Mom looks to medical marijuana to cure daughter’s seizures

“Kaercher said no matter what treatments Grace is on, the seizures continue. She has tried every option except medical marijuana, which isn’t legal in Pennsylvania,

Kaercher said. “Marijuana isn’t that extreme compared to all these other things we have done,” Kaercher said. Kaercher, 45, has watched her daughter suffer from seizures since Grace was a baby. Kaercher said Grave is so brave for going out into the world every day and her heart breaks every time Grace has a seizure.“It’s been a long road for us,” Kaercher said. “We hope medical marijuana will be a viable option for her.””


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The Neuroscience Of Munchies: Why The Scent Of A Burger Gives Us A High – npr

We Didn't Make This Up: The scientists who performed the study on how cannabis triggers the munchies through the sense of smell commissioned an artist to put this illustration together.

“From cinnamon buns in the morning to a burger after a long run, food never smells as good as when you’re superhungry.

Now scientists have uncovered a clue as to why that might be — and it lies in the munchies and marijuana.

Receptors in the brains of mice that light up when the animals are high are also activated when the critters are fasting, French scientists reported Sunday in the journal Nature Neuroscience.

In other words, skipping a meal triggered the same hunger-inducing brain receptors that marijuana does. And it works, at least in mice, by boosting the sense of smell, neuroscientist Giovanni Marsicano and his team at the Universite de Bordeaux report.

That’s because the receptors that get activated are located in the smelling center of the brain. And sense of smell is known to be a key factor driving appetite.

In case you’re wondering, the mice didn’t toke up. The researchers injected the rodents withTHC, the active ingredient in marijuana.”

“The endocannabinoid system controls food intake via olfactory processes.”

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The endocannabinoid system controls food intake via olfactory processes.

“Hunger arouses sensory perception, eventually leading to an increase in food intake, but the underlying mechanisms remain poorly understood. We found that cannabinoid type-1 (CB1) receptors promote food intake in fasted mice by increasing odor detection.

CB1 receptors were abundantly expressed on axon terminals of centrifugal cortical glutamatergic neurons that project to inhibitory granule cells of the main olfactory bulb (MOB).

Local pharmacological and genetic manipulations revealed that endocannabinoids and exogenous cannabinoids increased odor detection and food intake in fasted mice by decreasing excitatory drive from olfactory cortex areas to the MOB.

Consistently, cannabinoid agonists dampened in vivo optogenetically stimulated excitatory transmission in the same circuit.

Our data indicate that cortical feedback projections to the MOB crucially regulate food intake via CB1 receptor signaling, linking the feeling of hunger to stronger odor processing.Thus, CB1 receptor-dependent control of cortical feedback projections in olfactory circuits couples internal states to perception and behavior.”

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Cannabinoids inhibit cholinergic contraction in human airways through prejunctional CB1 receptors

“Here, we sought to assess the effects of natural and synthetic cannabinoids on cholinergic bronchial contraction…

Delta-9-tetrahydrocannabinol, WIN55,212-2 and CP55,940 induced concentration-dependent inhibition of cholinergic contraction… 

Conclusions and implications

Activation of prejunctional CB1-receptors appears to mediate the inhibition of electrical field stimulation-evoked cholinergic contraction in human bronchus.

This feature may explain the acute bronchodilation produced by marijuana smoking.”

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Altered Expression of the CB1 Cannabinoid Receptor in the Triple Transgenic Mouse Model of Alzheimer’s Disease.

“The endocannabinoid system has gained much attention as a new potential pharmacotherapeutic target in various neurodegenerative diseases, including Alzheimer’s disease (AD).

…The altered CB1 levels appear, rather, to be age-and/or pathology-dependent, indicating an involvement of the endocannabinoid system in AD pathology and supporting the ECS as a potential novel therapeutic target for treatment of AD.”

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Neuroprotective effects of the cannabinoid agonist HU210 on retinal degeneration.

“Cannabinoids have been demonstrated to exert neuroprotective effects on different types of neuronal insults.

Here we have addressed the therapeutic potential of the synthetic cannabinoid HU210 on photoreceptor degeneration, synaptic connectivity and functional activity of the retina in the transgenic P23H rat, an animal model for autosomal dominant retinitis pigmentosa (RP)…

These data suggest that cannabinoids are potentially useful to delay retinal degeneration in RP patients.”

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Involvement of the endocannabinoid system in osteoarthritis pain.

“Increasing evidence from preclinical studies supports the interest of the endocannabinoid system as an emerging therapeutic target for osteoarthritis pain.

