BRUCE MCCONNELL PHD

 Introduction

The shank of a century has passed since Albert Hofmann’s discovery of LSD; yet its definitive pharmacology has eluded us in the absence of knowing the biological roles of our internal hallucinogens. This glaring omission can be explained largely by a diversion of priorities from their neurobiology into a single preoccupation with their spectacular psychological effects on the vast majority of users, patients and psychotherapists.   Recently, unquestionable long-term improvement in the psychological well-being of carefully selected volunteers and sufferers of PTSD has been shown by researchers, undoubtedly inspired more by popular literature on the hallucinogen’s psychic  gifts, rather than by any knowledge of their neurophysiology.   Some physiological roles have been suggested, but miss the depth consistent with the hallucinogen’s profound and mysterious introduction to new existential meanings for good or ill that embody heuristic insights lasting a lifetime.   After all this time in the dark, one might look elsewhere to define the biological role of the hallucinogens, accepting that psychology may have only a peripheral role to play in a larger process that can be defined in precise neurobiological terms.  The path to this resolution, born by some of LSD’s rare effects, is described here.

The following,  “Rare Hallucinogen Effects and Twilight sleep: I and II”, respectively, report evidence for the function of endogenous hallucinogens at the time of birth as mediators of fetal memory consolidation and as activators of fetal movement, further suggesting their daily role in  autonomic healing of accumulated noxious memory and the real meaning of flashbacks.  Their peripheral psychological work is in support of the mother during her labor.  The evidence, taking the form of birth memory recall and fetal movement in an adult on LSD, represents rare drug responses traceable to the birthing method called “Twilight Sleep” and its use of scopolamine.  As involuntary and exclusively physical effects, these are not “subjective” effects of drug inebriation easily subject to varying interpretations. These are real data, the description and interpretation of which is limited and articulated by the human experimental animal.  The implications of these results in newborn development, hallucinogen pharmacology and trauma research follow all too easily to avoid as new conclusions. Furthermore, this connection between hallucinogens, birth and trauma may not have been found any other way.

The evidence described in this first report took the form of narcosis, catalepsy and robust skull sensations that arrived soon after LSD ingestion, linking the hallucinogen pharmacology of this adult subject to a similar hallucinogen mechanism within his fetal state at the time of birth when the memory was first consolidated.  This connection is based on the close consistency between the sequence of these somatic effects and documented obstetric manipulations during expulsion of the newborn in the Twilight Sleep protocol.  The complete erasure of this memory in a stepwise manner was revealed by diminishing encores of the skull sequence (flashbacks) over several days following, leading to two conclusions:  1) This particular trauma was reversible and describable by a simple, stepwise “open/closed” model, involving the well documented action of 5-HT1a agonists on the activity of brainstem raphe nuclei and 2) noxious impulses emerging from the open memory substrate must reach cortical interpretation (flashbacks) for continuance of stepwise erasure.   The spontaneity of this erasure suggests a natural autonomic mechanism for the day to day resolution of noxious memory involving the secretion of internal hallucinogens during REM sleep.  These findings are traced to the use of scopolamine in the Twilight Sleep birthing procedure.

Materials and Methods  

LSD was purchased in blotter form as a street drug sold in the mid 1970s and stored under refrigeration.  At the time, street blotter LSD was known to have undergone analysis by spectroscopic equipment of the university.  The authenticity of LSD was consistent with subjective accounts of more “classical” LSD experiences from other self-experimenters with this particular lot.  Confirmation was provided for this lot by the consistency of effect for a variety of other hallucinogens, as described in the following paper.

 A small 4mm blotter square containing approximately 100ug (micrograms) of the drug was divided into four sections with a razor blade, cutting from corner to corner.   The assumed dose of 25ug was based on the assumption that the alleged 100ug was distributed evenly within the blotter material.  The drug was taken using oral mastication and water by a 85kg naïve male subject (the author) in his mid 40s in a restful, attractive and safe atmosphere under the care of a man and wife alert to any needs that might arise.  Aside from occasional checking, the subject was left alone.  The session was recorded in a logbook the next day.

