Biomedicine: 2023; 43(2): 625-629 March-April 2023

Research article
Effect of valeric acid on the neurotransmitter levels of hippocampus on Alzheimer’s
induced rats
Blessina1, Bindhu S.2, Pramod K. L.3, Ashaiba Asiamma4
Department of 1Anatomy, 3Forensic Medicine and Toxicology,4Microbiology, Yenepoya Medical College, Yenepoya (Deemed
to be University), Mangalore, Karnataka, India
2
Department of Anatomy, K S Hegde Medical Academy, Nitte (Deemed to be University), Mangalore, Karnataka, India
(Received: February 2023 Revised: March 2023 Accepted: April 2023)
Corresponding author: Bindhu S. Email: [email protected]
ABSTRACT
Introduction and Aim: Though there are many drugs approved for treatment of Alzheimer’s disease (AD), there is
scope for exploring newer molecules for AD management, especially considering the side effects and drug interaction
profile of the existing drugs. The present study was conducted to assess the neuroprotective properties of valeric acid
by estimating the five neurotransmitters in the hippocampus of Wistar albino rats in an aluminium induced AD model.
Materials and Methods: In this experimental study design effects of valeric acid, piracetam and rivastigmine were
evaluated for changes in neurotransmitter levels. Seven groups were made out of 42 Wistar albino rats (male).
Aluminum chloride (AlCl3) (100 mg/kg body weight) was given orally for 42 days to cause AD. As a treatment,
valeric acid (50 mg/kg body weight) was administered to rats in group 3, piracetam was given to group 4, rivastigmine
to group 5, and a combination of piracetam and valeric acid to group 6 and valeric acid and rivastigmine to group 7
rats. After this, rat hippocampus is used to estimate acetylcholine (ACH), GABA, glutamate, dopamine, and serotonin
levels.
Results: ACH levels of the hippocampus in all treated groups (groups 3 to 7) showed more increase in comparison
to positive control (group 2) group. And remaining all groups demonstrated a considerable rise in GABA, glutamate,
dopamine, and serotonin levels, demonstrating the reversed AlCl3-induced impairment.
Conclusion: The neurotransmitter levels in aluminum chloride-induced neurological impairment appear to be
significantly improved by valeric acid and its use in combination with piracetam and rivastigmine.
Keywords: Alzheimer’s disease; acetylcholine; GABA; glutamate; dopamine; serotonin; valeric acid.
INTRODUCTION belonging to the statin group, has been shown “per se”
protecting its role against neuronal injury caused by

C
holinergic dysfunction as a component of
aluminium salts in hippocampus and cortex (3). An
Alzheimer’s disease (AD) is well established.
active component of green tea, epigallocatechin-
Among many animal models to evaluate the
gallate, loaded in nanoparticles, is shown to have a
effects of new molecules and treatment modalities,
protective role against aluminum induced
aluminum chloride induced AD in rats has carved its
neurobehavioral changes in AD induced rats (2).
own importance in terms of ease of performance of
Further, it is shown that co-administration of
behavioral studies, brain tissue accessibility and
rivastigmine and aluminium chloride normalizes the
histopathological documentation of amyloid bodies
expression of BACE1 (5), AChE and IL1B genes
specifying the neurodegeneration (1). It is proven on
indicating neuroprotection (6). Medicinal plants and
several studies that aluminum chloride at doses of 100
herbal treatments are currently attracting more
to 200 mg/kg body weight produces cognitive
attention and are a great source for developing
impairments mimicking AD in rats (2,3).
medicine for Alzheimer's (7). The anti-inflammatory
Quantification of neurotransmitters at after exposure
and antioxidant properties are suggested as possible
have shown that there is increase in aluminum in
mechanisms for beneficial effects (8). Systematic
hippocampus of the rat brains proving its
reviews of herbal medicines for dementia conclude
neurodegenerative effects (4). These accumulations
positively indicating a promising role in AD
are significant given the fact that hippocampus and
management (7,9). However, the quest for newer and
cerebral cortex are the areas of learning and memory.
better molecules for AD is ongoing. Though many
Therefore, it is prudent to utilize this established AD
drugs are approved for treatment of AD, there is scope
rat model for evaluation of study drugs among many
for exploring newer molecules for AD management,
researchers across the globe.
especially considering the side effects and drug
There is growing evidence that a plethora of drugs that interaction profile of the existing drugs.
were hitherto indicated for other medical conditions
Epilepsy, anxiety, and sleep disorders are routinely
improve cognitive dysfunction in aluminum induced
treated with herbal supplements that are widely used
AD models. Simvastatin, a lipid lowering agent
and generated from root extracts of Valeriana

