Exposure from excessive noise exposure in occupational and

to noise is major contribution factor to acquired hearing loss. Hearing loss
caused by acoustic overexposure is associated with cochlea injury including the
loss of sensory hair cells and primary auditory neurons in cochlea. Hearing
loss is the greatest cause sensory disability (WHO) affecting up to 1 in 6 of the population. It is estimated
that approximate 20% of the burden is generated from excessive noise exposure
in occupational and leisure setting (Thorne
et al 2008). Sustain exposure to sound pressure level >85dBa noise lead
to irreversible damage to the sensory structure of cochlea. Once damage, the
mammalian sensory hair cells do not regenerate and the loss of hearing is
permanent. NIHL (Noise induce hearing loss) also excerts effects beyond the
classical pathway. NIHL suppress neurogenesis in hippocampus and alter the
spatial tuning of hippocampus, neurons as animals navigate through a maze (Goble et al. 2009; Kraus 2010; Newmann
2015). Hearing loss has been
associated with cognitive decline in the elderly and is considered to be an
independent risk factor for dementia. One of the most common causes for
acquired sensorineural hearing loss is exposure to excessive noise, which has
been found to impair learning ability and cognitive performance in human
subjects and animal models. The mechanisms underlying the decline of cognitive
functions after noise exposure are not entirely clear (Lijie Liu et al

Uran et al 2012 reported that a mild
disruption in the hippocampal region after noise exposure along with
significant behavioral abnormalities and also hypothesized that an exposure of
developing rats to noise of moderate intensity was sufficient trigger change in
the hippocampus that could underlie the observed behavioral effect. Another study
was done on male SD rats to observe the effect of chronic noise reported that
expression of N-methyl-D-aspartic acid receptor 2B (NR2B) decreased
significantly which resulted in tau hyper phosphorylation and neural apoptosis
in hippocampus. It may play a role in chronic noise induced neural apoptosis
and cognition impairment. (Cui Bo et al. 2013). Noise could persistently
suppress cell proliferation thereby reducing neurogenesis and also showed a
reduced number of DCX labeled precursor and the rate of cells in noise exposed
rats. A similar connection between total number of neuronal precursors and rate
of cell proliferation has been observed in earlier studies (Kraus 2010),

Currently, prosthetic devices such as hearing
aids and cochlear implants are the only treatments for NIHL. Both options are
costly, and neither can mitigate cochlear injury. Therefore, there is a strong
demand for novel pharmacological or molecular treatments of hearing loss. Targeting
adenosine receptors
in the cochlea has recently shown promise for the treatment of hearing loss S.M.
Vlajkovic 2014). Adenosine is an endogenous neuromodulator and a cyto-protective
substance released from tissues in response to stress (S.H. Snyder 1985).
Adenosine can enhance endogenous antioxidant defenses, increase oxygen supply,
improve blood flow, inhibit glutamate release, trigger anti-inflammatory
responses, and promote antiapoptotic pathways (B.B. Fredholm 2007).
Adenosine can also promote angiogenesis, which may be crucial in tissue repair after
injury (T. H. Adair 2005).

In this study, we focused on the role of adenosine
receptor in development of neural injury in cochlea and different region of
hippocampus i.e. CA1, CA3, DG
associated with acoustic overexposure. Adenosine is an endogenous
neuromodulator whose effects are mediated by four types G-protein coupled
adenosine (A1, A2A, A2B, A3) are
differentially localized in cochlea tissues with the strongest immune
expression in sensory hair cell, supporting deiters cells, spiral ganglion
cells (SGN), (Vljkovic et al 2007)
and in hippocampus i.e. CA1, CA3, DG
region. Thus, drugs that increase the concentration of endogenous
adenosine or directly activate adenosine receptors could play a pivotal role in
the protection of the organ of Corti against cisplatin cytotoxicity.

In this paper
investigates the role of adenosine A2Areceptor signaling in the
regulation of noise induce hearing loss, memory impaired and explores the
therapeutic potential of selective adenosine A2A receptor agonist CGS21680
in mitigating noise induce hearing and memory impairment.

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