J Allan Hobson, has never shied form making bold departures from existing trends when it comes to dream research. At the time when Freudian notions of dream interpretation and dreams-as wish-fulfillment were at it speak, he proposed a theory that dreaming or the subjective state be distinguished from the underlying REM sleep physiological brain state and that dreaming or subjective experience thereof may be an epiphenomenon associated with the underlying physiology. In other words REM sleep may have a function, but the dream state accompanying it is just an epiphenomenon- our minds trying to make sense of random internally generated signals, in the absence of signals from the external world.
In between Hobson has written a book titled Dreaming as Delirium, in which he compares dream state to that of the psychotic state, especially the delirium accompanying such psychotic states. while dream sttes are naturally cut-off from reality ( no sense inputs or motor outputs) , psychosis, that is indeed characterized by lack of contact with reality, may also thus be predominantly internally generated and close to the dream state in its characterization.
In his most recent review paper in Nature reviews Neuroscience , he compares the dream state to that of proto consciousness. As per him, proto consciousness is made up of raw emotions and perceptions while secondary consciousness is made up of awareness about perceptions and emotions and meta cognitive processes. He now endows dreams/REM state with some functional significance. He believes that dreams provide and opportunity for inbuilt genetic scripts and schema to be played out and fine tuned against external real-world scenarios. In this view dreams would still be significant as they provide a window to out internal scripts that are present from birth. He doesn’t put this across in so many words and this is my interpretation, but that is what I could sort of intuit. You are encouraged to read the original paper which is relatively much more accessible as compared to his 1977 paper.
While some people even deny any function to consciousness and call it an epiphenomenon, and thus it would be very hard to convince them of any significance to the bizarreness of dreams; yet I believe that Dreams , not of the garden variety type, but those that we ourselves consider significant, do have a significance and are not mere epiphenomenon. It may be akin to everyday consciousness not having any major role than that of post-hoc narrative weaving; but at some time free will does assert itself and conscious will rules at some rare occasions. So not all dreams are created equal, some indeed are more than epiphenomenon. They may be delirium like in nature but perhaps tend towards more of hyper consciousness than proto consciousness.
Hat tip: Neuroskeptic
Hobson, J. (2009). REM sleep and dreaming: towards a theory of protoconsciousness Nature Reviews Neuroscience, 10 (11), 803-813 DOI: 10.1038/nrn2716
We all know that depression is marked by an increase in REM Sleep or dreaming and their are various theories of why this increased dreaming may be a root cause of depression itself. One theory posits that having too much dreams or emotional negativity even while sleeping (most dreams have negative content) may lead to maintenance of downward spiral of depressive cognitive and emotional style. Another theory posits that having too much negative dreams may lead us to get exhausted and the morning weariness found in depression is due to this fact.
I’ll not comment regarding the purported mechanism and causal direction of link between depression and dreaming. Suffice it to note few pertinent facts:
- Depressives dream 3 -4 times more than normal people.
- Most Anti-depressants cause REM sleep to be suppressed and this may underlie their therapeutic action or may just be a side-effect.
- There is mixed evidence as to whether REM sleep is also altered in Mania (although a decrease in REM sleep is not mentioned in literature- if anything REM increases just like in depression)
Now I’ll like to highlight an important experiment conducted by Wisconsin Madison scientists. They deprived rats of REM sleep and found that such rats became idiots in terms of survival sense and failed all standard test of survival. I’ll first describe the procedure and their results and then theorize:
What happens when a rat stops dreaming? In 2004, researchers at the University of Wisconsin at Madison decided to find out. Their method was simple, if a bit devilish. Step 1: Strand a rat in a tub of water. In the center of this tiny sea, allot the creature its own little desert island in the form of an inverted flowerpot. The rat can swim around as much as it pleases, but come nightfall, if it wants any sleep, it has to clamber up and stretch itself across the flowerpot, its belly sagging over the drainage hole.
In this uncomfortable position, the rat is able to rest and eventually fall asleep. But as soon as the animal hits REM sleep, the muscular paralysis that accompanies this stage of vivid dreaming causes its body to slacken. The rat slips through the hole and gets dunked in the water. The surprised rat is then free to crawl back onto the pot, lick the drops off its paws, and go back to sleep—but it won’t get any REM sleep.
Step 2: After several mostly dreamless nights, the creature is subjected to a virtual decathlon of physical ordeals designed to test its survival behaviors. Every rat is born with a set of instinctive reactions to threatening situations. These behaviors don’t have to be learned; they’re natural defenses—useful responses accrued over millennia of rat society.