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Blessina et al: Effect of valeric acid on the neurotransmitter levels of hippocampus on Alzheimer’s induced rats

officinalis (10). It has preventive effects against weight) (12). These oral medications were
neurodegenerative diseases like Parkinson's disease administered for 30 days (15) to treat the aluminum
(11) and interacts with various neurotransmitter chloride-induced cognitive alterations in rats. In group
systems. It can also control anxiety (12) and insomnia 6 and 7 with combination oral medication, a second
(13) by interacting with various neurotransmitter drug was administered after 30 minutes of first drug
systems (14). Neurological diseases have been treated administration.
with valeric acid, a straight chain alkyl carboxylic acid
All rats were sacrificed by cervical dislocation 24
that is naturally present in the Valeriana officinalis
hours after the treatment and their hippocampuses
(10,14). By measuring the five neurotransmitters in
separated from their brains on ice. The hippocampus
the hippocampus of Wistar albino rats using an
was homogenized in phosphate buffer with a pH of
aluminum-induced AD model, valeric acid
7.4, the homogenates centrifuged at 2000 rpm for 20
neuroprotective effects were assessed in the current
min, and the supernatant of the homogenates was
work.
utilized for the quantitative determination of the
MATERIALS AND METHODS neurotransmitters.
The effects of valeric acid, piracetam, and Quantification of neurotransmitters in homogenate of
rivastigmine on alterations in neurotransmitter levels hippocampus was performed using specific ELISA
were assessed in this experimental study design which kits (Rat Acetylcholine, Rat Gamma-aminobutyric
was carried out in the Dept. of Anatomy, Yenepoya Acid, Rat Dopamine D2 Receptor, Rat Glutamate and
Medical College, Mangalore in 2020. The study was Rat Serotonin, Bioassay Technology Laboratory,
approved by the Institutional Animal Ethics China), according to the manufacturer’s instructions.
Committee (approval letter number:
Quantification of neurotransmitters
YU/IAEC25/01/2020) and it was confined to the
CPCSEA's (Committee for the Purpose of Control and ACH, GABA, glutamate, dopamine, and serotonin
Supervision of Experiments on Animals) rules and levels
standards. In these tests, high sensitivity conjugates were used to
Experimental animals find the protein in samples of hippocampal
homogenate. For a 40μl sample, 10μl anti-GABA
We used 42 male Wistar albino rats, aged 4-6 months,
antibody is added for GABA estimation. For a 40μl
weighing 220-250g. They were kept in appropriate
sample, 10μl anti-ACHR antibody is added for
climatic conditions and housed in polypropylene
glutamate estimation. For a 40μl sample, 10μl anti-
cages at a temperature of 22±1°C. Rats used in the
GLM antibody is added for glutamate estimation. For
study were bred at the Liveonbiolabs in Bangalore
40μl sample, 10μl anti-D2R antibody is added for the
(Registration no. 1610/ROBiBt/S/2012/CPCSEA).
dopamine estimation. For a 40μl sample, 10μl anti-ST
They were maintained during the tests in
antibody is added for the serotonin estimation. The
dry polypropylene cages with husk. Four rats were
sample wells were then incubated for 1 hour at 37°C
housed in a single cage. Rats were marked on the head,
with 50μl of streptavidin-HRP. After 5 times washing
body, and tail with their cage number to help with
with a wash buffer, soaked wells with 0.35 ml wash
identification (15,16).
buffer for 1 minute for each wash. Positive samples
Rat model of Alzheimer’s disease obtained blue color when 50μl of substrate solution A
and 50μl of substrate solution B added to each well
Rats were categorized into seven groups. Group
and incubated (10 min) at 37°C in the dark. After
1(negative control) rats were given distilled water
adding 50μl of stop solution to the reaction, it was
orally, whereas remaining group rats were given
stopped, and within 10 minutes the absorbance at 450
aluminum chloride (AlCl3) at a dosage of 100 mg/kg
nm was measured. By comparing the samples' OD
body weight orally for 42 days to induce Alzheimer's
value to the standard curve, it was possible to estimate
disease (17). Group 2 was considered as positive
the amounts of neurotransmitters present in the
control and was not administered any medication to
samples.
address the aluminum induced defects.
Statistical analysis
Study drug administration
All the groups were subjected to one-way analysis of
Study drugs were administered on the 47th day. Group
variance (ANOVA) followed by Tukey Kramer’s test.
3 rats were given valeric acid (50 mg/kg body weight).
Statistical significance was set at P < 0.05.
Group 4 was administered with piracetam (200mg/kg
body weight) (13). Group 5 was given rivastigmine RESULTS
(0.5 mg/kg body weight) (14). Group 6 rats were given
ACH levels of the hippocampus in all treated groups
a combination of valeric acid (50 mg/kg body weight)
(groups 3 to 7) showed significant increase in
and piracetam (200 mg/kg body weight). Group 7 rats
comparison to positive control group (group 2) (table
were given a combination of valeric acid (50 mg/kg
1). This indicated significant reversal of impairment
body weight) and rivastigmine (0.5 mg/kg body

