2. Neuronal Signaling GPCR/G Protein
  3. Monoamine Oxidase 5-HT Receptor
  4. 5,7-Dihydroxytryptamine hydrobromide

5,7-Dihydroxytryptamine hydrobromide  (Synonyms: 5,7-DHP hydrobromide)

Cat. No.: HY-N18471A
Handling Instructions Technical Support

5,7-Dihydroxytryptamine (5,7-DHT) hydrobromide is an autofluorescent (Ex ≈ 365 nm), selective neurotoxin and a transport substrate for MAO-A and 5-HT. 5,7-Dihydroxytryptamine hydrobromide can specifically target and damage central and peripheral 5-HTergic neurons, while affecting 5-HT-related pathways and neurotransmitter balance. 5,7-Dihydroxytryptamine hydrobromide can be used to establish 5-HTergic neuron injury models for studies on neural development, neurodegenerative diseases, as well as mechanisms related to platelet function and retinal neurons.

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5,7-Dihydroxytryptamine hydrobromide

5,7-Dihydroxytryptamine hydrobromide Chemical Structure

CAS No. : 1841081-30-8

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Other Forms of 5,7-Dihydroxytryptamine hydrobromide:

5,7-Dihydroxytryptamine hydrobromide Related Antibodies

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Description

5,7-Dihydroxytryptamine (5,7-DHT) hydrobromide is an autofluorescent (Ex ≈ 365 nm), selective neurotoxin and a transport substrate for MAO-A and 5-HT. 5,7-Dihydroxytryptamine hydrobromide can specifically target and damage central and peripheral 5-HTergic neurons, while affecting 5-HT-related pathways and neurotransmitter balance. 5,7-Dihydroxytryptamine hydrobromide can be used to establish 5-HTergic neuron injury models for studies on neural development, neurodegenerative diseases, as well as mechanisms related to platelet function and retinal neurons[1][2][3].

In Vitro

5,7-dihydroxytryptamine hydrobromide (25 μM; 60 min at 37°C) specifically labels serotonergic cells (but not dopaminergic cells) in 10-day-old primary mesencephalic cultures from 14-day-old Wistar rat foetuses[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

5,7-Dihydroxytryptamine hydrobromide Related Antibodies
In Vivo

5,7-Dihydroxytryptamine (12.5-50.0 μg; intracerebroventricular administration; single dose) hydrobromide depletes norepinephrine and 5-HT in the hippocampus of mice. The depletion of norepinephrine is blocked by non-selective MAO inhibition but not by selective MAO-B inhibition[1].
5,7-Dihydroxytryptamine (10 μg base; intracerebroventricular injection; single administration; 10 days prior to seizure induction) hydrobromide depletes 5-HT levels in the spinal cord of rats, but does not affect electrically induced spinal cord seizures in rats[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Wistar rats (adult male, 175-200 g at surgery)[1]
Dosage: 8 μg
Administration: bilateral stereotaxic infusion into nucleus accumbens; over 2 min, injector left in place for 1 additional min post-infusion
Result: Increased mean amplitude of the acoustic startle reflex significantly across all stimulus intensities in the absence of background noise compared to the Sham-lesion group.
Showed no significant differences in startle amplitude between the DHT-lesion, Sham-lesion, and intact groups at any stimulus intensity in the presence of background noise.
Confirmed nearly complete loss of serotonergic neurons in the nucleus accumbens via immunohistochemistry.
Animal Model: C57BL/6 (male, 2 and 10 months old, 20-30 g)[2]
Dosage: 12.5 μg; 25 μg; 50 μg
Administration: i.c.v.; single dose
Result: Had a damaging effect on the noradrenergic system, and this effect was independent of the age of the mice.
Exerted stronger toxic effects on serotonergic neurons in young individuals.
Animal Model: M/511-Wistar (male, 240-280 g)[4]
Dosage: 4 µg (calculated as the base) per injection site
Administration: stereotactic injection; 1 µl/min rate; needle left in situ for 1 min post-injection
Result: Reduced ³H-5-HT uptake but did not change ³H-NA uptake in the cortex (medial bundle lesion group).
Reduced ³H-NA uptake to 75% of control (non-significant) in the cortex (medial plus lateral bundle lesion group).
Induced mouse killing behavior in 4 of 8 rats (medial bundle lesion group) and 6 of 7 rats (medial plus lateral bundle lesion group).
Required significantly more trials to reach habituation criterion for touch (both lesion groups).
Required significantly more trials for acoustic stimulation habituation (only medial plus lateral lesion group).
Showed a significantly higher number of boxing positions in the shock elicited fighting test (both lesion groups).
Showed no significant changes in home cage activity (both lesion groups).
Molecular Weight

273.13

Formula

C10H13BrN2O2
CAS No.
SMILES

NCCC1=CNC2=C(C=C(C=C12)O)O.Br
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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5,7-Dihydroxytryptamine hydrobromide Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

5,7-Dihydroxytryptamine1841081-30-85,7-DHPMonoamine Oxidase5-HT ReceptorMAOSerotonin Receptor5-hydroxytryptamine Receptornoradrenergic neurotoxicityserotonin transporterparkinson's diseaseserotoninMAO Ahyperacusisserotonergic neuronsalzheimer's diseaseratsmiceInhibitorinhibitorinhibit

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