Cannabinoid Receptor Found to Help Suppress Habitual Behavior

“A mouse study finds that CB1 protein in orbitofrontal cortex neurons mediates the ability to switch between habitual and active-learning behaviors when needed.

Everyone carries out daily habits and routines. As David Lovinger, Ph.D., chief of the Laboratory for Integrative Neuroscience at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), explained, “If your brain does not habitualize familiar tasks or places, it would be very difficult to focus because you’re constantly processing all these sensory inputs.”

Nonetheless, it’s important that the brain can shift from habit mode to a more active, goal-directed mindset. While an occasional lapse is normal, a chronic inability to exit from habitual behavior is a critical element of both addiction and obsessive-compulsive disorders. A new study carried out by Lovinger and colleagues adds to the understanding of the brain circuits responsible for the habitual/goal-directed shift.

The results, published June 15 in Neuron, also point to a receptor called cannabinoid type 1 (CB1) as a key regulator of this circuitry.

The findings were made possible using a training strategy that enabled mice to push levers for food in both a habitual and goal-directed manner. The mice were placed in enclosures with differing visual decorations; the lever in the first dropped a food reward after it was pressed a certain number of times, while the lever in the second would drop a reward at a random time after the lever had been pressed once.

“In the first scenario, the mouse makes the connection quickly that pressing the lever 20 times, for example, gets it a reward,” Lovinger told Psychiatric News. “In the second enclosure, that contiguity is disrupted. The mouse knows that pressing will eventually lead to reward, but it doesn’t know how many, so it will just start pressing at a periodic rate.”

On alternate testing days, the mice were allowed to eat their treats prior to the testing, and on these days—termed the devalued state because the desire for the reward is lessened—mice pressed the lever far less in the goal-directed enclosure, but still roughly the same amount in the random-time enclosure—much like a habit.

The researchers then tried these tests out on mice in which the neurons that travel between the orbitofrontal cortex (OFC) and dorsal striatum (DS, which links decision making and reward behaviors) were blocked and observed that the mice kept pressing a lot in both enclosures, suggesting an inability to switch out of habit mode.

“Normally, on devalued days the urge to default to the habit of pressing the lever repeatedly gets suppressed in some way because the brain is providing information that the food isn’t as valuable,” Lovinger said.

With the OFC-DS connection identified, the next question was what part of these neurons was responsible for suppressing habits? Some previous work by Lovinger’s colleague and study coauthor Rui Costa, Ph.D., an investigator at the Champalimaud Institute for the Unknown in Lisbon, Portugal, pointed to CB1 as a potential candidate; the CB1 receptor interacts with endocannabinoids, natural messenger molecules in the body that are strikingly similar to THC, the active compound in marijuana.

When mice lacking the CB1 receptor in their OFC neurons were trained, they reduced their lever pressing in both enclosures on devalued days, reflective of a state in which the mice always used goal-directed behaviors because they could not form habits.

Having found CB1 as the receptor that Helps suppress habits, Lovinger said the next step would be to find the agent in the OFC-DS neural circuit that strengthens habits—and that should provide major clues about how drugs of abuse like alcohol and marijuana disrupt the normal process of habituation.

While the NIAAA is more focused on the addiction side, Lovinger thinks the current knowledge gained on weakened habits could be valuable in neuropsychiatry as well.

“It may be a bit of a stretch, but ADHD could be mediated in part by reduced habit-forming potential,” he said. “If someone is trying to pay attention to all potential outcomes in every decision, it could explain the lack of focus displayed by people with ADHD.””

http://psychnews.psychiatryonline.org/doi/full/10.1176/appi.pn.2016.7b25

Multiple Mechanistically Distinct Modes of Endocannabinoid Mobilization at Central Amygdala Glutamatergic Synapses

“The central amygdala (CeA) is a key structure at the limbic-motor interface regulating stress responses and emotional learning. Endocannabinoid (eCB) signaling is heavily implicated in the regulation of stress-response physiology and emotional learning processes; however, the role of eCBs in the modulation of synaptic efficacy in the CeA is not well understood. Here we describe the subcellular localization of CB1 cannabinoid receptors and eCB synthetic machinery at glutamatergic synapses in the CeA and find that CeA neurons exhibit multiple mechanistically and temporally distinct modes of postsynaptic eCB mobilization. These data identify a prominent role for eCBs in the modulation of excitatory drive to CeA neurons and provide insight into the mechanisms by which eCB signaling and exogenous cannabinoids could regulate stress responses and emotional learning.”

http://www.cell.com/neuron/abstract/S0896-6273(14)00017-8

Cannabis Targets Receptors in the Amygdala Linked to Anxiety

“Marijuana may hijack cannabinoid receptors in the amygdala to reduce anxiety.”