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Blessina et al: Effect of valeric acid on the neurotransmitter levels of hippocampus on Alzheimer’s induced rats

caused by AlCl3. Among all the treatment groups, between negative control and piracetam group (group
Group 3 (valeric acid) showed more ACH levels. 4).
There was a statistical difference between ACH levels
Table 1: Comparison of acetylcholine (ACH) levels of hippocampus between animal groups
Group number Animal Groups ACH levelsin µ/ml (mean ± SD)
1 Distilled water (DW) (Negative control) 177.57 ± 20.77
2 AlCl3(Positive control) 112.53±21.58a
3 Valeric acid 221.04±21.58b
4 Piracetam 189.02±12.78b
5 Rivastigmine 215.79±26.31b
6 Valeric acid+ Piracetam 199.72±31.16b
7 Valeric acid+ Rivastigmine 198.52±26.12b
Animal groups (n=6 rats in each group); p˂0.05 (values in comparison with negative control group) and bp˂0.05 (values in
a

comparison with positive control group)

All the treatment groups (groups 3 to 7) showed values in the treatment groups. There was statistical
marked increase in the level of GABA after the difference between GABA levels between negative
treatment showed reversal of impairment in the control and valeric acid group (group 3) and
neurotransmitter levels caused by AlCl3 (table 2). rivastigmine group (group 5).
Group 6 (valeric acid+ piracetam) reported the highest
Table2: Comparison of GABA levels of hippocampus between animal groups
Group number Animal Groups GABA levels in nmol/L (mean ± SD)
1 DW (Negative control) 440.52±72.61
2 AlCl3(Positive control) 181.46±63.8a
3 Valeric acid 449.07±74.15b
4 Piracetam 403.05±104.03b
5 Rivastigmine 436.34±97.29b
6 Valeric acid+ Piracetam 480.05±123.3b
7 Valeric acid+ Rivastigmine 409.48±48.16b
Animal groups (n=6 rats in each group); ap˂0.05 (values in comparison with negative control group) and bp˂0.05 (values in
comparison with positive control group)
All the treatment groups (groups 3 to 7) showed valeric acid group (group 3) showed no statistical
significant increase in the dopamine after the difference in comparison to negative control. There
treatment showing reversal of impairment caused by was a statistical difference among groups 4 to 7.
AlCl3 (table 3). Among all the treatment groups,
Table3: Comparison of Dopamine levels of hippocampus between animal groups
Group number Animal Groups Dopamine in ng/L (mean ± SD)
1 DW (Negative control) 1158.4±62.29
2 AlCl3(Positive control) 594.6±94.11@
3 Valeric acid 1185.29±123.56*
4 Piracetam 1024.9±158.08*
5 Rivastigmine 936.12±175.3*
6 Valeric acid+ Piracetam 932.43±126.96*
7 Valeric acid+ Rivastigmine 981.15±374.5*
Animal groups (n=6 rats in each group); @p˂0.05 (values in comparison with negative control group) and *p˂0.05 (values in
comparison with positive control group)
All the treatment groups (groups 3 to 7) showed treatment showing reversal of impairment caused by
significant increase in the glutamate after the AlCl3 (table 4).
Table4: Comparison of glutamate levels of hippocampus between animal groups
Group number Animal Groups Glutamate in µg/ml (mean ± SD)
1 DW (Negative control) 26.32±4.45
2 AlCl3(Positive control) 11.42±4.81@
3 Valeric acid 35.67±6.48*
4 Piracetam 31.66±6.96*
5 Rivastigmine 35.58±5.415*
6 Valeric acid+ Piracetam 35.26±6.11*
7 Valeric acid+ Rivastigmine 35.53±5.47*
Animal groups (n=6 rats in each group); @p˂0.05 (values in comparison with negative control group) and *p˂0.05 (values in
comparison with positive control group)