RESULTS

The six to seven hour LSD session was dominated by intense sensations of palate pressure and skull shearing forces (below).  Previous to this, about a half hour after ingestion, feelings of “healing”, calm physical relaxation, pleasurable anticipation and increased intestinal sound activity preceded the onset of skull sensations.  During this early time a brief hallucination appeared as a short interval of watching an amusing dreamlike movie.  This event was followed by a comfortable feeling of dulled narcosis, pleasurable body sensations, relaxed gazing and the desire to remain motionless, best characterized as the “stoned” state of narcosis.  This continued to varying degrees throughout the following sensory events.

Soon, intense feelings of alarming pressure began with the palate and proceeded upward into the bony maxillae area above the upper teeth, then across the bridge of the nose and into the forehead.  These sensations were not superficial, but seemed deep in the bone.  As shown in Figure 1, the sequence was divided into specific locations in the skull, each sensation having its own time frame: First, the palate (the palatine process of the maxilla), then, the bone holding the upper teeth (the maxilla), the nasal bone and finally, the forehead (frontal squama of the frontal bone). These sensations, traversing from the palate upwards along the front of the skull, continued to repeat in the same order, but eventually, only the palate and maxilla sensations were felt.   The forehead sensations were felt as a line of shearing, as if the left and the right sides were forced along the suture in opposite directions.   The initial sequence of pressure and shearing was alarming, but not painful and appeared within a background of “narcosis” (above).

 

 Flashbacks

The skull sensations continued on spontaneously and sporadically over a period of several days, diminishing in intensity to the point of complete disappearance.  The palate pressure was the last to disappear.   These flashbacks returned most often a short time after the subject awakened from sleep in the morning and sometimes in the afternoon during normal work activities.  

 Source of Skull Sensations

A few weeks after this session, the author learned that these palate and skull sensations would be those of a fetus during an obstetric procedure fashionable in the 1930s (Grof, personal communication).  In this obstetric protocol the mother was given a mixture of morphine and scopolamine to promote anesthesia, sleep and amnesia.  Because this “twilight sleep” protocol would diminish the contractions, the baby, now incapacitated under the influence of these drugs in the placental blood, is worked out of the birth canal by the roof of its mouth with the first two fingers of the doctor’s hand.  Until this explanation by Dr. Stanislav Grof, neither the observers involved nor the author had any inkling of the meaning of these skull sensations, putting to rest the question of hallucinogen suggestibility.   The author recalled, as a teenager,  his mother’s comment that this birth was the easiest of the three children; She learned of the birth only after she awoke, asking a frequent question seen in Twilight Sleep, "When does it begin?".

Discussion

Like Albert Hofmann's discovery of LSD in April, 1943, this LSD retrieval of a birth memory needs no statistical test of its reality and, like Hofmann's could not be obtained in any way other than the experimental animal's nuanced  articulation of the experience.  This represents a different kind of science than that normally publishable, but it is science, nonetheless, short on data, but long on the discussion of immediate and unavoidable insights, obviously pointing to new approaches in the study of memory, trauma therapy, obstetric management and newborn development not to mention the first clue to the real biological role of hallucinogens, having escaped workers for seventy or more years of intensive scrutiny.  LSD triggered the surge of a certain kind of memory quite different from the kind recalled willfully as information about life episodes or facts.  As seen in posttraumatic stress disorder (PTSD) the recall was involuntary and appeared as a recapitulation of somatic insults imposed previously, in this case, 4.5 decades later, but unlike PTSD, it erased itself completely.   Enumerating a number of obvious claims: 1) The rarity of this LSD effect derives from the rarity of the subject’s birth by an obstetric method used between 1900 and 1970 called, Twilight Sleep (TS), 2) Consolidation of this memory during the original trauma does not involve cerebral elements, owing to the anticholinergic effects of the TS drug, scopolamine, on the hypothalamus and hippocampus, as well as the spinal horns and cortical areas of the parturient fetus and mother, 3) Once triggered, this memory is erased completely by spontaneous processes in steps, each introduced by flashbacks, revealing the necessity for cortical interpretation of these impulses to initiate each step; Flashbacks are not toxic aberrations, as commonly thought, but signs of spontaneous autonomic healing, as in a laceration, 4) A regular schedule of healing noxious memory is implied, involving the secretion of endogenous hallucinogens during REM sleep to open memory substrates for erasure, or to consolidate recent insults into updated memory. These claims will be discussed in this order.  5) A reversible “open”/”closed” anatomical model of this memory can be described by a reversible neural mechanism for sub-cerebral memory control, based on the documented 5-HT1a (serotonergic) receptor influence within the brainstem raphe (Ra) nuclei to release blocked impulses within a reticular nucleus (RN), i.e., the (RaRN model).  6) The reversible property of this memory forms the basis for specific caveats about the clinical, spiriual and recreational use of hallucinogens.