The dream-deprived rats flubbed each of the tasks. When plopped down in a wide-open field, they did not scurry to the safety of a more sheltered area; instead, they recklessly wandered around exposed areas. When shocked, they paused briefly and then went about their business, rather than freezing in their tracks the way normal rats do. When confronted with a foreign object in their burrow, they did not bury it; instead, they groomed themselves. Had the animals been out in the wild, they would have made easy prey.
The surprise came during Step 3. Each rat was given amphetamines and tested again; nothing changed. If failure to be an effective rat were due to mere sleep deprivation, amphetamines would have reversed the effect. But that didn’t happen. These rats weren’t floundering because they were sleepy. Something else was going on—but what?
To me it seems that what is happening in these dream-deprived rats is an unlearning of learned helplessness paradigm. In learned helplessness, one stops exploring the environment and becomes extremely cautious. Learned helplessness is an extremely influential theory of depression and I have blogged about it previously. In the dream-deprived rats something exactly the opposite is happening – they are becoming more exploratory and sort of unlearning the basic survival instincts .
To me all this seems to nicely fit together. Dreams may be instrumental in rehearsal learning and when the rat (or human) has been repeatedly exposed to inescapable shocks (unavoidable stress), then it may lose the desire to explore not only in the real world, but also in the dream world – the primary purpose of which is to generate alternative strategies to previously un-encountered negative situations. When one loses or fails to find creative solutions to the inescapable situations, one falls in a negative dream loop whereby one fails to explore adequately new strategies or to reassess the environment in light of new evidences. Instead as one has failed to find creative solutions earlier, one;s dreams become pre-occupied with failure- and with each failure prompts more vigorous search for answers in the dream -thus leading to more REM sleep. Also, as REM sleep is required for thus maintaining the new (unhealthy) associations hence as long as adequate REM sleep is available one stays stuck with the learned negative associations and the learned helplessness.
SSRIs and other anti-depressants , by blocking the REM sleep , may be providing one additional step whereby dreaming stops for some duration and the synapses that underlie negative associations (that were constantly strengthened during dreams) are given time to naturally become weak. Thus events no longer have automatic negative connotations, but can be appraised afresh with a new outlook. This may be one putative mechanism of how anti-depressants work. This may also explain why anti-depressants take so much time to become effective. When dreaming stops, the unlearning doesn’t happen in a day- the weakening of associations would take weeks and months to materialize and have an effect.
Cognitive – behavioral theory may also be working on the level of dreams and it would be interesting to note how much dreaming is reduced and brought to normal levels as CBT starts showing effects.
The behavior of the dream deprived rat seems almost manic- unconcerned with survival and unnecessarily risk-taking. One experiment that can be conducted is to first induce learned helplessness in rats (by exposing them to unavoidable shocks) and then dream-deprive them as per the above methodology. If dream-deprivation restores the normalcy in rats and removes the depressive symptomatology we have a new theory of how depression works. This is not a difficult experiment to do and can be easily performed. I’m sure it will lead to positive results. I look forward to hearing from some readers of this blog as to how the experiment actually went (I myself am in no position to conduct such experiments). Do let me know via comments the experimental results- even if they are negative.
This post is about an article by Schacter et al (pdf) regarding how the constructiveness of memories may crucially be due to the need to simulate future scenarios. But before I go to the main course, I would like to touch upon a starter: Jeff Hawkins Heirarchical Temporla Memory (HTM) hypothesis. I would recommend that you watch this excellent video.
As per Jeff Hawkins, we humans are basically prediction machines, constantly predicting the external causes and our responses to them. Traditionally, the behaviorist account has been that we are nothing but a bundle of associations- either conditioned pavlovian associations between stimuli and stimulus-response or a skinerrian association between our operant actions and environmental rewards. Thus every behavior we indulge in is guided by our memory of past associations and the impending stimulus. Jeff Hawkins refines this by postulating that we are not passive responders to environmental stimuli, but actively predict what future causes (stimuli) are expected and what our response to those stimuli may be. Thus in his HTM model, the memory of past events not only exerts influence via a bottom up process of responding to impending stimulus; but it is also used for a top-down expectation or prediction of incoming stimulus and our responses to it. Thus, we are also prediction machines constantly using our memory to predict future outcomes and our possible responses.
Now lets get back to the original Schacter article. Here is the abstract:
Episodic memory is widely conceived as a fundamentally constructive, rather than reproductive, process that is prone to various kinds of errors and illusions. With a view toward examining the functions served by a constructive episodic memory system, we consider recent neuropsychological and neuroimaging studies indicating that some types of memory distortions reflect the operation of adaptive processes. An important function of a constructive episodic memory is to allow individuals to simulate or imagine future episodes, happenings, and scenarios. Because the future is not an exact repetition of the past, simulation of future episodes requires a system that can draw on the past in a manner that flexibly extracts and re-combines elements of previous experiences. Consistent with this constructive episodic simulation hypothesis, we consider cognitive, neuropsychological, and neuroimaging evidence showing that there is considerable overlap in the psychological and neural processes involved in remembering the past and imagining the future.