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All rats in the treatment groups (groups 3 to 7) showed serotonin. statistical difference in comparison to
significant increase in the serotonin after the treatment negative control. There was no statistical difference
(table 5). Among all the treatment groups, between negative control and groups 3, 4, 6 and 7.
rivastigmine group (group 5) showed lowest level of
Table5: Comparison of serotonin levels of hippocampus between animal groups
Group Animal Groups Serotonin in ng/ml (mean ± SD)
number
1 DW (Negative control) 52.41±5.27
2 AlCl3(Positive control) 16.59±12.8@
3 Valeric acid 55.96±9*
4 Piracetam 56.56±18.35*
5 Rivastigmine 45.88±6.13 *
6 Valeric acid+ Piracetam 53.7±11.59*
7 Valeric acid+ Rivastigmine 55.08±5.55*
Animal groups (n=6 rats in each group); @p˂0.05 (values in comparison with negative control group) and *p˂0.05 (values in
comparison with positive control group)
DISCUSSION have increased the overall effect of cognitive
impairment.
Systematic review of 13 studies evaluating herbal
medicines either as monotherapy or adjunct to routine Imbalance between GABAergic and glutaminergic
medications resulted significantly better outcomes neurotransmission contributes to the neuro
(15). However, there are innumerable methodological degenerative process in animal model AD (19).
drawbacks and differences among these studies that Among many functions of astrocytes, maintenance of
hinder unequivocal recommendation of herbal glutamate-glutamate shuttle is necessary for normal
medicines for regular human use. Many of these cognitive functions and for AD progression (20).
herbal extracts employ either direct or indirect effects Lavender extract effects on Amyloid beta 1–42
of ACH and acetylcholinesterase inhibition (8). induced AD rat model showed significant lower levels
Considering multiple targets including anti-oxidative of GABA and glutamate in comparison to positive
neuroprotective mechanism of actions by use of controls (21). Outcomes of our study agree with this
combination of approved drugs and herbal extracts study in aluminum model of rat AD.
provide extended opportunity to address the cognitive
There are no established direct links between
impairment at early stages.
dopamine-serotonin alterations and cognitive
First neurotransmitter imbalance implicated in dysfunctions of AD in humans (22). However, links of
cognitive changes in dementia is ACH (16). A marker serotonin and early depression characteristics of AD is
for cholinergic neuronal loss in the brain, acetyl well established (23). Functional interdependence
cholinesterase, is utilized to quantify the between dopamine and serotonin is the key factor in
neuroprotective role of green tea component designing and exploring new opportunities to address
epigallocatechin-gallate and it was proven that the early cognitive deterioration in AD (24). In this regard,
administration of nanoparticles of this component as pointed out from dopamine and serotonin
resulted in significant decrease on cholinergic normalization after use of valeric acid in our study aids
neuronal loss among aluminum induced AD rats (2). in understanding the interdependence of these two
Memory problems linked to brain monocyte varied neuro-signaling pathways.
infiltration were lessened by simvastatin treatment
CONCLUSION
(17). In another perspective the inhibition of
degradation of synaptic acetylcholine by rivastigmine When aluminum chloride causes neurological
is found effective in AD rats (6). Rivastigmine is impairment, valeric acid and its combination with
different from other cholinesterase inhibitors. It piracetam and rivastigmine seem to be effective at
inhibits both acetylcholinesterase and raising neurotransmitter levels. Valeric acid may
butyrylcholinesterase in a partially irreversible way therefore be a helpful choice in the treatment of
(18). Therefore, in these lines, along with neurodegenerative diseases like AD, which justifies
rivastigmine, donepezil and galantamine are in vogue more investigation into this area.
for AD management. In the present study, CONFLICT OF INTEREST
cholinesterase is not quantified. However, as increase
ACH levels found in this study may be partly Authors have no conflicts of interest to declare.
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