Indeed, pharmacological studies have shown the anti-nociceptive effects of cannabinoids in different rodent models of osteoarthritis, and compelling evidence suggests an active participation of the endocannabinoid system in the pathophysiology of this disease.

The ubiquitous distribution of cannabinoid receptors, together with the physiological role of the endocannabinoid system in the regulation of pain, inflammation and even joint function further support the therapeutic interest of cannabinoids for osteoarthritis.

…review summarizes the promising results that have been recently obtained in support of the therapeutic value of cannabinoids for osteoarthritis management.”

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No more pain upon Gq -protein-coupled receptor activation: role of endocannabinoids.

“Marijuana has been used to relieve pain for centuries. The analgesic mechanism of its constituents, the cannabinoids, was only revealed after the discovery of cannabinoid receptors (CB1 and CB2 ) two decades ago.

The subsequent identification of the endocannabinoids, anandamide and 2-arachidonoylglycerol (2-AG), and their biosynthetic and degradation enzymes discloses the therapeutic potential of compounds targeting the endocannabinoid system for pain control.

Inhibitors of the anandamide and 2-AG degradation enzymes, fatty acid amide hydrolase and monoacylglycerol lipase, respectively, may be superior to direct cannabinoid receptor ligands as endocannabinoids are synthesized on demand and rapidly degraded, focusing action at generating sites.

Recently, a promising strategy for pain relief was revealed in the periaqueductal gray (PAG). It is initiated by Gq -protein-coupled receptor (Gq PCR) activation of the phospholipase C-diacylglycerol lipase enzymatic cascade, generating 2-AG that produces inhibition of GABAergic transmission (disinhibition) in the PAG, thereby leading to analgesia.

Here, we introduce the antinociceptive properties of exogenous cannabinoids and endocannabinoids, involving their biosynthesis and degradation processes, particularly in the PAG. We also review recent studies disclosing the Gq PCR-phospholipase C-diacylglycerol lipase-2-AG retrograde disinhibition mechanism in the PAG, induced by activating several Gq PCRs, including metabotropic glutamatergic (type 5 metabotropic glutamate receptor), muscarinic acetylcholine (M1/M3), and orexin 1 receptors.

Disinhibition mediated by type 5 metabotropic glutamate receptor can be initiated by glutamate transporter inhibitors or indirectly by substance P, neurotensin, cholecystokinin and capsaicin. Finally, the putative role of 2-AG generated after activating the above neurotransmitter receptors in stress-induced analgesia is discussed.”

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Anandamide in primary sensory neurons: too much of a good thing?

“The quest for possible targets for the development of novel analgesics has identified the activation of the cannabinoid type 1 (CB1) receptor outside the CNS as a potential means of providing relief from persistent pain, which currently constitutes an unmet medical need.

Increasing tissue levels of the CB1 receptor endogenous ligand N-arachidonoylethanolamine (anandamide), by inhibiting anandamide degradation through blocking the anandamide-hydrolysing enzyme fatty acid amide hydrolase, has been suggested to be used to activate the CB1 receptor.

However, recent clinical trials revealed that this approach does not deliver the expected relief from pain. Here, we discuss one of the possible reasons, the activation of the transient receptor potential vanilloid type 1 ion channel (TRPV1) on nociceptive primary sensory neurons (PSNs) by anandamide, which may compromise the beneficial effects of increased tissue levels of anandamide.

We conclude that better design such as concomitant blocking of anandamide hydrolysis and anandamide uptake into PSNs, to inhibit TRPV1 activation, could overcome these problems.”

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Endocannabinoids and neuropathic pain: focus on neuron-glia and endocannabinoid-neurotrophin interactions.

“Although originally described as a signalling system encompassing the cannabinoid CB1 and CB2 receptors, their endogenous agonists (the endocannabinoids), and metabolic enzymes regulating the levels of such agonists, the endocannabinoid system is now viewed as being more complex, and including metabolically related endocannabinoid-like mediators and their molecular targets as well.

The function and dysfunction of this complex signalling system in the molecular and cellular mechanisms of pain transduction and control has been widely studied over the last two decades.

In this review article, we describe some of the latest advances in our knowledge on the role of the endocannabinoid system, in its most recent and wider conception, in pain pathways, by focusing on: (1) neuron-glia interactions; and (2) emerging data on endocannabinoid cross-talk with neurotrophins, such as nerve growth factor and brain-derived neurotrophic factor.”

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