As per the paper the same brain areas and mechanisms are involved in both remembering a past event and imagining a future one – and the regions involved include the hippocampus. These findings in itself are not so fascinating, but the argument that Schacter et al give for , as to why, the same regions are involved in both memory retrieval and future imaginings, and how this leads to confabulations and false recognitions is very fascinating. As per them , because we need to simulate the future events, and as the future events are never an exact replica of past events, hence we do not store the past events verbatim, but store a gist of the event, so that we can recombine the nebulous gist to create different possible future scenarios. Due to this fact (the need for simulation of future events), the memory is not perfect, and in normal individuals it is possible that they confabulate (attribute the source of their memory erroneously) or make false recognitions on memory tests like the DRM.
Fisrt a bit of background on DRM paradigm. In this test, a list of related words are presented to a subject: eg yawn, bed, night, pillow, dream, rest etc. All of these relate to the theme of sleep. Later in a recall test, when this thematically related word is presented to normal subjects, they most often say that they had encountered the word sleep earlier. However given an unrelated word like hunger, most are liable to recognize that the word was not encountered previously. What Schachter et al found was , that in those subjects that had damage to hippocampus/ other memory areas and were amnesics, this effect of confabulating the gist word was reduced. In other words, those with brain damage to memory areas were less likely to say that they had encountered the related word sleep during the original trial. this, despite their poor performance in overall remembering of old list items as compared to controls. This clearly indicates that remembering the gist vis-a-vis details is very important memory mechanism.
I believe that we should also take into account the prototype versus exemplar differences in categorization between the males and females into account here. I would be very interested to know whether the data collected showed the expected differences between males and females and hopefully the results are not confounded due to not taking this gender difference into account.
Anyway , returning to the experimental methodology, another sticking point seems to be the extending of results obtained with semantic memory (like that for word lists) to episodic memory.
Keeping that aside, the gist and false recognition data results clearly indicate that the constructive nature of memory is an adaptation (it is present in normal subjects) and is disrupted in amnesics/ people with dementia.
Thus, now that it is established that memory is reconstructive and that this reconstruction is adaptive, the question arises why it is reconstructive and not reproductive. To this Schacter answers that it is because the same brain mechanism used for reconstructing memory from gist are also used for imagining or simulating future scenario. They present ample neuropsychological, neuroimaging and cognitive evidence on this and I find that totally convincing.
The foregoing research not only provides insights into the constructive nature of episodic memory, but also provides some clues regarding the functional basis of constructive memory processes. Although memory errors such as false recognition may at first seem highly dysfunctional, especially given the havoc that memory distortions can wreak in real-world contexts (Loftus 1993; Schacter 2001), we have seen that they sometimes reflect the ability of a normally functioning memory system to store and retrieve general similarity or gist information, and that false recognition errors often recruit some of the same processes that support accurate memory decisions. Indeed, several researchers have argued that the memory errors involving forgetting or distortion serve an adaptive role.
However, future events are rarely, if ever, exact replicas of past events. Thus, a memory system that simply stored rote records of what happened in the past would not be well-suited to simulating future events, which will likely share some similarities with past events while differing in other respects. We think that a system built along the lines of the constructive principles that we and other have attributed to episodic memory is better suited to the job of simulating future happenings. Such a system can draw on elements of the past and retain the general sense or gist of what has happened. Critically, it can flexibly extract, recombine, and reassemble these elements in a way that allows us to simulate, imagine, or ‘pre-experience’ (Atance & O’Neill 2001) events that have never occurred previously in the exact form in which we imagine them. We will refer to this idea as the constructive episodic simulation hypothesis: the constructive nature of episodic memory is attributable, at least in part, to the role of the episodic system in allowing us to mentally simulate our personal futures.
I’ll finally like to end with the conclusions the author drew:
In a thoughtful review that elucidates the relation between, and neural basis of, remembering the past and thinking about the future, Buckner and Carroll (2007) point out that neural regions that show common activation for past and future tasks closely resemble those that are activated during “theory of mind” tasks, where individuals simulate the mental states of other people (e.g., Saxe & Kanwisher 2003). Buckner and Carroll note that such findings suggest that the commonly activated regions may be specialized for, and engaged by, mental acts that require the projection of oneself in another time, place, or perspective”, resembling what Tulving (1985) referred to as autonoetic consciousness.
