House of Mind

"Biology gives you a brain. Life turns it into a mind" - Jeffrey Eugenides

  • 14th May
    2013
  • 14

Long-term Effects of Cannabis Use on Memory and Executive Function

Cannabis is easily the most widely used illegal substance in the world. Although it still illegal at federal level, Washington and Colorado have legalized recreational cannabis use. Studies examining the relationship between marijuana use and neuropsychological function should be taken into consideration when making/reforming laws and  health policies.  I have received multiple questions regarding the effects of marijuana on memory and health and recently found a longitudinal study on this matter.

Prior evidence suggests that long-term, heavy cannabis use may cause enduring neuropsychological impairment beyond the period of acute intoxication (i.e. being high). Moreover, the magnitude and persistence of impairment depends on several factors including: quantity, frequency, duration and age of onset. Greater quantities, more frequent and earlier onset of use are associated with a poorer neuropsychological outcome. However, studies that compare pre-initiation neuropsychological functioning with longitudinal data on post-initiation functioning are scarce. 

Meier et. al investigated the association between persistent cannabis use  and neuropsychological functioning (assessed over a 20 year period) in over 1,000 individuals. Subjects received neuropsychological testing prior to onset of use (childhood; 1985-1986) and after some had developed a persistent pattern of use (~38 years old; 2010-2012). 

Important findings included: 

  1. Subjects with more persistence cannabis dependence showed greater IQ decline. Those who never experienced cannabis experienced a slight increase in IQ. 
  2. Subjects with more persistent cannabis dependence generally showed greater neuropsychological impairment across different areas of mental function: executive function, memory, processing speed, perceptual reasoning and verbal comprehension. The greatest impairments were in the domains of executive function and processing speed. 
  3. Neuropsychological deficits induced by cannabis use were still significant  even when the researchers controlled for: past 24 hour cannabis use, past-week cannabis use, persistent tobacco, alcohol and/or hard drug dependence, and schizophrenia (all of which alternative explanations for poorer neuropsychological function). 
  4. The effect of cannabis dependence on cognitive decline remained significant even after controlling for years of education. Persistent cannabis users with a high school education or less experienced greater IQ decline. 
  5. Subjects who had an adolescent onset of use and were diagnosed with dependence prior to 18 years of age tended to become more persistent users. Importantly, adult-onset cannabis users did not appear to experience IQ decline as a function of cannabis use. 
  6. Within-person IQ decline was apparent regardless of whether cannabis was used frequently or infrequently a year before testing. Thus, cessation of cannabis use did not restore neuropsychological functioning among adolescent-onset former persistent cannabis users. 


So it looks like persistent use of cannabis is particularly detrimental with adolescent onset. Some have speculated that this may be due to puberty, a critical period of brain development in which circuits related to decision-making, executive-function, and reward are undergoing reorganization/rewiring. Neurotransmitter systems like dopamine are also vulnerable during this period as they have not fully matured yet. Thus, the authors suggest that cannabis use exerts neurotoxic effects during this developmental period. 

However, one must remember that although the authors show compelling data, their data correlational and is not sufficient to establish causation. Furthermore, there is no mechanism underlying the negative impact of cannabis use on neuropsychological function- merely speculations (see above). It is also possible that there is another variable related to cannabis use and neuropsychological decline that the authors did not rule out. Another limitation of the study was the heavy reliance on self-reporting measures like self-reported frequency of use. Finally, it is hard to estimate dosages due to the variety of strains and potency of cannabis. 

I would personally suggest taking this information for what it’s worth. Neuroimaging studies in adolescents (humans) reveal structural and functional brain differences associated with cannabis use so we know that cannabis use changes the brain. I personally believe that cannabis use has negative effects on memory and general health, but I do not think that it’s as simple as the “Weed will make you stupid.” notion that some adults try to instill in adolescents.  After all, we already KNOW about the dangers and costs of alcohol/tobacco use and people still use them. For me, the key is to delay onset of use (if you must use) and to prevent adolescent use of cannabis. If you are a teenager with cannabis dependence, it is never to late to quit and try to remedy the effects.

Source:  (Click on the link for abstract)


Meier et. al. (2012). Persistent cannabis users show neuropsychological decline from childhood to midlife. Proceedings of the National Academy of Science (PNAS). 109 (40): 2657-64. 

  • 26th January
    2013
  • 26
I've been looking for scholarly articles on neurotransmitters and their relations to learning, and memory. Would you be able to recommend any? Greatly appreciated.