1)  In the 1930s the standard drill for some Twilight Sleep (TS) acolytes was to work the fetus’ head through the birth canal, with the first and second fingertips of doctor’s hand placed at the roof of its mouth, producing the exact sequence of local skull sensations experienced by this adult with LSD, i,e., first, serious pressure on the fetal palate, followed by gross distortion of the maxilla and nasal bone from the upward force and some shearing of the frontal bone suture as the head emerges asymmetrically from the cervical opening.  The early narcosis and unwillingness to move are convincing as part of this sequence, as these are consistent with the early injection of scopolamine and morphine (S&M) to the mother to make her sleep and ensure amnesia of the ordeal (Van Hoosen and Shaw, 1915).  

2) This obstetric manipulation of the fetus identifies Twilight Sleep as the method used to deal with the flaccid, unconscious state of the fetus and the mother's diminished uterine contractions that resulted from the presence of scopolamine (S) and morphine (M), the drugs producing the titular symptoms.  As a powerful anti-cholinergic (muscarinic) drug, (S) blocks both the storage of memory by the hippocampus (Hasselmo et al, 1996; Kaakkola and Ahtee (1977) and sub-cerebral to cerebral communication through another key M3 cholinergic organ, the hypothalamus (McGeer et al, 1987; Kandel et al, 2001).  The unwillingness of this subject to move is consistent with the well known potentiation of morphine catalepsy and anesthesia by scopolamine (Sperber ES, Romero MT, Bodnar RJ, 1986).  However, scopolamine’s cholinergic antagonism per se actually reverses catalepsy (Morelli & DiChiara, 1985) and the administration of S&M by TS practitioners emphasizes S alone for the second and third injections (van Hooten & Shaw, 1915).   Since catalepsy-like symptoms did occur for this subject, it may reflect scopolamine’s known potentiation of hallucinogenic catalepsy (Chiu & Mishra,1980, consistent with the discussion below on the role of endogenous hallucinogens in birth.  These results support the proposition that, like the mother, the fetus has no cerebral memory of the birth, as S&M easily pass the placental barrier and were found in fetal secretions fifteen minutes after the last injection (van Hooten & Shaw, 1915).  The cerebral memory in a baby otherwise born would include some rudimentary alarm and depression mediated by the amygdale-hippocampus axis, although pain awareness at this stage is mediated largely by the thalamus (Diamond et al, 1985).  Because there were only physical sensations in this memory recall, it’s concluded from well known scopolamine pharmacology that the memory holding these fetal insults could not have been stored cerebrally, but stored within an (un-idendified) cerebellar nucleus, as amply documented by the work of Thompson others on Pavlovian memory (Thompson, 2005; Thompson and Krupa, 1994).  it is concluded that a non-human or human experimental model can be created to study isolated sub-cerebral effects, free of cerebral contamination.