This Seems to be a very promising direction. The ‘another time and place’ can normally be simulated withing hippocampus that also specializes in cognitive maps. We may use the cognitive maps to not only remember past events, but also simulate new events. In this respect the importance of dreams may be paramount. Dreams (and asleep) may be the mechanism whose primary purpose is not memory consolidation; rather I suspect that the primary function of dreams is to work on the gist of the memory from the previous day, simulate possible future scenarios, and then keep in store those memories that would help and are likely to be encountered in future. Thus, while dreaming we are basically predicting future scenarios and sorting information as per their future relevance. Not a particularly path-breaking hypothesis, but I’m not aware of any thinking is this direction. Do let me know of any other similar hypothesis regarding the function of dream as predictors and not merely as consolidators.
In a study that could have potentially far-reaching effects for the Bipolar research and treatment, Dr Colleen and her group have reported on a mouse model of bipolar disorder.
The association between circadian rhythms and bipolarity is well established and a bipolar episode is characterized with disruptions in daily sleeping, eating rhythms etc. Till now the biological basis of this was not clear.
In this study, mice with Clock gene knocked out were tested on a number of measures of bipolairty and it was found that these mice lacking the Clock gene, which is essential for proper circadian rhythms, suffered from human manic like symptoms. Moreover treating these bipolar mice with lithium resulted in the subsiding of symptoms.
The study included putting the mutant mice through a series of tests, during which they displayed hyperactivity, decreased sleep, decreased anxiety levels, a greater willingness to engage in “risky” activities, lower levels of depression-like behavior and increased sensitivity to the rewarding effects of substances such as cocaine and sugar.
“These behaviors correlate with the sense of euphoria and mania that bipolar patients experience,” said Dr. McClung. “In addition, there is a very high co-morbidity between drug usage and bipolar disorder, especially when patients are in the manic state.”
During the study, lithium was given to the mutant mice. Lithium, a mood-stabilizing medication, is most commonly used in humans to treat bipolar patients. Once treated with the drug on a regular basis, the majority of the study’s mice reverted back to normal behavioral patterns, as do humans.
The clock gene is expressed widely in the human brain, but the focus till now was only on the area called suprachiasmatic nucleus. In this study the area of brain associated with reward learning, VTA/ Striatum etc was studied and expressing the clock gene there in KO mice resulted in subsiding of symptoms.
The researchers also injected a functional Clock gene protein – basically giving the mice their Clock gene back – into a specific region of the brain that controls reward functions and where dopamine cells are located. Dopamine is a neurotransmitter associated with the “pleasure system” of the brain and is released by naturally rewarding experiences such as food, sex and the use of certain drugs. This also resulted in the mice going back to normal behaviors.
This is an exciting news as it makes a mice model for Bipolairty readily available and would help in clinical testing of new anti psychotics and mood stabilizers.
New research has established that mice dream and during their sleep there is a two-way dialog between the hippocampal recent day memory area and the neo-cortex that is believed to be involved in long-term memory.
The content of the mice dream is also no longer secret. In the sleep they are replaying the sequence of steps that they had executed in a maze, but in a reverse order, and in lesser time and in general are rehearsing the structure of the maze (the mouse trap). Learning, it is to be remembered, arises from these replays of fast rewinds and sleep it seems is necessary for learning.
Some quotes from the article:
During nondreaming sleep, the neurons of both the hippocampus and the neocortex replayed memories — in repeated simultaneous bursts of electrical activity — of a task the rat learned the previous day.
Earlier this year Dr. Wilson reported that after running a maze, rats would replay their route during idle moments, as if to consolidate the memory, although the replay, surprisingly, was in reverse order of travel. These fast rewinds lasted a small fraction of the actual time spent on the journey.
In the findings reported today, the M.I.T. researchers say they detected the same replays occurring in the neocortex as well as in the hippocampus as the rats slept.
The rewinds appeared as components of repeated cycles of neural activity, each of which lasted just under a second. Because the cycles in the hippocampus and neocortex were synchronized, they seemed to be part of a dialogue between the two regions.
Because the fast rewinds in the neocortex tended to occur fractionally sooner than their counterparts in the hippocampus, the dialogue is probably being initiated by the neocortex, and reflects a querying of the hippocampus’s raw memory data, Dr. Wilson said.
“The neocortex is essentially asking the hippocampus to replay events that contain a certain image, place or sound,” he said. “The neocortex is trying to make sense of what is going on in the hippocampus and to build models of the world, to understand how and why things happen.”
PS: My blog post has deliberately used words like ‘dream’, ‘mouse’ and ‘traps’ instead of the correct ‘sleep’, ‘rats’ and ‘mazes’: just to come up with a juicy headline!!