ABSTRACT
ABSTRACT: Cannabidiol and other cannabinoids are being used more frequently for sports medicine-related conditions. This review will help sports medicine clinicians answer questions that their athletes and active patients have about the potential effectiveness of cannabinoids on common sports medicine conditions. In the article, the authors compare cannabidiol and delta-9-tetrahydrocannabinol effects, noting the difference on the endocannabinoid and nonendocannabinoid receptors. The theoretical benefits of these two compounds and the current legality in the United States surrounding cannabidiol and delta-9-tetrahydrocannabinol use also are addressed.
Subject(s)
Cannabidiol/therapeutic use , Cannabinoids/therapeutic use , Sports Medicine , Athletic Performance , Brain Concussion/drug therapy , Cannabidiol/adverse effects , Cannabidiol/metabolism , Cannabinoids/adverse effects , Cannabinoids/metabolism , Cannabis/chemistry , Cannabis/classification , Chronic Pain/drug therapy , Dronabinol/metabolism , Dronabinol/therapeutic use , Endocannabinoids/metabolism , Endocannabinoids/pharmacology , Humans , Medical Marijuana , Osteoarthritis/drug therapy , Receptor, Serotonin, 5-HT1A/metabolism , Receptors, Cannabinoid/metabolism , TRPV Cation Channels/metabolism , United StatesABSTRACT
Traumatic brain injury (TBI) constitutes a heterogeneous cerebral insult induced by traumatic biomechanical forces. Mitochondria play a critical role in brain bioenergetics, and TBI induces several consequences related with oxidative stress and excitotoxicity clearly demonstrated in different experimental model involving TBI. Mitochondrial bioenergetics alterations can present several targets for therapeutics which could help reduce secondary brain lesions such as neuropsychiatric problems, including memory loss and motor impairment. Guanosine (GUO), an endogenous neuroprotective nucleoside, affords the long-term benefits of controlling brain neurodegeneration, mainly due to its capacity to activate the antioxidant defense system and maintenance of the redox system. However, little is known about the exact protective mechanism exerted by GUO on mitochondrial bioenergetics disruption induced by TBI. Thus, the aim of this study was to investigate the effects of GUO in brain cortical and hippocampal mitochondrial bioenergetics in the mild TBI model. Additionally, we aimed to assess whether mitochondrial damage induced by TBI may be related to behavioral alterations in rats. Our findings showed that 24 h post-TBI, GUO treatment promotes an adaptive response of mitochondrial respiratory chain increasing oxygen flux which it was able to protect against the uncoupling of oxidative phosphorylation (OXPHOS) induced by TBI, restored the respiratory electron transfer system (ETS) established with an uncoupler. Guanosine treatment also increased respiratory control ratio (RCR), an indicator of the state of mitochondrial coupling, which is related to the mitochondrial functionality. In addition, mitochondrial bioenergetics failure was closely related with locomotor, exploratory and memory impairments. The present study suggests GUO treatment post mild TBI could increase GDP endogenous levels and consequently increasing ATP levels promotes an increase of RCR increasing OXPHOS and in substantial improve mitochondrial respiration in different brain regions, which, in turn, could promote an improvement in behavioral parameters associated to the mild TBI. These findings may contribute to the development of future therapies with a target on failure energetic metabolism induced by TBI.
Subject(s)
Brain Concussion/drug therapy , Energy Metabolism/drug effects , Guanosine/therapeutic use , Locomotion/drug effects , Memory, Long-Term/drug effects , Mitochondria/drug effects , Animals , Brain Concussion/metabolism , Brain Concussion/pathology , Cerebral Cortex/drug effects , Cerebral Cortex/metabolism , Cerebral Cortex/pathology , Energy Metabolism/physiology , Guanosine/pharmacology , Hippocampus/drug effects , Hippocampus/metabolism , Hippocampus/pathology , Locomotion/physiology , Male , Memory, Long-Term/physiology , Mitochondria/metabolism , Mitochondria/pathology , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Rats , Rats, WistarABSTRACT
The present review paper aims to update the definition and classification of cerebral concussion, highlighting its pathophysiological mechanisms. The high prevalence of cerebral concussion in emergency rooms around the world makes it necessary to know its proper management to avoid its late sequelae, which traditionally compromise cognitive aspects of behavior. New evidence on potential neuroprotective treatments is being investigated.