3) Progressively diminishing flashbacks of this trauma memory, appearing spontaneously long after the drug was gone, were exact encores of the memory retrieval until they never returned, even with subsequent trials with hallucinogens.  Thus, these simple flashbacks are heralds of a healing process that would underlie and be fundamental to those more persistent flashbacks seen in post-traumatic stress disorder (PTSD), which include traumatizing emotions from the amygdala that would be reconsolidated into noxious memory.  The implication is that, fundamentally, flashbacks of this episode are not the lingering aftermath of hallucinogen “toxicity”, as commonly held (Halpern and Pope, 2004).  The persistence of LSD flashbacks seen in the clinic or ER originate largely from recreational use, in which the retrieval of past trauma or frightening visions represent the cerebral effects of the vast majority of users, that is, those born more naturally than this subject.  Accordingly, flashbacks seen In a therapeutic context  are much less a problem (Nichols, 2004).  By contrast, flashbacks in this TS-born adult were highly simplified physical sensations that were consolidation under conditions obviating cortical and subcortical (hippocampus) input.  Upon activation of this hidden memory, these flashbacks were, indeed, cortical interpretations that accompanied each step within a spontaneous process of memory erasure.  In the simplest of terms, this fixes cortical interpretation of incoming sensory impulses as the sine-qua-non for continuance of memory erasure, an old concept derived from psychiatry.  Furthermore, the spontaneity of this process in discrete steps indicates the existence of a natural schedule for autonomic removal of noxious memory, both cerebral and sub-cerebral on a reglar, ongoing basis. The success of this autonomic process would depend upon the amplitude of the associated factors contributing to the trauma, as in cases of robust PTSD symptoms.  Failing this by autonomic processes is likely to lead to some kinds of chronic depression, as discussed below.  Rather than erasure, a cerebrally complicated memory would be merely updated by further trauma from the PTSD symptoms themselves, to explain their persistence. Consistent with this notion is the dramatic improvement of PTSD (cerebral) symptoms when the influence of the amygdala on hippocampus beta receptors is removed by propranolol ( Pitman et al, 2002). 

4) These results and conclusions derived from this view of flashbacks conform to a simple "open/closed" property of the memory substrate, in which the imprint or engram is "opened" by a receptor agonist (LSD) and closed with its disappearance by dilution or by oxidase destruction.   In one crude scheme (Figure 2) a “closed” substrate (MS) is “opened” by LSD, allowing the contents to reach cortical awareness. As suggested in the drawing, impulses reaching the cortical realm begin a feedback cycle to liberate more contents into awareness until the memory substrate is “empty”. The necessity of reaching the cortex for continuation of the cycle is implicit from the sensory awareness of the flashbacks.  Here, both the horizontal and left vertical openings are the same, requiring LSD or an endogenous hallucinogen, respectively.

 

The inclusion of “DMT+” (any or all congeners of dimethytryptamine) is introduced in Figure 2 to account for continuing memory erasure long after LSD has gone. Also, DMT+ is the basis for the mechanism of memory control presented below, in which the memory of Figure 2 is “opened” in the presence of DMT+ and closed in its absence, accounting for its reversibility and erasure.  The key assumption for this inclusion of DMT+ is that the pharmacological state of this adult on LSD is the same as that of his fetal form during parturition; fetal “hallucinogenic” indoles are secreted for the memory’s original consolidation. The same process re-opened the memory 45 years later by an external indole. Basically, the process to be discussed below involves the un-blocking of memory impulses by the activation of a brainstem reticular nucleus (RN) due to the inhibition of serotonergic (5-HT) neurons within brainstem raphe nuclei (Ra) and is referred to as the RaRN model or mechanism..  This raphe inhibition is first initiated by LSD and later by DMT+ , both as ligands binding to the raphe 5-HT1a receptor.

 Like LSD, DMT+ congeners bind strongly to the same serotonergic receptors as LSD, notably the (hallucinogenic) 5HT2a/2c within the pyramidal layers of the prefrontal cortex and the (non-hallucinogenic) 5-HT1a of the brainstem raphe nuclei (Nichols, 2004). These endogenous congeners, collectively designated as DMT+, are:  dimethyltryptamine (DMT), 5-methoxyDMT and bufotenin (dimethylserotonin), known for several decades to reside in the human brain and body (Barker et al, 2001; Forstrom et al, 2001 and references therein).  Their synthetic enzymes are all found in the pineal gland (Weichmann et al, 1985; Reiter, 1981; Wurtman & Anton-Tay 1969).  Pineal melatonin, secreted in the light-controlled diurnal cycle to promote sleep (Kennaway & Voltsios 1998; Tan & Khoo, 1981)  is almost identical structurally to the most powerful of DMT+ hallucinogen, 5-methoxyDMT, except for the substituent on the terminal ethyl nitrogen: carbonyl for melatonin and dimethyl for 5-methoxyDMT,  the latter indole having by far the highest affinity of the others for the 5-HT1a receptor (Ray, 2010; Kent, 2010).  This receptor is the centerpiece of the suggested memory control mechanism, as represented by a proposed description of the relevant neuroanatomy (below).

