.

Publication source: International Review of Neurobiology (2016)
Treating Addiction: Perspectives from EEG and Imaging Studies on Psychedelics:  (PDF)
This chapter outlines relevant EEG and brain imaging studies evaluating the effects of psychedelics on the brain. This chapter also reviews evidence of the use of psychedelics as adjunct therapy for a number of psychiatric and addictive disorders. In particular, psychedelics appear to have efficacy in treating depression and alcohol-use disorders.

Publication source: Psychopharmacology journal: (October 2016):
Alterations of consciousness and mystical-type experiences after acute LSD in humans (Full-text/PDF)
LSD not as effective in facilitating a mystical experience as psilocybin.

Publication source: Journal of Humanistic Psychology (October 2016):
A Comparison of Psychedelic and Nonpsychedelic Mystical Experiences
This study was authored by researchers from:

• University of Pennsylvania, Philadelphia, PA, USA
• University of North Carolina, Chapel Hill, NC, USA
• University of Melbourne, Parkville, Victoria, Australia
• New York University, New York, NY, USA
• Thomas Jefferson University, Philadelphia, PA, USA
• University of Tennessee at Chattanooga, Chattanooga, TN, USA

Experiences of profound existential or spiritual significance can be triggered reliably through psychopharmacological means using psychedelic substances. However, little is known about the benefits of religious, spiritual, or mystical experiences (RSMEs) prompted by psychedelic substances, as compared with those that occur through other means. In this study, 739 self-selected participants reported the psychological impact of their RSMEs and indicated whether they were induced by a psychedelic substance. Experiences induced by psychedelic substances were rated as more intensely mystical (d = .75, p < .001), resulted in a reduced fear of death (d = .21, p < .01), increased sense of purpose (d = .18, p < .05), and increased spirituality (d = .28, p < .001) as compared with nonpsychedelically triggered RSMEs. These results remained significant in an expanded model controlling for gender, education, socioeconomic status, and religious affiliation. These findings lend support to the growing consensus that RSMEs induced with psychedelic substances are genuinely mystical and generally positive in outcome. 

Publication source: Neuroimage: clinical (2016)
The mixed serotonin receptor agonist psilocybin reduces threat-induced modulation of amygdala connectivity (Full-text/PDF)
Highlights:

• We measured BOLD signals during a threat-inducing pictures task.
• Subjects were treated with psilocybin (a serotonergic hallucinogen) and placebo.
• We compared effective connectivity changes between psilocybin and placebo using DCM.
• We found that psilocybin decreased top-down connectivity from the amygdala to visual cortex.
• Results point at a neural mechanism underlying emotional shifts induced by psilocybin

Since the amygdala plays a key role in PTSD, this is another good reason for the DoD and/or Veterans Administration to conduct a Clinical Trial utilizing psilocybin to treat PTSD.

Publication source:  Therapeutic Advances in Psychopharmacology (June 2016):
Antidepressive, anxiolytic, and anti-addictive effects of ayahuasca, psilocybin and lysergic acid diethylamide (LSD): a systematic review of clinical trials published in the last 25 years (PDF)
In conclusion, ayahuasca, psilocybin and LSD may be useful pharmacological tools for the treatment of drug dependence, and anxiety and mood disorders, especially in treatment-resistant patients. These drugs may also be useful pharmacological tools to understand psychiatric disorders and to develop new therapeutic agents. However, all studies reviewed had small sample sizes, and half of them were open-label, proof-of-concept studies. Randomized, double-blind, placebo-controlled studies with more patients are needed to replicate these preliminary findings.

Publication source: The Baltimore Sun: (September 2016):
Growing research finds psychedelics effective in treating disease
Since Johns Hopkins is in Baltimore, this article mostly likely arose due to their proximity.

Low dose psilocybin erases conditioned fear in mice faster than high dose psilocybin and has potential as treatment for PTSD

Effects of psilocybin on hippocampal neurogenesis and extinction of trace fear conditioning
Drugs that modulate serotonin (5-HT) synaptic concentrations impact neurogenesis and hippocampal (HPC)-dependent learning. The primary objective is to determine the extent to which psilocybin (PSOP) modulates neurogenesis and thereby affects acquisition and extinction of HPC-dependent trace fear conditioning. PSOP, the 5-HT2A agonist 25I-NBMeO and the 5-HT2A/C antagonist ketanserin were administered via an acute intraperitoneal injection to mice. Trace fear conditioning was measured as the amount of time spent immobile in the presence of the conditioned stimulus (CS, auditory tone), trace (silent interval) and post-trace interval over 10 trials. Extinction was determined by the number of trials required to resume mobility during CS, trace and post-trace when the shock was not delivered. Neurogenesis was determined by unbiased counts of cells in the dentate gyrus of the HPC birth-dated with BrdU co-expressing a neuronal marker. Mice treated with a range of doses of PSOP acquired a robust conditioned fear response. Mice injected with low doses of PSOP extinguished cued fear conditioning significantly more rapidly than high-dose PSOP or saline-treated mice. Injection of PSOP, 25I-NBMeO or ketanserin resulted in significant dose-dependent decreases in number of newborn neurons in hippocampus. At the low doses of PSOP that enhanced extinction, neurogenesis was not decreased, but rather tended toward an increase. Extinction of "fear conditioning" may be mediated by actions of the drugs at sites other than hippocampus such as the amygdala, which is known to mediate the perception of fear. Another caveat is that PSOP is not purely selective for 5-HT2A receptors. PSOP facilitates extinction of the classically conditioned fear response, and this, and similar agents, should be explored as potential treatments for post-traumatic stress disorder and related conditions. 
Catlow BJ, Song S, Paredes DA, Kirstein CL, Sanchez-Ramos. J. 
Exp Brain Res. 2013 Jun 2. [Epub ahead of print] 
PMID: 23727882 
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