Role of endogenous cannabinoids in synaptic signaling.
The synthetic pathways of endocannabinoids are discussed, along with the putative mechanisms of their release, uptake, and degradation, and the fine-grain anatomical distribution of the neuronal cannabinoid receptor CB1 is described in most brain areas, emphasizing its general presynaptic localization and role in controlling neurotransmitter release.
Brain monoglyceride lipase participating in endocannabinoid inactivation
- T. Dinh, D. Carpenter, D. Piomelli
- BiologyProceedings of the National Academy of Sciences…
- 22 July 2002
The results suggest that hydrolysis by means of MGL is a primary mechanism for 2-AG inactivation in intact neurons, and not on the accumulation of anandamide, another endocannabinoid lipid.
Presynaptically Located CB1 Cannabinoid Receptors Regulate GABA Release from Axon Terminals of Specific Hippocampal Interneurons
The results suggest that cannabinoid-mediated modulation of hippocampal interneuron networks operate largely via presynaptic receptors on CCK-immunoreactive basket cell terminals, the likely mechanism by which both endogenous and exogenous CB1 ligands interfere with hippocampal network oscillations and associated cognitive functions.
Distribution of CB1 Cannabinoid Receptors in the Amygdala and their Role in the Control of GABAergic Transmission
It is proposed that these anatomical and physiological features, characteristic of CB1 receptors in several forebrain regions, represent the neuronal substrate for endocannabinoids involved in retrograde synaptic signaling and may explain some of the emotionally relevant behavioral effects of cannabinoid exposure.
Regulation of endoplasmic reticulum turnover by selective autophagy
Severe disruption of Fam134b in mice causes expansion of the ER, inhibits ER turnover, sensitizes cells to stress-induced apoptotic cell death and leads to degeneration of sensory neurons, so selective ER-phagy via FAM134 proteins is indispensable for mammalian cell homeostasis and controls ER morphology and turnover in mice and humans.
Subcellular Arrangement of Molecules for 2-Arachidonoyl-Glycerol-Mediated Retrograde Signaling and Its Physiological Contribution to Synaptic Modulation in the Striatum
- M. Uchigashima, M. Narushima, M. Fukaya, I. Katona, M. Kano, Masahiko Watanabe
- Biology, ChemistryJournal of Neuroscience
- 4 April 2007
2-AG is identified as the major endocannabinoid mediating retrograde suppression at excitatory and inhibitory synapses of MS neurons, and CB1 cannabinoid receptor, the main target of 2-AG, was present at high levels on GABAergic axon terminals of MS neuron and parvalbumin-positive interneurons and at low levels on excitatories corticostriatal afferents.
Molecular Composition of the Endocannabinoid System at Glutamatergic Synapses
It is shown, by using two independent riboprobes, that principal cell populations of the hippocampus express high levels of diacylglycerol lipase α (DGL-α), the enzyme involved in generation of the endocannabinoid 2-arachidonoyl- glycerol (2-AG), which may contribute to homosynaptic plasticity of excitatory synapses and to heterosynptic plasticity between excitatories and inhibitory contacts.
Endocannabinoid signaling as a synaptic circuit breaker in neurological disease
Recent advances show that endocannabinoid signaling is a key regulator of synaptic communication throughout the central nervous system and offers new therapeutic opportunities for the selective control of deleterious neuronal activity in several neurological disorders.
Endocannabinoid Signaling in Rat Somatosensory Cortex: Laminar Differences and Involvement of Specific Interneuron Types
This work combined multiple immunolabeling with whole-cell recordings to investigate the morpho-functional characteristics of cannabinoid signaling in rat somatosensory cortex and found a unique population of large pyramidal neurons in layer VB that received much less perisomatic innervation from CB1-expressing GABAergic axon terminals and, accordingly, showed no depolarization-induced suppression of inhibition.