Asked by: aebl

Mol Neurobiol. 2011 Dec;44(3):449-64. doi: 10.1007/s12035-011-8214-0. Epub 2011 Nov 11.

Serotonin and prefrontal cortex function: neurons, networks, and circuits.

Puig MV, Gulledge AT.

Source

The Picower Institute for Learning and Memory and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. mvpuig@mit.edu

Abstract

Higher-order executive tasks such as learning, working memory, and behavioral flexibility depend on the prefrontal cortex (PFC), the brain region most elaborated in primates. The prominent innervation by serotonin neurons and the dense expression of serotonergic receptors in the PFC suggest that serotonin is a major modulator of its function. The most abundant serotonin receptors in the PFC, 5-HT1A, 5-HT2A and 5-HT3A receptors, are selectively expressed in distinct populations of pyramidal neurons and inhibitory interneurons, and play a critical role in modulating cortical activity and neural oscillations (brain waves). Serotonergic signaling is altered in many psychiatric disorders such as schizophrenia and depression, where parallel changes in receptor expression and brain waves have been observed. Furthermore, many psychiatric drug treatments target serotonergic receptors in the PFC. Thus, understanding the role of serotonergic neurotransmission in PFC function is of major clinical importance. Here, we review recent findings concerning the powerful influences of serotonin on single neurons, neural networks, and cortical circuits in the PFC of the rat, where the effects of serotonin have been most thoroughly studied.

Mol Brain. 2010 May 13;3:15. doi: 10.1186/1756-6606-3-15.

Emotional enhancement of memory: how norepinephrine enables synaptic plasticity.

Tully K, Bolshakov VY.

Source

Department of Psychiatry, McLean Hospital, Harvard Medical School, 115 Mill Street, Belmont, Massachusetts 02478, USA. ktully@mclean.harvard.edu

Abstract

Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.

Neuropharmacology. 2010 Jun;58(7):951-61. doi: 10.1016/j.neuropharm.2010.01.008. Epub 2010 Jan 21.

Neurotransmitter roles in synaptic modulation, plasticity and learning in the dorsal striatum.

Lovinger DM.

Source

Laboratory for Integrative Neuroscience, NIAAA/NIH, 5625 Fishers Lane, Rockville, MD 20852, USA. lovindav@mail.nih.gov

Abstract

The dorsal striatum is a large forebrain region involved in action initiation, timing, control, learning and memory. Learning and remembering skilled movement sequences requires the dorsal striatum, and striatal subregions participate in both goal-directed (action-outcome) and habitual (stimulus-response) learning. Modulation of synaptic transmission plays a large part in controlling input to as well as the output from striatal medium spiny projection neurons (MSNs). Synapses in this brain region are subject to short-term modulation, including allosteric alterations in ion channel function and prominent presynaptic inhibition. Two forms of long-term synaptic plasticity have also been observed in striatum, long-term potentiation (LTP) and long-term depression (LTD). LTP at glutamatergic synapses onto MSNs involves activation of NMDA-type glutamate receptors and D1 dopamine or A2A adenosine receptors. Expression of LTP appears to involve postsynaptic mechanisms. LTD at glutamatergic synapses involves retrograde endocannabinoid signaling stimulated by activation of metabotropic glutamate receptors (mGluRs) and D2 dopamine receptors. While postsynaptic mechanisms participate in LTD induction, maintained expression involves presynaptic mechanisms. A similar form of LTD has also been observed at GABAergic synapses onto MSNs. Studies have just begun to examine the roles of synaptic plasticity in striatal-based learning. Findings to date indicate that molecules implicated in induction of plasticity participate in these forms of learning. Neurotransmitter receptors involved in LTP induction are necessary for proper skill and goal-directed instrumental learning. Interestingly, receptors involved in LTP and LTD at glutamatergic synapses onto MSNs of the “indirect pathway” appear to have important roles in habit learning. More work is needed to reveal if and when synaptic plasticity occurs during learning and if so what molecules and cellular processes, both short- and long-term, contribute to this plasticity.

(c) 2009. Published by Elsevier Ltd.

Curr Med Chem. 2009;16(7):796-840.

Neuro-transmitters in the central nervous system & their implication in learning and memory processes.

Reis HJ, Guatimosim C, Paquet M, Santos M, Ribeiro FM, Kummer A, Schenatto G, Salgado JV, Vieira LB, Teixeira AL, Palotás A.