Functional Neuro-anatomy of RaRN: The appropriate anatomical slice of the brainstem is shown in the sketch of Figure 3, illustrating the reciprocal activities Ra and RN with color changes from red (active) to blue (inactive). Agonist binding at the Ra 5-HT1a shuts down 5-HT neurons of the raphe magnus within the center of this slice, activating the neighboring reticular nuclei within the reticular formation.  From the initial palate insult of the birthing fetus, pain impulses first originate from the palate nocireceptors and are sent to the nucleus solitarius in the caudal pons/rostral medulla, which relays them to one or both reticular nuclei at this level, the lateral reticular nucleus (LRN) or the reticular gigantocellular nucleus (Nolte , 2002; Kandel et al, 2001).  Fiber connections between RaMagnus and LRN are shown in these references, as well as the connections between LRN and deep cerebellar nuclei for memory storage. Thus, release of DMT+ “opens” the memory substrate to send pain impulses to the cortical S1 and S11 for pain interpretation.  

Figure 4 illustrates the reversible and bi-directional nature of impulse traffic between memory storage and cerebral awareness.  In the absence of 5-HT1a agonist (Fig. 4 A), the 

usual direct route for pain to the cortex occurs via the thalamus, where pain impulses to cortical regions (SI and SII) are attenuated by negative feedback through collateral fibers within the thalamic reticular nucleus (Nolte, 2002).  Figure 4B represents the adult subject on LSD, where inhibition of the raphe magnus and activation of LRN allows the relay of pain impulses from a cerebellar storage nucleus into cortical interpretation.  In this case, the palate is out of the picture and sensations are not attenuated by TRN.  

Assignment for the location of the memory substrate within a deep cerebellar nucleus is consistent with its Pavlovian quality inferred from the connection between the timed sequence of LSD sensations reaching awareness, beginning with narcosis and progressing into the skull sensations.  Thompson and co-workers have shown from bell-ring/eye blink experiments that the indispensible memory location, i.e., one that persists after selective ablation of all other brain parts, resides as a bi-synaptic junction within the interpostis nucleus deep in the cerebellum (Thompson, 2005; Thompson & Krupa, 1994).  In the Pavlovian sense, the onset of narcosis from the LSD birth memory and the following sequence of skull sensations would represent a cascade corresponding to the “conditioned stimulus” (CS) or the rabbit’s blink, but each acting as the unconditioned stimulus for the next, corresponding to the air puff in Thompson’s experiments.  These studies support the sub-cerebral location of this LSD memory.

Of course, the binding of an agonist to the 5HT1a receptor isn’t the only way to affect raphe activity.  Acetylcholine, gama-aminobutyric acid (GABA) and norepinephrine affect the REM-ON and REM-OFF states (see “Contents” link R2  in biosublime.com).  Also, the raphe dorsalis, supplying most of the 5-HT synapses to the brain, contains the inhibitory gamma-aminobutyric acid (GABA) system from one or more of its six to eight sub-nuclei (wikipedia.org/wiki/Dorsal_raphe_nucleus). The lateral habenula, a diurnal cycle nucleus adjacent to the pineal gland, controls raphe activity through direct enervation for inhibiting midbrain dopamine neurons to dampen activities associated with negative reward (Aghajanian,1977; Matsumoto &Hikosaka, (2007); Morris et al,1999.).  However, the 5-HT1a mechanism triggered by LSD is the most consistent with the close similarity between the initial memory recall and its subsequent flashbacks.

