The aim of this review is to highlight the chemistry, pharmacological effects and experimental values of scopolamine. It is a tropane alkaloid drug with muscarinic antagonist effects, also known as Hyoscine. It is on the World Health Organization’s List of Essential Medicines. Chemically it is 6,7b-epoxide of hyoscyamine, formed from hyoscyamine via 6b-hydroxyhyoscyamine. It is used to treat postoperative nausea and vomiting, gastrointestinal spasms, irritable bowel syndrome, etc. It is sometimes used as a premedication to surgery. It is experimentally used to evaluate nootropic and cholinergic drugs. Therefore it is further applied as a model for discovery and evaluation of new drugs and natural bioactive affecting cognitive function.
Scopolamine is a tropane alkaloid drug with muscarinic antagonist effects, also known as Hyoscine. Scopolamine exerts its effects by acting as a competitive antagonist at muscarinic acetylcholine receptors; it is thus classified as an anti cholinergic (anti muscarinic) drug. Although it is generally mentioned as a nonspecific antagonist, there is secondary evidence for M1-receptor subtype specificity. It is on the World Health Organization’s List of Essential Medicines, the most important medications needed in a basic health system. Scopolamine is named after the plant genus Scopolia. The name “hyoscine” is derived from the scientific name of henbane (Hyoscyamus Niger). Scopolamine has a number of uses in medicine, where it is used to treat postoperative nausea and vomiting, gastrointestinal spasms, irritable bowel syndrome, etc. It is sometimes used as a premedication (especially to reduce respiratory tract secretions) to surgery, most commonly by injection [1,2].
Scopolamine, which is the 6,7b-epoxide of hyoscyamine, is formed from hyoscyamine via 6b-hydroxyhyoscyamine. Both reactions are catalysed by hyoscyamine-6b-hydroxylase (H6H), which is a 2-oxoglutarate-dependent deoxygenase. The enzyme is localized in the pericycle of the root and is especially active in cultured roots, but absent in aerial parts of the plant [3-5].
A. Brown et al.  suggested that Scopolamine may impair temporal attention through a decrease in tonic alertness and that this decrease in alertness can be temporarily
compensated by a phasic alerting response to a salient stimulus.
B. Dandan et al.  examined harmine effects on scopolamine induced memory impairment mice and APP/PS1 transgenic mice as one of the models for Alzheimer’s disease, using Morris Water Maze test.
C. Wohleb et al.  proposed that scopolamine reverses the inhibitory inter neurons in the PFC causing disinhibition of pyramidal neurons and amplified extracellular glutamate that stimulates the quick antidepressant reactions to these mediators.
D. Changrun et al.  showed that the treatment with scopolamine significantly increased the escape latency time, decreased the number of crossings, and shortened the time spent in the target quadrant, while poly galacic acid reversed this scopolamine induced effects.
E. Andrea et al.  suggested that the administration of scopolamine increases the activity marker Fos in the medial prefrontal cortex, including the infralimbic (IL) and prelimbic (PrL) subregions. Scopolamine micro infusions into the IL or the PrL formed substantial antidepressant reactions in the forced swim test, and neuronal silencing of IL or PrL obstructed the antidepressant properties of systemic scopolamine. The consequences also reveal that the systemic administration of a selective muscarinic acetylcholine receptor antagonist, VU0255035, created an antidepressant reaction and stimulated mechanistic target of rapamycin complex 1 signaling in the PFC, related to the
actions of scopolamine.
A. Badruddeen et al.  examined the imaginable
protective result of hydro-alcoholic extract of Salvia
haematodes Wall root (HESH) on cognitive purposes in
scopolamine-induced amnesia in adult Sprague Dawley rats.
This study was observed acquisition SDL, retention SDL
and locomotor activity significantly decreased while Ach
E activity significantly increased in scopolamine-treated
group as compared to normal control group. The acquisition
SDL, retention SDL and locomotor activity were significantly
increased while; Ach E activity was significantly decreased
with all the doses of HESH as compared to scopolaminetreated
B. Memory impairment was induced in male Wistar
rats by administration of scopolamine (1mg/kg intra
peritoneally). Rats received oral doses of ramipril (0.225mg/
kg) and losartan (2.25mg/kg) for a period of four weeks.
Passive avoidance paradigm was used to assess learning and
memory. Ramipril and losartan pre-treatment overturned
the scopolamine-induced memory impairment, oxidative
stress and hippocampal degeneration which were marked
by the results from behavioral, biochemical and histological
C. Saline or scopolamine (16mg/kg, i.p.) was administered
to male Wistar rats. The other three groups were pre-treated
with Nigella sativa oil (NSO) (1ml/kg, p.o.), wheat germ oil
(WGO) (170mg/kg, p.o.) and donepezil used as a reference
drug (10mg/kg, p.o.) for 14 days before scopolamine
injection. Cognitive and biochemical measurements were
then assessed. NSO and WGO treated rat’s expressively
overturned scopolamine-induced shortage of spatial and
non-spatial functioning memory deficiency in the T maze
change task and object recognition test, respectively .
D. Naringenin (50 and 100mg/kg) and donepezil (2.5mg/
kg) were orally administered for 7 successive days. At the
end of the treatment period, dementia was prompted by a
single injection of scopolamine (20mg/kg; i.p). Scopolamine
caused memory impairment that was combined by
modifications in the projected neurotransmitters and acetyl
cholinesterase action as well as enlarged brain oxidative
stress. Pre-treatment with naringenin in both doses eased
scopolamine-induced behavioural, neuro chemical and
histological alterations in a manner similar to donepezil
E. Morris water maze scale was engaged to test the
amnesic influence of scopolamine and its reversal by B.
monniera. Rota rod test was conducted to screen muscle
coordination activity of mice. Scopolamine expressively
reduced the acquisition and recovery of memory making
both antero grade and retrograde amnesia .
i. In normal rats, Bifemelane Hydrochloride (30mg/
kg, i.p.) slightly increased acetylcholine (ACh) content in
the cerebral cortex. Scopolamine (1mg/kg, i.p.) decreased
ACh level and pre-treatment of Bifemelane Hydrochloride
attenuated the decrement of ACh level in the rats .
ii. The properties of cholinesterase inhibitors, cholinergic
agonists, dopaminergic agonists and dopaminergic
antagonists on the hyperactivity resulted by the muscarinic
cholinergic antagonist scopolamine were assessed in mice.
Scopolamine (0.3-10mg/kg) produced a dose-related
increase in loco motor activity, with a peak effect at 3.0mg/
iii. Atropine and scopolamine in low doses intensify
basic activity, increase amphetamine stereotypy, and
suppress catalepsy induced by injection of haloperidol. High
doses lower body temperature, antagonize amphetamine
stereotypy, and intensify the hypnotic action of chloral