Abstract

This review article gives an overview of a number of central neuro-transmitters, which are essential for integrating many functions in the central nervous system (CNS), such as learning, memory, sleep cycle, body movement, hormone regulation and many others. Neurons use neuro-transmitters to communicate, and a great variety of molecules are known to fit the criteria to be classified as such. A process shared by all neuro-transmitters is their release by excocytosis, and we give an outline of the molecular events and protein complexes involved in this mechanism. Synthesis, transport, inactivation, and cellular signaling can be very diverse when different neuro-transmitters are compared, and these processes are described separately for each neuro-transmitter system. Here we focus on the most well known neuro-transmitters: acetyl-choline, catechol-amines (dopamine and nor-adrenalin), indole-amine (serotonin), glutamate, and gamma-amino-butyric acid (GABA). Glutamate is the major excitatory neuro-transmitter in the brain and its actions are counter-balanced by GABA, which is the major inhibitory substance in the CNS. A balance of neuronal transmission between these two neuro-transmitters is essential to normal brain function. Acetyl-choline, serotonin and catechol-amines have a more modulatory function in the brain, being involved in many neuronal circuits. Apart from summarizing the current knowledge about the synthesis, release and receptor signaling of these transmitters, some disease states due to alteration of their normal neuro-transmission are also described.

Prog Brain Res. 2008;172:567-602. doi: 10.1016/S0079-6123(08)00927-8.

Serotonin/dopamine interaction in learning.

Olvera-Cortés ME, Anguiano-Rodríguez P, López-Vázquez MA, Alfaro JM.

Source

Laboratorio de Neurofisiología Experimental, Centro de Investigación Biomédica de Michoacán, Instituto Mexicano del Seguro Social, Morelia, México. maesolco@yahoo.com

Abstract

Dopamine (DA)-serotonin interactions dealing with learning and memory functions have been apparent from experimental approaches over the past decade. However, since the former evidence showing that these cerebral neurotransmitter systems are involved in the regulation of the same cognitive processes, few experimental studies have been done to further clarify the nature of DA-serotonin interactions for cognitive processes sharing common brain structures. Nevertheless, a regulatory role of 5-HT/DA interactions in cognition and the prefrontal cortex (PFC) and the striatum as a neuroanatomical substrate for these DA/5-HT interactions, are now recognized. Experimental evidence indicates that pharmacological disruption of serotonin neurotransmission results in a facilitative effect on the processing of mnemonic information by cerebral regions under strong, functional DA modulation, such as the striatum and the PFC; on the other hand, increased serotonin neurotransmission appears to have a detrimental effect on cognitive functions integrated in these structures. These effects seem to occur through the interaction of different pre- and postsynaptic DA and serotonin receptor subtypes acting as opposite systems underlying cognitive abilities. Some studies, focused on DA-serotonin interactions underlying the pathophysiology of neurological and psychiatric diseases, which evolve with cognitive dysfunctions in human beings, have shown that drugs that are able to modify DA or serotonin neurotransmission may exert beneficial effects on cognitive functions, even though improvement of motor, mood and behavioural disturbances are the main objectives of pharmacological treatment of these diseases. The complete significance of DA-serotonin interactions in cognitive functions could be addressed by future experimental and clinical studies.

Hi!
I searched and found these on PubMed. The first 3 are available as free downloads. Enjoy!
  • 31st August
    2012
  • 31
Upcoming Events at the New York Academy of Sciences

Being a graduate student at NYU has many perks. One of the best ones, in my opinion, is that we get a paid student membership to the New York Academy of Sciences (NYAS) for the entire duration of your Ph.D. study. Amazing, I know! Sometimes I actually feel a little guilty about not taking the maximum advantage of this opportunity. Thus, this year I have decided to be more proactive about going to the NYAS neuroscience events and actually get myself over there. 
While searching for the closest upcoming events, I discovered that the majority of these events are open to everybody for a small registration fee of $10 if you are a student/postdoc/fellow or $15 if you are a nonmember. 
Below is a list of the 3 upcoming NYAS Neuroscience events, but I will be posting about the other events throughout the year. Also, the NYAS events span a wide variety of topics like: 
  • Life Sciences and Biomedical Research
  • Physical Sciences and Engineering
  • Environmental Studies and Sustainability
  • Social Sciences
  • Science, Society and Culture
  • Science Education
  • Career Development
Click on the link for the full menu of upcoming events. Also, they have a Science and the Seven Deadly Sins series that seems fantastic, check it out! 
 Wednesday, October 10, 2012 | 7:00 PM - 8:30 PM

The Thinking Ape: The Enigma of Consciousness

Panelists: David Chalmers (Australian National University), Daniel Kahneman (Princeton University, Prof. Em.), Laurie Santos (Yale University), Nicholas D. Schiff (Weill Cornell Medical College)
Moderator: Steve Paulson (To the Best of Our Knowledge — WPR)

Nobel laureate psychologist Daniel Kahneman, philosopher David Chalmers, expert in primate cognition Laurie Santos, and physician-scientist Nicholas Schiff discuss the origin and nature of consciousness, with a special emphasis on what makes humans unique with respect to our cognitive, aesthetic, and ethical behaviors.