The irony in proposing the roles of DMT+ is that measuring its secretion may not be possible or extremely difficult during the changes in physiology expected for relevant on-going processes such as parturition and REM sleep (below).  Pineal melatonin and DMT+ are secreted directly into cerebral spinal fluid (CSF) within the tiny (2 ml) third ventricle and descend through the cerebral aqueduct to bathe the brainstem, presumably supplying DMT+ to the raphe receptors. Afterwards,  DMT+ remaining is either diluted 150-fold within the entire CSF volume of the cerebral ventricles  via the fourth ventricle or further by descent into the spinal column (Tan &  Khoo, 1981; Tricoire et al, 2002). As secretory products of the pineal gland, DMT+ would reach a maximum concentration below that of melatonin, peaking to only 9 picomolar after four hours into the sleep cycle.  Integrating a parabola with this maximum during this time gives about 160 picomoles.  It is unlikely that a significant amount of DMT+ would be found in the easiest sampling source, the saliva, after dilution in the blood supply and their notorious instability from monoamine oxidases. To ensure  homeostasis of psychic balance, DMT+ must be the brains “little secret”, cloistering the agonist in this small vetrincular space and utilizing its short lifetime before its oxidized.  In respect for this necessity, methyl/carbonyl exchange enzymes (putatively) to convert melatonin to 5-methoxyDMT within the raphe nuclei  themselves, is an attractive, but even more elusive possibility for detection and measurement.

5) REM Sleep and the RaRN model:  REM sleep (REMS), occurs 2 or 3 times a night on a regular schedule and is the attractive choice the functional location for opening and erasing the noxious memory acquired during the day.  As cortical manifestations of autonomic attempts to erase noxious memory, it is not untoward to suggest that flashbacks appear as dreams, particularly if the memory’s origin was cerebral (see below).  REMS is necessary for the next day’s functioning (Shumard, 2002) and has been viewed by others as a healing process associated with deep personal issues (Crick & Mitchison, 1983; Shapiro & Forrest, 1997).  Jung’s earlier findings that negative personal issues revealed by an individual’s dreams diminish over time and are replaced by dreams having a “numinous” quality (Jung, 1943). prompting this empirical scientist to claim the healing property of dreaming.  The natural progression of awakening, beginning with the REM phase of sleep, is consistent with the morning appearance of flashbacks soon after this subject arose from sleep.

Both the REMS and the hallucinogenic states share several attributes: 1) The REM state is initiated by direct application of 5-HT1a agonists to raphe nuclei within the brainstem and is inhibited by similar application of 1a antagonists (Monti & Monti, 2000: Monti et al, 2002).  Also, it has been shown that, while the dorsal raphe 5-HT neurons are active during deep sleep, they are completely inactive during REMS (Wu et al, 2004).  Although the 5-HT1a receptor is non-hallucinogenic, DMT+ released during REMS would find the hallucinogenic 5-HT2a/2c receptors within the pyramidal layers of the prefrontal cortex as well (Nichols, 2004).  2) Reticular activation associated with an increased level of cognition, is common to both (Szara, 1994).  3) The muscle atonia characteristic of the REM state is seen as paralysis at high dose/weight ratios of hallucinogens in humans and is consistent with hallucinogen cataplexy in animal research (Chiu & Mishra, 1980). 4) REMS dreams are similar to hallucinogenic visions with their vivid distorted imagery (McNamara et al, 2007, ‘09) and are generally negative in tone, extending into the next day as depression (Robert & Zadra, 2008).  This is consistent with the nature of this subject’s birth memory as traumatic recall and may imply that REM dreams are really cerebral flashbacks originating either from sub-cerebral memory or cerebral memory by the same RaRN mechanism. The plausibility of the latter is consistent with control of nuclei within the hippocampus via enervation from the dorsal raphe nucleus (Freund, 1990; Ma et al, 1991).  The notion that the REM state would be hallucinogenic finds interesting consistency with sleeping habits of pre-industrial Europe when the absence of artificial lighting forced people to retire early and awaken at midnight for highly creative activities within an altered mental state ( Ekirch, 2005).

