Cannabis, psychosis and the thalamus: a theoretical review.
Zoran Vukadinovic, Merrill S Herman, Ivana Rosenzweig
Neuroscience and biobehavioral reviews May 1, 2013 DOI: 10.1016/j.neubiorev.2013.02.013 via PubMed
Summary
Cannabis use is a strong environmental risk factor for schizophrenia, but the mechanism is unknown. This theoretical paper argues that exogenous cannabinoids may directly affect T-type calcium channels in the thalamus. These channels are critical for amplifying corticothalamic inputs and generating neuronal burst firing, which is important for trans-thalamic cortico-cortical interactions. Interference with burst firing could impair these interactions, leading to a relative disconnection between cortical areas, reduced ability to recognize re-afferent sensory inputs, and psychosis. Δ(9)THC may be more detrimental than cannabidiol because it increases thalamic neuron excitability through its direct effect on T-type calcium channels.
Study at a glance
| Characteristics | Theoretical or philosophical paper Peer reviewed |
|---|---|
| Key finding | The pathomechanism by which cannabis use increases schizophrenia risk may involve direct effects of exogenous cannabinoids on T-type calcium channels in the thalamus, leading to impaired cortico-cortical interactions and psychosis. |
Abstract
The role of cannabis in the etiology of schizophrenia has been documented as possibly the strongest environmental risk factor. However, the pathomechanism whereby cannabis use increases this risk has not yet been identified. We argue that this pathomechanism may involve direct effects of exogenous cannabinoids on T-type calcium channels in the thalamus. These channels are crucial for amplification of corticothalamic inputs, as well as for the ability of the thalamus to generate neuronal burst firing. Cortically induced thalamic burst firing has been found to be important in trans-thalamic cortico-cortical interactions. Therefore, any potential interference with the burst firing mode in the thalamus could lead to an impairment in these interactions, which in turn causes a relative disconnection between cortical areas. This in turn could result in reduced ability to recognize re-afferent sensory inputs and psychosis. We also argue that the effects of Δ(9)THC are more detrimental compared with the effects of cannabidiol, as the former may increase the excitability of thalamic neurons by its direct effect on T-type calcium channels.