Post by Admin on Feb 11, 2019 17:44:09 GMT
Long_term behavioral and biochemical effects of an ultra_low dose of D9_tetrahydrocannabinol (THC)- neuroprotection and ERK signaling
Abstract
We have previously reported that a single
injection of an ultra-low dose of delta-9-tetrahydrocannabinol (THC; the psychoactive ingredient of marijuana)
protected the brain from pentylenentetrazole (PTZ)-
induced cognitive deficits when applied 1–7 days before or
1–3 days after the insult. In the present study we expanded
the protective profile of THC by showing that it protected
mice from cognitive deficits that were induced by a variety
of other neuronal insults, including pentobarbital-induced
deep anesthesia, repeated treatment with 3,4 methylenedioxymethamphetamine (MDMA; ‘‘ecstasy’’) and exposure to carbon monoxide. The protective effect of THC
lasted for at least 7 weeks. The same ultra-low dose of
THC (0.002 mg/kg, a dose that is 3–4 orders of magnitude
lower than the doses that produce the known acute effects
of the drug in mice) induced long-lasting (7 weeks) modifications of extracellular signal–regulated kinase (ERK)
activity in the hippocampus, frontal cortex and cerebellum
of the mice. The alterations in ERK activity paralleled
changes in its activating enzyme MEK and its inactivating
enzyme MKP-1. Furthermore, a single treatment with the
low dose of THC elevated the level of pCREB (phosphorylated cAMP response element–binding protein) in the
hippocampus and the level of BDNF (brain-derived neurotrophic factor) in the frontal cortex. These long-lasting
effects indicate that a single treatment with an ultra-low
dose of THC can modify brain plasticity and induce longterm behavioral and developmental effects in the brain.
Keywords Cannabinoid Neuroprotection
Preconditioning Cognitive deficit
Extracellular signal–regulated kinase (ERK)
Source: cdn.doctorsonly.co.il/2013/05/Long-term-behavioral-and-biochemical-effects.pdf
Abstract
We have previously reported that a single
injection of an ultra-low dose of delta-9-tetrahydrocannabinol (THC; the psychoactive ingredient of marijuana)
protected the brain from pentylenentetrazole (PTZ)-
induced cognitive deficits when applied 1–7 days before or
1–3 days after the insult. In the present study we expanded
the protective profile of THC by showing that it protected
mice from cognitive deficits that were induced by a variety
of other neuronal insults, including pentobarbital-induced
deep anesthesia, repeated treatment with 3,4 methylenedioxymethamphetamine (MDMA; ‘‘ecstasy’’) and exposure to carbon monoxide. The protective effect of THC
lasted for at least 7 weeks. The same ultra-low dose of
THC (0.002 mg/kg, a dose that is 3–4 orders of magnitude
lower than the doses that produce the known acute effects
of the drug in mice) induced long-lasting (7 weeks) modifications of extracellular signal–regulated kinase (ERK)
activity in the hippocampus, frontal cortex and cerebellum
of the mice. The alterations in ERK activity paralleled
changes in its activating enzyme MEK and its inactivating
enzyme MKP-1. Furthermore, a single treatment with the
low dose of THC elevated the level of pCREB (phosphorylated cAMP response element–binding protein) in the
hippocampus and the level of BDNF (brain-derived neurotrophic factor) in the frontal cortex. These long-lasting
effects indicate that a single treatment with an ultra-low
dose of THC can modify brain plasticity and induce longterm behavioral and developmental effects in the brain.
Keywords Cannabinoid Neuroprotection
Preconditioning Cognitive deficit
Extracellular signal–regulated kinase (ERK)
Source: cdn.doctorsonly.co.il/2013/05/Long-term-behavioral-and-biochemical-effects.pdf