**Nora Laaris et. al., "Δ9-tetrahydrocannabinol is a full agonist at CB1 receptors on GABA neuron axon terminals in the hippocampus." Neuropharmacology, Vol. 59, No. 1-2, 121-127. 2010.[
**A. Hoffman, "Mechanisms of Cannabinoid Inhibition of GABA-A Synaptic Transmission in the Hippocampus." J. Neurosci., 20(7):2470-2479. 2000.
Marijuana causes a physiological reaction that causes anxiety.
Depression of growth hormone and cortisol response to insulin-induced hypoglycemia after prolonged oral delta-9-tetrahydrocannabinol administration in man.
Six hospitalized volunteer male subjects were given insulin, 0.15 U/kg, before and after 14 days of administration of delta-9-tetrahydrocannabinol (THC) at a dose of 210 mg/day. A diminished maximal serum human growth hormone (GH) increase followed the prolonged THC ingestion. The mean maximal GH response was: 52.6 ng/ml /- 8.7 ( /-SE) before THC and 18.8 ng/ml /- 6.7 ( /-SE) during THC, P less than 0.01; corresponding cortisol responses were 20.1 mug/dl /- 3.0 before THC and 10.0 mug/dl /- 1.1 during THC, P less than 0.05. The data suggest suppression of the hypothalamic-pituitary axis after prolonged high dose THC use. This is consistent with other reported endocrine effects of marijuana in man.
Gamma-aminobutyric acid B receptor 1 mediates behavior-impairing actions of alcohol in Drosophila: adult RNA interference and pharmacological evidence.
Department of Psychiatry, Psychiatric Institute, University of Illinois, Chicago, IL 60612, USA.
In addition to their physiological function, metabotropic receptors for neurotransmitter gamma-aminobutyric acid (GABA), the GABA(B) receptors, may play a role in the behavioral actions of addictive compounds. Recently, GABA(B) receptors were cloned in fruit flies (Drosophila melanogaster), indicating that the advantages of this experimental model could be applied to GABA(B) receptor research. RNA interference (RNAi) is an endogenous process triggered by double-stranded RNA and is being used as a tool for functional gene silencing and functional genomics. Here we show how cell-nonautonomous RNAi can be induced in adult fruit flies to silence a subtype of GABA(B) receptors, GABA(B)R1, and how RNAi combined with pharmacobehavioral techniques (including intraabdominal injections of active compounds and a computer-assisted quantification of behavior) can be used to functionally characterize these receptors. We observed that injection of double-stranded RNA complementary to GABA(B)R1 into adult Drosophila selectively destroys GABA(B)R1 mRNA and attenuates the behavioral actions of the GABA(B) agonist, 3-aminopropyl-(methyl)phosphinic acid. Moreover, both GABA(B)R1 RNAi and the GABA(B) antagonist CGP 54626 reduced the behavior-impairing effects of ethanol, suggesting a putative role for the Drosophila GABA(B) receptors in alcohol's mechanism of action. The Drosophila model we have developed can be used for further in vivo functional characterization of GABA(B) receptor subunits and their involvement in the molecular and systemic actions of addictive substances.
Cannabis has been known to inhibit GABA-A transmission. This would be the same as the anxiety one would get if your blood level of benzos got low and you are dependent. There would not be enough GABA to cover the receptors that manage fear and anxiety.
Then again if you want to dismiss oral consumption there is still the fact of shortness of breath and anxiolytics (sp?) that are in tobacco smoke or your method of smoking induces shortness of breath.
Other then that I believe its likely much more complex than that, both anxiety and paranoia, are a result of your brain reacting to the abstinence of the drug you've so frequently "flooded" it with. With cannabis, smoking it would typically induce positive feelings. excessive drug use will trick your brain into relying on exogenous rather than endogenous sources. Therefore, cessation of whatever drug you typically used will leave your body without feeling comfortable, and thus responds with the opposite feeling (i.e. paranoia in the absence of calmness).
benzos respectively, are of course antianxiety/sleep aids etc, and help with such anxious/paranoid thinking. On the flip side though, CB1 induced suppresion of inhibiton at GABA receptors will lead to increased dopamine release. Both rewarding and perhaps, like other DA releasers could cause paranoia/anxiety. I guess suppression of inhibition induced DA relese is of a far smaller magnitude than that caused by stimulants and such.
Everyone is diffirent but still I think long-term smokers can expect a little bit of anxiety. Who doesn't though?