Several publications seem to contradict this proposed RaRN-REMS connection, but some authors deal only with cognitive hippocampal memory, ignoring sub-cerebral memory.  Others involve irrelevant memory definitions (Vertes & Eastman, 2000; Vogel et al, 1990) and yet others present conflicting notions on origin of dreams (Vogel et al, 1990; Solms, 2000; Jouvet, 19622; McCarley & Hobson, 1975).  A more serious conflict with the RaRN model is the inhibition of REMS by systemic 5-HT1a agonists (McCarley & Hobson, 1975) and monoamine oxidase (MAO) inhibitors (Wyatt et al, 1979); The opposite would be expected according to the RaRN model.  Moreover, the protection of DMT and acetylcholine by MAO inhibitors has been shown and direct application of 5-HT1a agonists and antagonists to the raphe turns REM on and off, respectively (Monti & Monti, 2000: Monti et al, 2002;S1).

Summarizing, a highly plausible case has been made for the biological role of endogenous hallucinogens as subcortical mediators of memory consolidation at the time of birth.  Perhaps more than detecting the elusive DMT+ hallucinogens, the 5-HT1a receptor may be more significant for utilizing many known agonists to examine these claims about human parturition and pharmacology. This receptor is the most widespread of all the serotonergic receptors in the human brain and is generally known as the key to neuro-protection and neuro-recovery after stroke and infarction (Berends et al, 2005; Kline et al, 2001; Jordan et al, 2002; Dunn et al, 1989).  In relation to the pineal gland, the 5-HT1a  “modifies” circadian rhythm, further implicating the endogenous hallucinogens (Tominaga et al, 1982 ).  In particular, documentation on this receptor is central these present results in all aspects of interpretation, including the control of REM sleep and the reversibility of its agonist interactions.  Hallucinogenic effects of DMT+ would arise as well from the 5-HT2a/2c cortical receptors to bolster the mother’s alertness and positive mentality, as has been seen often by midwives, obstetric nurses and indigenous people using plants as the source of the agonist (England 7&Horowitz,1998; Harrison, 2007).  The origin of this rare kind of LSD recall may be exclusive to those having little or no cerebral memory of their birth, due to the anticholinergic and potentiating effects of scopolamine mixed with morphine in anesthesia, i.e., Twilight Sleep.  

It is noteworthy that the RaRN model, thus far discussed as a sub-cerebrak mechanism, might be applied as well to mechanisms of cerebral trauma, owing to the documented influence of the dorsal raphe on the amygdala-hippocampus axis through direct enervation (Jackson et al, 2008; Freund et al, 1990).  Cerebrally , the “open”/”closed” memory would be less reversible, but now updatable, as the renewed fear, mediated by the amygdala/hippocampus after the onset of PTSD symptoms themselves, would add to new insults to a memory opened by DMT+ (Pitman et al, 2002; McConnell, 2008).  This erasable and updatable property of trauma memory would account both for the persistence of PTSD symptoms and for the newly documented relief of PTSD with MDMA, a 5HT1a agonist ( Sprouse  et al, 1989), as shown in recent studies  ( Mithoefer & Mithoefer 2010).

The "open/closed" model supported by this evidence of LSD memory activation and erasure brings certain caveats into the use of hallucinogens for clinical, recreational or spiritual purposes.  With this model the memory substrate remains open in the presence of the hallucinogen, not only to release stored impulses into cerebral awareness, but also to receive new information for consolidation, such as certain emotional preoccupations that may plague the subject at that time. Closing of the memory substrate with retreat of the hallucinogen would add another unconscious influence over future decisions and psychic well-being.  This is borne out with the observation that the quality of the experience among diverse individuals injected with DMT corresponds closely with the habitual mental preferences of the subject, running from the extremes in histories of chronic negativity to histories of positive, outward directed care and spirituality, with intermediate experiences for those of spotty lifetimes (Strassman et al, 1994).

The next report, “Rare LSD Effects and Twilight Sleep Birth II---“ introduces a new hallucinogen pharmacological target, thus far unknown, that mediates fetal activation and movement in a sequence of three discrete phases that are biologically coupled.

 

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