Wednesday, October 24, 2012 | 8:30 AM - 7:00 PM

Sixth Annual Parkinson’s Disease Therapeutics Conference

Chair: Kalpana Merchant (Eli Lilly and Company)

Michael J. Fox Foundation-funded investigators will discuss novel therapeutic targets for Parkinson’s disease, biomarkers for early detection and assessment of disease progression, and strategies to alleviate symptoms or to slow disease progression.

Wednesday, November 14, 2012 | 7:00 PM - 8:30 PM

The Mystery of Memory: In Search of the Past

Panelists: André Aciman (City University of New York Graduate Center), Joseph LeDoux (New York University), Daniel Schacter (Harvard University), Alison Winter (University of Chicago)
Moderator: Steve Paulson (To the Best of Our Knowledge — WPR)

Psychologist Daniel Schacter, neuroscientist Joseph LeDoux, science historian Alison Winter, and novelist and comparative literature professor André Aciman discuss how memory impacts our perception, our personality, and our experience of the world.

  • 15th July
    2012
  • 15
ikenbot: Marijuana Reveals Memory Mechanism Glial cells, not neurons, are responsible for marijuana-induced forgetfulness Until recently, most scientists believed that neurons were the all-important brain cells controlling mental functions and that the surrounding glial cells were little more than neuron supporters and “glue.” Now research published in March in Cell reveals that astrocytes, a type of glia, have a principal role in working memory. And the scientists made the discovery by getting mice stoned. Marijuana impairs working memory—the short-term memory we use to hold on to and process thoughts. Think of the classic stoner who, midsentence, forgets the point he was making. Although such stupor might give recreational users the giggles, people using the drug for medical reasons might prefer to maintain their cognitive capacity. To study how marijuana impairs working memory, Giovanni Marsicano of the University of Bordeaux in France and his colleagues removed cannabinoid receptors—proteins that respond to marijuana’s psychoactive ingredient THC—from neurons in mice. These mice, it turned out, were just as forgetful as regular mice when given THC: they were equally poor at memorizing the position of a hidden platform in a water pool. When the receptors were removed from astrocytes, however, the mice could find the platform just fine while on THC. The results suggest that the role of glia in mental activity has been overlooked. Although research in recent years has revealed that glia are implicated in many unconscious processes and diseases [see “The Hidden Brain,” by R. Douglas Fields; Scientific American Mind, May/June 2011], this is one of the first studies to suggest that glia play a key role in conscious thought. “It’s very likely that astrocytes have many more functions than we thought,” Marsicano says. “Certainly their role in cognition is now being revealed.” Unlike THC’s effect on memory, its pain-relieving property appears to work through neurons. In theory, therefore, it might be possible to design THC-type drugs that target neurons—but not glia—and offer pain relief without the forgetfulness.

ikenbot:

Marijuana Reveals Memory Mechanism

Glial cells, not neurons, are responsible for marijuana-induced forgetfulness

Until recently, most scientists believed that neurons were the all-important brain cells controlling mental functions and that the surrounding glial cells were little more than neuron supporters and “glue.” Now research published in March in Cell reveals that astrocytes, a type of glia, have a principal role in working memory. And the scientists made the discovery by getting mice stoned.

Marijuana impairs working memory—the short-term memory we use to hold on to and process thoughts. Think of the classic stoner who, midsentence, forgets the point he was making. Although such stupor might give recreational users the giggles, people using the drug for medical reasons might prefer to maintain their cognitive capacity.

To study how marijuana impairs working memory, Giovanni Marsicano of the University of Bordeaux in France and his colleagues removed cannabinoid receptors—proteins that respond to marijuana’s psychoactive ingredient THC—from neurons in mice. These mice, it turned out, were just as forgetful as regular mice when given THC: they were equally poor at memorizing the position of a hidden platform in a water pool. When the receptors were removed from astrocytes, however, the mice could find the platform just fine while on THC.