“An international group of researchers led by Vanderbilt University has discovered for the first time that there are cannabinoid receptors in the amygdala. The amygdala is one of the primary brain regions involved in regulating anxiety and the flight-or-fight response.

“The discovery may help explain why marijuana users say they take the drug mainly to reduce anxiety” said Sachin Patel, M.D., Ph.D., the paper’s senior author and professor of Psychiatry and of Molecular Physiology and Biophysics at Vanderbilt. He said, “this could be highly important for understanding how cannabis exerts its behavioral effects.”

The study titled, “Multiple Mechanistically Distinct Modes of Endocannabinoid Mobilization at Central Amygdala Glutamatergic Synapses” is published in the March 2014 issue of the journal Neuron.”

https://www.psychologytoday.com/blog/the-athletes-way/201403/cannabis-targets-receptors-in-the-amygdala-linked-anxiety

New Study Finds Marijuana To Be Effective Against Depression, Migraine and Anxiety

“Research has suggested that cannabis may be a promising treatment option for a number of different physical and mental health conditions, from post-traumatic stress disorder to chronic pain. A study released this week suggests that depression , anxiety and migraine can be added to that list.

Neuroscientists from the University of Buffalo’s Research Institute on Addictions found that endocannabinoids — chemical compounds in the brain that activate the same receptors as THC, an active compound in marijuana — may be helpful in treating depression, anxiety and migraine that results from chronic stress.

In studies on rats, the researchers found that chronic stress reduced the production of endocannabinoids, which affect our cognition, emotion and behavior, and have been linked to reduced feelings of pain and anxiety, increases in appetite and overall feelings of well-being. The body naturally produces these compounds, which are similar to the chemicals in cannabis. Reduction of endocannabinoid production may be one reason that chronic stress is a major risk factor in the development of depression.

Then, the research team administered marijuana cannabinoids to the rats, finding it to be an effective way to restore endocannabinoid levels in their brains — possibly, thereby, alleviating some symptoms of depression.

“Using compounds derived from cannabis — marijuana — to restore normal endocannabinoid function could potentially help stabilize moods and ease depression,” lead researcher Dr. Samir Haj-Dahmane said in a university press release.

Recent research around marijuana’s effect on symptoms of post-traumatic stress disorder further bolsters the Buffalo neuroscientists’ findings, since both disorders involve the way the brain responds to stress. A study published last year in the journal Neuropsychopharmacology, for instance, found synthetic cannabinoids triggered changes in brain centers associated with traumatic memories in rats, preventing some of the behavioral and physiological symptoms of PTSD. Another study published last year found that patients who smoked cannabis experienced a 75 percent reduction in PTSD symptoms.

However, it’s important to note that the relationship between marijuana and depression  is complex. Some research has suggested that regular and heavy marijuana smokers are at a higher risk for depression, although a causal link between cannabis use and depression has not been established. More studies are needed in order to determine whether, and how, marijuana might be used in a clinical context for patients with depression.”  http://painphysicianjournal.co/2016/06/30/new-study-finds-marijuana-to-be-effective-against-depression-migraine-and-anxiety/

New Study Finds Marijuana To Be Effective Against Depression, Migraine and Anxiety

New Study Finds Endocannabinoids May Help OCD

OCD and cannabis research

“Obsessive-Compulsive Disorder (OCD) may look different in each affected individual. One person might feel it is necessary to wash their hands constantly while others might feel obligated to count something over and over.

According to the National Institute of Mental Health, OCD is a common disorder in which a person has uncontrollable and reoccurring obsessions and compulsions. Obsessions often cause anxiety in a person, so they feel by doing compulsions, or certain behaviors, they might relieve their anxiety.

There are many treatments and medications used to combat OCD, however research is now showing that endocannabinoids can also play a huge role in OCD. The new study was funded by the The National Institute of Alcohol Abuse and Alcoholism (NIAA) and was conducted with mice. Researchers probed the brain mechanisms that are used when a mouse transitions from goal-directed behavior to habitual behaviors. They then led the mouse to receive food two ways. One way the mice received food was through doing a goal-directed behavior while the second way was through doing a habitual behavior. They then found that by deleting a certain endocannabinoid receptor, mice didn’t form habits.

