Cannabinoids can modulate motor behaviour, learning and memory, cognition and pain perception. These effects correlate with the expression of the cannabinoid receptor 1 (CB1) and with the presence of endogenous cannabinoids in the brain. In trying to obtain further insights into the mechanisms underlying the modulatory effects of cannabinoids, CB1-positive neurons were determined in the murine forebrain at a single cell resolution. We performed a double in situ hybridization study to detect mRNA of CB1 in combination with mRNA of glutamic acid decarboxylase 65k, neuropeptide cholecystokinin (CCK), parvalbumin, calretinin and calbindin D28k, respectively. Our results revealed that CB1-expressing cells can be divided into distinct neuronal subpopulations. There is a clear distinction between neurons containing CB1 mRNA either at high levels or low levels. The majority of high CB1-expressing cells are GABAergic (gamma-aminobutyric acid) neurons belonging mainly to the cholecystokinin-positive and parvalbumin-negative type of interneurons (basket cells) and, to a lower extent, to the calbindin D28k-positive mid-proximal dendritic inhibitory interneurons. Only a fraction of low CB1-expressing cells is GABAergic. In the hippocampus, amygdala and entorhinal cortex area, CB1 mRNA is present at low but significant levels in many non-GABAergic cells that can be considered as projecting principal neurons. Thus, a complex mechanism appears to underlie the modulatory effects of cannabinoids. They might act on principal glutamatergic circuits as well as modulate local GABAergic inhibitory circuits. CB1 is very highly coexpressed with CCK. It is known that cannabinoids and CCK often have opposite effects on behaviour and physiology. Therefore, we suggest that a putative cross-talk between cannabinoids and CCK might exist and will be relevant to better understanding of physiology and pharmacology of the cannabinoid system.

Expression of the cannabinoid receptor CB1 in distinct neuronal subpopulations in the adult mouse forebrain

TMS and drugs

TMS and drugs revisited 2014

State of the art: Pharmacologic effects on cortical excitability measures tested by transcranial magnetic stimulation.

Interaction of acamprosate with ethanol and spermine on NMDA receptors in primary cultured neurons.

The possible effects on psychomotor performance, concentration, attention, and mood of acamprosate (calciumacetylhomotaurinate) were assessed using a randomized, double-blind, cross-over, placebo-controlled design involving 12 healthy male volunteers. Acamprosate 2 g daily per os or placebo was administered for seven days and separated by washout intervals of at least 21 days. Objective tests evaluated psychomotor functions (simple reaction time measurement, binary choice reaction test, computerized visual searching task, sustained attention test). Mood was assessed using the Beck Depression Inventory and the Beschwerde-Liste to assess subjective physical impairment. Additionally, a visual 3-D illusion paradigm was applied to measure the psychotomimetic effect. A dose of acamprosate of 2 g/day for seven days was free of any significant effects on mood, concentration, attention, psychomotor performance and did not produce any subjective sedation, excitation or psychotomimetic effects. Language: en

Lack of psychotomimetic or impairing effects on psychomotor performance of acamprosate.

Acamprosate is effective in reducing alcohol intake in weaned alcoholics. We were interested if acamprosate had an effect on the excitability of cortical motoneurons determined by transcranial magnetic stimulation (TMS). We studied 12 male healthy volunteers (mean age 29.5 years, SD = 4.8) who were either treated with 6 tablets of acamprosate (each containing 333 mg verum) per day or placebo (randomized cross-over design) for 1 week. TMS was performed after each treatment session including a paired stimulation paradigm. Motor evoked potentials (MEPs) of the placebo and verum group did not differ with respect to paired stimulation. However, motor threshold increased in the acamprosate group (verum: 61.5% (SD = 7.9) vs. placebo: 58.9% (SD = 8.8), p = 0.036). We conclude that acamprosate leads to a hypoexcitability of the motor cortex. This might be due to subcortical mechanisms, e.g. thalamocortical pathways since intracortical inhibition and facilitation was not affected.

Acamprosate reduces motor cortex excitability determined by transcranial magnetic stimulation.

Objective: Several studies have shown acamprosate (calciumacetylhomotaurinate) to increase abstinence rates in weaned alcoholics. Chronic alcoholics often suffer from cognitive deficits. Since acamprosate appears to interact with N-methyl-D-aspartate (NMDA) receptors, a subclass of glutamate receptors playing an important role in learning and memory processes, this study was performed in order to investigate different cognitive functions during administration of acamprosate. Method: A randomized, double-blind, cross-over, placebo-controlled design, involving 12 healthy male volunteers was used. Acamprosate 2 g daily per os or placebo were administered for 7 days respectively, with a wash-out interval of 21 days between phases. Mood and different memory functions (i.e., working memory, delayed recall, recognition tasks) were assessed. Results: It was shown that a dose of acamprosate 2 g/day for 7 days may produce an impairment in delayed free recall. Recognition tasks, short term working memory and mood we...

Effects of acamprosate on memory in healthy young subjects.

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Lack of psychotomimetic or impairing effects on psychomotor performance of acamprosate.

Acamprosate reduces motor cortex excitability determined by transcranial magnetic stimulation.

Effects of acamprosate on memory in healthy young subjects.