Molecular Targets of Cannabinoids Associated with Depression

2021 ◽  
Vol 28 ◽  
Author(s):  
Pradeep Paudel ◽  
Samir Ross ◽  
Xing-Cong Li
Keyword(s):  
Gaba Receptor ◽  
Rational Design ◽  
Cannabinoid Receptors ◽  
Molecular Targets ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Binding Modes ◽  
Novel Therapeutic Strategies ◽  
New Treatments ◽  
Synthetic Derivatives

: Novel therapeutic strategies are needed to address depression, a major neurological disorder affecting hundreds of millions of people worldwide. Cannabinoids and their synthetic derivatives have demonstrated numerous neurological activities and may potentially be developed into new treatments for depression. This review highlights cannabinoid (CB) receptors, monoamine oxidase (MAO), N-methyl-D-aspartate (NMDA) receptor, gamma-aminobutyric acid (GABA) receptor, and cholecystokinin (CCK) receptor as key molecular targets of cannabinoids that are associated with depression. The anti-depressant activity of cannabinoids and their binding modes with cannabinoid receptors are discussed, providing insights into rational design and discovery of new cannabinoids or cannabimimetic agents with improved druggable properties.

Gamma-aminobutyric acid (GABA) receptor binding selectively depleted by viral induced granule cell loss in hamster cerebellum

1976 ◽  
Vol 105 (2) ◽  
pp. 365-371 ◽  
Author(s):  
Rabi Simantov ◽  
Mary Lou Oster-Granite ◽  
Robert M. Herndon ◽  
Solomon H. Snyder
Keyword(s):  
Receptor Binding ◽  
Granule Cell ◽  
Gaba Receptor ◽  
Cell Loss ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid

A comparison of similar ionic responses to gamma-aminobutyric acid and acetylcholine

1978 ◽  
Vol 41 (3) ◽  
pp. 531-541 ◽  
Author(s):  
J. Yarowsky ◽  
D. O. Carpenter
Keyword(s):  
Gaba Receptor ◽  
Aminobutyric Acid ◽  
Identified Neurons ◽  
Ionic Conductance ◽  
Gamma Aminobutyric Acid ◽  
Gaba Antagonists ◽  
Conductance Increase ◽  
Alpha Bungarotoxin ◽  
Cl Conductance

1. Fast Na+-, Cl-, and K+-Conductance increase responses to gamma-aminobutyric acid (GABA) show times to peak similar to the comparable ionic responses to acetylcholine (ACh). 2. On some identified neurons, both putative transmitters elicit responses due to the same conductance change. For example, in cell R2 both substances cause an increase in Cl- conductance. Receptors for GABA and ACh on R2 do not cross desensitize and therefore are distinct. The ACh but not the GABA response is blocked by alpha-bungarotoxin and strychnine. 3. In R2 both responses reverse at -58 mV, and the Cl- ionophore (for both responses) appears to be partially permeant to propionate and isethionate, but impermeant to acetate, sulfate, and methylsulfate. 4. The Cl- responses but not the Na+ responses to both ACh and GABA are blocked by both picrotoxin and bicuculline, the classical GABA antagonists. 5. These results are compatible with the hypothesis that the ionophores associated with receptors to different neurotransmitters but mediating the same ionic conductance change have many common properties and may, in fact, be identical. Bicuculline and picrotoxin may be specific blockers of the Cl- ionophore, not the GABA receptor.

Respiratory depression produced by activation of GABA receptors in hindbrain of cat

1981 ◽  
Vol 51 (5) ◽  
pp. 1278-1286 ◽  
Author(s):  
K. A. Yamada ◽  
P. Hamosh ◽  
R. A. Gillis
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Respiratory Depression ◽  
Gaba Receptors ◽  
Gaba Receptor ◽  
Respiratory Activity ◽  
Aminobutyric Acid ◽  
Neural Pathways ◽  
Gamma Aminobutyric Acid ◽  
Respiratory Responses

Respiratory responses to activation of gamma-aminobutyric acid (GABA) receptors in the hindbrain were measured in chloralose-anesthetized cats using a Fleisch pneumotachograph. GABA receptors were activated by intracisternal injections of muscimol and GABA. Muscimol (0.05--6.65 micrograms) administered to seven animals caused a depression of respiratory activity with apnea occurring in each animal. Before apnea occurred, a decrease in tidal volume was observed (from 25.7 +/- 0.9 to 14.7 +/- 1.1 ml). Respiratory rate and inspiratory and expiratory durations were unchanged. GABA (0.05--12.15 mg) administered to five animals produced the same effect as muscimol on respiratory activity. Apnea produced by both agents was reversed by intracisternal administration of the GABA-receptor antagonist drug, bicuculline. Administration of bicuculline to four naive animals increased tidal volume (from 31.3 +/- 1.7 to 36.5 +/- 0.7 ml) but had no effect on either respiratory rate or inspiratory duration. These results indicate that activation of GABA receptors causes respiratory depression and suggest that GABA may be an important neurotransmitter in CNS neural pathways involved in regulating respiratory activity.

Gamma-aminobutyric acid (GABA) receptor rho (GABRR) polymorphisms and risk for essential tremor

2010 ◽  
Vol 258 (2) ◽  
pp. 203-211 ◽  
Author(s):  
Elena García-Martín ◽  
Carmen Martínez ◽  
Hortensia Alonso-Navarro ◽  
Julián Benito-León ◽  
Oswaldo Lorenzo-Betancor ◽  
...  
Keyword(s):  
Essential Tremor ◽  
Gaba Receptor ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid
Sign in / Sign up

Export Citation Format

Share Document