This discovery led scientists to the conclusion that endocannabinoids, which are natural messengers in our bodies similar to cannabinoids found in cannabis, have a lot to do with how our brains make decisions.

George F. Koob, Ph.D. is the Director of the NIAA stated that their study revealed a mechanism in the brain that controls the transition between goal-directed behaviors and habitual behaviors. He went on to explain, “As we learn more about this mechanism, it could reveal how the brain forms habits and, more specifically, how both endocannabinoids and cannabinoid abuse can influence habitual behavior pathophysiology.”

This conclusion that our bodies natural endocannabinoids and the active ingredients in cannabis can affect memory and decision-making may give scientists a glimpse into new medications and treatments for OCD.” http://ireadculture.com/new-study-finds-endocannabinoids-may-help-ocd/

New Study Finds Endocannabinoids May Help OCD

Study reveals central role of endocannabinoids in habit formation

National Institutes of Health (NIH) - Turning Discovery into Health

“Daily activities involve frequent transitions between habitual behaviors, such as driving home, and goal-directed behaviors, such as driving to a new destination on unfamiliar roads. An inability to shift between habitual and non-habitual behaviors has been implicated in obsessive-compulsive disorder (OCD), addiction, and other disorders characterized by impaired decision-making.

In a new study conducted with mice, scientists report that endocannabinoids, natural messengers in the body that are chemically similar to the active compound in marijuana, play an important role in how the brain controls this fundamental process.

The National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, funded the study.

“The new findings point to a previously unknown mechanism in the brain that regulates the transition between goal-directed and habitual behaviors,” said George F. Koob, Ph.D., NIAAA director. “As we learn more about this mechanism, it could reveal how the brain forms habits and, more specifically, how both endocannabinoids and cannabinoid abuse can influence habitual behavior pathophysiology.” A report of the findings is now online in the journal Neuron.

Previous work in NIAAA’s Laboratory for Integrative Neuroscience suggested that reduced activity in the brain’s orbitofrontal cortex (OFC) underlies habit formation. Endocannabinoids are known to generally reduce the activity of neurons. In the current study, the authors, hypothesized that endocannabinoids in the OFC could be playing a key role in habit formation. The researchers used a newly developed procedure that allowed them to probe the brain mechanisms involved when a mouse shifts from goal-directed to habitual actions. By chemically inhibiting the activity of neurons in the OFC, they disrupted goal-directed behaviors and the mice relied on habitual actions instead. David Lovinger, Ph.D., chief of the NIAAA Laboratory for Integrative Neuroscience, Rui Costa, Ph.D., D.V.M., from the Champalimaud Centre for the Unknown in Lisbon, Portugal, and first author Christina Gremel, Ph.D. from NIAAA and the University of California, San Diego led the research team.

“Mice were trained to receive a food reward in two different ways,” said Dr. Lovinger. “One way required the animal to respond out of habit, while the second way demanded it to perform behaviors that were goal-directed.”

When Dr. Lovinger and his colleagues selectively deleted a particular endocannabinoid receptor, called cannabinoid type 1 (CB1), from OFC neurons, they found that mice that lacked these receptors did not form habits, but used goal-directed responses to receive the food reward. Animals with intact CB1 receptors preferentially used habitual responses to obtain the food reward. The authors say the new study points to a molecular mechanism through which endocannabinoids promote the formation of habits by reducing the flow of information in the OFC.

“Endocannabinoids appear to act as a brake in the OFC, allowing for habit formation,” said Dr. Gremel, an assistant professor of psychology and affiliated with the Neurosciences Graduate program at UCSD. “Our results suggest that alterations in the brain’s endocannabinoid system could be blocking the brain’s capacity to ‘break habits’ as observed in disorders that affect switching between goal-directed and habitual behaviors.”

The authors concluded that their findings demonstrate the existence of parallel brain circuits that mediate goal-directed and habitual behaviors. Drugs of abuse and neuropsychiatric disorders can affect decision-making by changing the balance between habitual and goal-directed actions. In particular, these mechanisms could help explain how cannabis drugs such as marijuana affect memory and decision-making.

