Abstracts should be prepared strictly according to the following instructions.
- Submissions should include all authors of the original research.
- Insert the author’s initials, last name and institute details. Indicate all affiliations with a lower-case letter immediately after the Author’s Name: a,b
- Do not add any titles or degrees: Prof, Dr, PhD, etc.
- First author should be the presenting author. All communication will be done with the presenting author
Please note that these guidelines may not be applicable for all disciplines. If you do not use experimental methods, you may suffice with an introduction, main research question and methods and/or theoretical approach.
All other abstracts should include the following:
- brief introduction to the research question, and aim(s) of the study
- methods used including statistical analysis methods
- summary of results containing real data and the outcome of statistical analyses
- disclosure on potential conflicts of interest and acknowledgement of funding
- Abstracts must be submitted in English (UK) (e.g. -ise not -ize).
- The title should not exceed 150 characters.
- Submit text with as little ‘formatting’ as possible (no italic or bold if you can avoid it)
- Use Times New Roman, 12 pts for text
- Write the title in lower case letters (except the first letter) and do not put a dot at the end. Please refrain from using all caps.
- Abstracts should have a minimum of 200 and a maximum of 250 words (excluding references).
- Tables, graphs and pictures are not allowed.
- Optionally, you can include up to five references to previous publications. In the body text, a publication should be referred to by a consecutive number between brackets, i.e. , , ,  and .
- Authors are responsible for the accuracy of references. Only published articles and those in press (the journal should be stated) may be included; unpublished results and personal communications should be cited as such in the body text.
- The references should be provided in accordance with Vancouver referencing guidelines; see below for examples:
1. Nichols DE. Psychedelics. Pharmacol Rev. 2016;(68):264–355.
Reference to a book
2. Halberstadt AL, Vollenweider FX, Nichols DE, editors. Current Topics in Behavioral Neurosciences. Behavioral Neurobiology of Psychedelic Drugs. 1st ed. Berlin: Springer-Verlag GmbH; 2018.
Reference to a chapter in a book
3. Preller KH, Vollenweider FX. Phenomenology, structure, and dynamic of psychedelic states. In: Halberstadt AL, Vollenweider FX, Nichols DE, editors. Current Topics in Behavioral Neurosciences. Behavioral Neurobiology of Psychedelic Drugs. 1st ed. Berlin: Springer-Verlag GmbH; 2018. p. 221–256.
An example of an abstract following our guidelines can be found below.
DMT and other hallucinogenic tryptamines exhibit substrate behavior at the serotonin uptake transporter and the vesicle monoamine transporter
Cozzia,b, NV, Shulgin, A.T.a,b, Sample authorc, Generic Authora,d, Another researchera, Person fiveb, Final authore
a Department of Psychiatry, Schulgin School of Medicine, CA, USA
b Department of Psychology, University of Groningen, Netherlands
c Neuroscience Department, King’s College, London, UK
d Harvard School of Thought, Boston, USA
e Private Practice, Berlin, Germany
N,N-dimethyltryptamine (DMT) is a potent plant hallucinogen that has also been found in human tissues. When ingested, DMT and related N,N-dialkyltryptamines produce an intense hallucinogenic state. Behavioral effects are mediated through various neurochemical mechanisms including activity at sigma-1 and serotonin receptors, modification of monoamine uptake and release, and competition for metabolic enzymes.
To further clarify the pharmacology of hallucinogenic tryptamines, we synthesized DMT, N-methyl-N-isopropyltryptamine (MIPT), N,N-dipropyltryptamine (DPT), and N,N-diisopropyltryptamine. We then tested the abilities of these N,N-dialkyltryptamines to inhibit [(3)H]5-HT uptake via the plasma membrane serotonin transporter (SERT) in human platelets and via the vesicle monoamine transporter (VMAT2) in Sf9 cells expressing the rat VMAT2. The tryptamines were also tested as inhibitors of [(3)H]paroxetine binding to the SERT and [(3)H]dihydrotetrabenazine binding to VMAT2.
Our results show that DMT, MIPT, DPT, and DIPT inhibit [(3)H]5-HT transport at the SERT with K ( I ) values of 4.00 +/- 0.70, 8.88 +/- 4.7, 0.594 +/- 0.12, and 2.32 +/- 0.46 microM, respectively. At VMAT2, the tryptamines inhibited [(3)H]5-HT transport with K ( I ) values of 93 +/- 6.8, 20 +/- 4.3, 19 +/- 2.3, and 19 +/- 3.1 muM, respectively. On the other hand, the tryptamines were very poor inhibitors of [(3)H]paroxetine binding to SERT and of [(3)H]dihydrotetrabenazine binding to VMAT2, resulting in high binding-to-uptake ratios.
High binding-to-uptake ratios support the hypothesis that the tryptamines are transporter substrates, not uptake blockers, at both SERT and VMAT2, and also indicate that there are separate substrate and inhibitor binding sites within these transporters. The transporters may allow the accumulation of tryptamines within neurons to reach relatively high levels for sigma-1 receptor activation and to function as releasable transmitters.
This work was supported by the Hallucinogen Research Institute.