The results suggest that the role of glia in mental activity has been overlooked. Although research in recent years has revealed that glia are implicated in many unconscious processes and diseases [see “The Hidden Brain,” by R. Douglas Fields; Scientific American Mind, May/June 2011], this is one of the first studies to suggest that glia play a key role in conscious thought. “It’s very likely that astrocytes have many more functions than we thought,” Marsicano says. “Certainly their role in cognition is now being revealed.”

Unlike THC’s effect on memory, its pain-relieving property appears to work through neurons. In theory, therefore, it might be possible to design THC-type drugs that target neurons—but not glia—and offer pain relief without the forgetfulness.

(via scinerds)

  • 6th March
    2012
  • 06
WiredScience: A pill that can erase painful memories forever?

Even though PTSD is triggered by a stressful incident, it is really a disease of memory. The problem isn’t the trauma—it’s that the trauma can’t be forgotten. Most memories, and their associated emotions, fade with time. But PTSD memories remain horribly intense, bleeding into the present and ruining the future. So, in theory, the act of sharing those memories is an act of forgetting them. 

In the past decade, scientists have come to realize that our memories are not inert packets of data and they don’t remain constant. Even though every memory feels like an honest representation, that sense of authenticity is the biggest lie of all.

Every memory begins as a changed set of connections among cells in the brain. If you happen to remember this moment—the content of this sentence—it’s because a network of neurons has been altered, woven more tightly together within a vast electrical fabric. This linkage is literal: For a memory to exist, these scattered cells must become more sensitive to the activity of the others, so that if one cell fires, the rest of the circuit lights up as well. Scientists refer to this process as long-term potentiation, and it involves an intricate cascade of gene activations and protein synthesis that makes it easier for these neurons to pass along their electrical excitement. Sometimes this requires the addition of new receptors at the dendritic end of a neuron, or an increase in the release of the chemical neurotransmitters that nerve cells use to communicate. Neurons will actually sprout new ion channels along their length, allowing them to generate more voltage. Collectively this creation of long-term potentiation is called the consolidation phase, when the circuit of cells representing a memory is first linked together. Regardless of the molecular details, it’s clear that even minor memories require major work. The past has to be wired into your hardware.

I just found this online and could not be more proud that I know and am professionally associated to these people. I’ve actually had the pleasure of meeting Dr. Karim Nader (he’s the coolest) at a GRC conference and hearing all he has to say about memory reconsolidation and zeta. And as for Joe Le Doux, well he’s the director for our institute (EBI). 

Anyhow, the link above is a strongly encouraged read, as it explains the persistence of PTSD (and traumatic memories) as well as memory mechanisms like reconsolidation. The molecular player in question, PKMzeta, is actually at the centerpiece of one of our current collaborations. 

In short, read read read!

  • 17th November
    2010
  • 17
Considering I’ve been suffering from lack of sleep lately, a post about sleep and cognitive performance seems appropriate. I visited this poster on my last day at SfN10 and I finally got around to blogging about it. So here it goes… Sleep is thought to benefit decision-making and creativity as well as aid in problem-solving, consolidation of memory and transitive relationships. To test the effect of sleep on cognitive performance, Karmakar and others assigned experimental subjects to one of two different sleep sessions and conducted a cognitive task after the 12-hour period. Both groups had 12 hour sessions, but one group had 12 hours (sleep time included, from PM-AM) before the test while the other had 12 hours awake (AM-OM) before the test. For example, the 12 hour session of the sleep group were from 8PM to 8AM and then they went to take the test.  Results: 1. Sleep improves memory recall.  2. Sleep increases accuracy of attribute recall.  3. Sleep decreased the perception of decision quality and the time of day did not account for differences in recall or perceived decision quality. (Individuals who slept before the exam had less confidence and were less satisfied with their choices.) 4. Sleep benefits recall of positive information and hinders recall of negative information. Author Abstract (Karmarkar et. al): Impact of Sleep on Attribute Recall and Choice Satisfaction A wealth of recent studies has illustrated a role of sleep in memory but also many other cognitive processes such as problem-solving and creativity. While sleep deprivation has been shown to diminish decision-making, to date, studies have failed to directly investigate the impact of sleep on decision-making or choice. Yet, we often follow the wisdom that “sleeping on it” is beneficial to decisions. Thus, we examined whether periods of sleep influence recall for information pertaining to a decision as well as subjective perceptions of decision quality. Across studies, participants attended two experimental sessions separated by 12 hrs, either spent awake (AM-PM) or containing sleep (PM-AM). All studies were incentive compatible. During the first session, participants were informed that their selection from a choice set would be honored if they were chosen in a later random drawing. Participants viewed several positive and negative attributes relating to each of four commonly used items (laptop messenger satchels). Following an unrelated filler task, recall was assessed and participants rated the valence of each remembered attribute. In the second session, recall was tested again in a similar manner. After this, participants then indicated their preferred item from the choice set and rated the ease of this decision process, their confidence and their satisfaction with their choice. Overall, sleep significantly benefited attribute recall. Individuals in the PM-AM group showed an increase in responses, while those in the AM-PM group showed a decrease. These results applied to the total attributes recalled (inclusive of errors) as well as the accurate attributes only. Data from subsequent experiments with balanced numbers of positive and negative attributes suggest that the differences between groups may be due to improved memory for positive compared to negative attributes after sleep. Notably, despite the boost in their knowledgeability, PM-AM participants found the choice process more difficult and were less confident and less satisfied with their decision. These findings do not appear to be dependent on time of day. Single-session control groups, tested in the AM or PM, revealed no differences in baseline recall performance or perceptions of decision quality. Emerging data suggest that single item (yes/no) choices also result in less satisfaction after “sleeping on” decision-relevant information. Thus our results suggest that sleep may have some negative consequences for decision-making, decreasing decision satisfaction, despite improving knowledgeability about the choice set.