The new findings suggest that strategies that target the brain’s endocannabinoid system might restore this balance and alleviate suffering in disorders involving these processes.”

https://www.nih.gov/news-events/news-releases/study-reveals-central-role-endocannabinoids-habit-formation?source=acsh.org

The synthetic cannabinoids attenuate allodynia and hyperalgesia in a rat model of trigeminal neuropathic pain.

 

“Trigeminal neuralgia is a disorder of paroxysmal and severely disabling facial pain and continues to be a real therapeutic challenge.

At present there are few effective drugs. Here we have evaluated the effects of the synthetic cannabinoid WIN 55,212-2 on mechanical allodynia and thermal hyperalgesia in a rat model of trigeminal neuropathic pain produced by a chronic constriction injury (CCI) of the infraorbital branch of the trigeminalnerve (ION).

Taken together, these results suggest that cannabinoids may be a useful therapeutic approach for the clinical management of trigeminal neuropathic pain disorders.”

The endocannabinoid system and Post Traumatic Stress Disorder (PTSD): From preclinical findings to innovative therapeutic approaches in clinical settings.

“Post-Traumatic Stress Disorder (PTSD) is a psychiatric chronic disease developing in individuals after the experience of an intense and life-threatening traumatic event. The post-traumatic symptomatology encompasses alterations in memory processes, mood, anxiety and arousal.

There is now consensus in considering the disease as an aberrant adaptation to traumatic stress. Pharmacological research, aimed at the discovery of new potential effective treatments, has lately directed its attention towards the “so-called” cognitive enhancers. This class of substances, by modulating cognitive processes involved in the development and/or persistence of the post-traumatic symptomatology, could be of great help in improving the outcome of psychotherapies and patients’ prognosis.

In this perspective, drugs acting on the endocannabinoid system are receiving great attention due to their dual ability to modulate memory processes on one hand, and to reduce anxiety and depression on the other.

The purpose of the present review is to offer a thorough overview of both animal and human studies investigating the effects of cannabinoids on memory processes.

First, we will briefly describe the characteristics of the endocannabinoid system and the most commonly used animal models of learning and memory. Then, studies investigating cannabinoid modulatory influences on memory consolidation, retrieval and extinction will be separately presented, and the potential benefits associated with each approach will be discussed.

In the final section, we will review literature data reporting beneficial effects of cannabinoid drugs in PTSD patients.”

http://www.ncbi.nlm.nih.gov/pubmed/27456243

Refractory trigeminal neuralgia responsive to nabiximols in a patient with multiple sclerosis.

“Nabiximols is a cannabinoid compound approved for the treatment of multiple sclerosis (MS)-related spasticity.

However, additional symptoms, such as pain, urinary urgency and sleep disturbance, may benefit from treatment.

CASE REPORT:

The present report describes a patient with secondary progressive MS and severe lower limbs spasticity who was started on treatment with nabiximols. The patient also suffered from trigeminal neuralgia, which he was not treating due to inefficacy or side effects of all previously tried medications. After nabiximols initiation the patient experienced a marked benefit on trigeminal neuralgia, which completely resolved, while spasticity responded only partially to treatment.

CONCLUSION:

Nabiximols mechanism of action is based on the interaction with CB1 and CB2 receptors, which are expressed by central nervous system neurons and are known to modulate pain among other effects. The present case indicates that nabiximols and other cannabinoids need to be further tested for the treatment of trigeminal neuralgia.”

http://www.ncbi.nlm.nih.gov/pubmed/27456876

“Therapeutic potential of cannabinoids in trigeminal neuralgia. Considering the pronounced antinociceptive effects produced by cannabinoids, they may be a promising therapeutic approach for the clinical management of trigeminal neuralgia.”  http://www.ncbi.nlm.nih.gov/pubmed/15578967

Should we care about sativex-induced neurobehavioral effects? A 6-month follow-up study.

“Sativex® is an exclusive cannabinoid-based drug approved for the treatment of spasticity due to Multiple Sclerosis (MS).

The most common side effects include dizziness, nausea, and somnolence. However, it is still under debate whether the drug could cause negative cognitive effects.

The aim of our study was to investigate the effect of Sativex® on functional and psychological status in cannabis-naïve MS patients.

After the treatment, we did not observe any significant neurobehavioral impairment in all the patients, but one.

Our findings suggest that Sativex® treatment does not significantly affect the cognitive and neurobehavioral functions.”

http://www.ncbi.nlm.nih.gov/pubmed/27460745