Considering I’ve been suffering from lack of sleep lately, a post about sleep and cognitive performance seems appropriate. I visited this poster on my last day at SfN10 and I finally got around to blogging about it. So here it goes…

Sleep is thought to benefit decision-making and creativity as well as aid in problem-solving, consolidation of memory and transitive relationships. To test the effect of sleep on cognitive performance, Karmakar and others assigned experimental subjects to one of two different sleep sessions and conducted a cognitive task after the 12-hour period. Both groups had 12 hour sessions, but one group had 12 hours (sleep time included, from PM-AM) before the test while the other had 12 hours awake (AM-OM) before the test. For example, the 12 hour session of the sleep group were from 8PM to 8AM and then they went to take the test. 

Results:

1. Sleep improves memory recall. 

2. Sleep increases accuracy of attribute recall. 

3. Sleep decreased the perception of decision quality and the time of day did not account for differences in recall or perceived decision quality. (Individuals who slept before the exam had less confidence and were less satisfied with their choices.)

4. Sleep benefits recall of positive information and hinders recall of negative information.

Author Abstract (Karmarkar et. al): Impact of Sleep on Attribute Recall and Choice Satisfaction

A wealth of recent studies has illustrated a role of sleep in memory but also many other cognitive processes such as problem-solving and creativity. While sleep deprivation has been shown to diminish decision-making, to date, studies have failed to directly investigate the impact of sleep on decision-making or choice. Yet, we often follow the wisdom that “sleeping on it” is beneficial to decisions. Thus, we examined whether periods of sleep influence recall for information pertaining to a decision as well as subjective perceptions of decision quality.

Across studies, participants attended two experimental sessions separated by 12 hrs, either spent awake (AM-PM) or containing sleep (PM-AM). All studies were incentive compatible. During the first session, participants were informed that their selection from a choice set would be honored if they were chosen in a later random drawing. Participants viewed several positive and negative attributes relating to each of four commonly used items (laptop messenger satchels). Following an unrelated filler task, recall was assessed and participants rated the valence of each remembered attribute. In the second session, recall was tested again in a similar manner. After this, participants then indicated their preferred item from the choice set and rated the ease of this decision process, their confidence and their satisfaction with their choice.

Overall, sleep significantly benefited attribute recall. Individuals in the PM-AM group showed an increase in responses, while those in the AM-PM group showed a decrease. These results applied to the total attributes recalled (inclusive of errors) as well as the accurate attributes only. Data from subsequent experiments with balanced numbers of positive and negative attributes suggest that the differences between groups may be due to improved memory for positive compared to negative attributes after sleep. Notably, despite the boost in their knowledgeability, PM-AM participants found the choice process more difficult and were less confident and less satisfied with their decision. These findings do not appear to be dependent on time of day. Single-session control groups, tested in the AM or PM, revealed no differences in baseline recall performance or perceptions of decision quality. Emerging data suggest that single item (yes/no) choices also result in less satisfaction after “sleeping on” decision-relevant information. Thus our results suggest that sleep may have some negative consequences for decision-making, decreasing decision satisfaction, despite improving knowledgeability about the choice set.