The World Health Organization (WHO) recently reported that hearing impairment affects around 5% of the world’s population, regardless of age, which will affect 1 in every 10 (or every 4 in those older than 60 years) by 2050. Hearing impairment has a higher possibility of occurrence in individuals with comorbidities like occlusive diseases, head trauma, CNS infection, autoimmune diseases or over exposure of ototoxic drugs with a specific reference to anticancer drugs like cisplatin, antibiotics and loop diuretics head and neck injury, ear infection, headaches, migraine, depression, epilepsy, traumatic brain injuries, coagulopathy, and other brain disorders. As a Research Assistant Professor in auditory neuroscience, I am curious like a monkey infant and committed to enhancing our understanding of hearing disorders. My work is centered on the use of a chicken as a simple model to gain insights into the functioning of auditory circuits at auditory brainstem.
Over the years, I have honed my expertise in electrophysiology, biochemistry, and molecular biology, and gained a deep understanding of the intricate cellular mechanisms of protein kinases that regulate neural activity in all areas of brain however I am focused on hippocampus, cortex, and auditory brainstem. My research has contributed to several studies that have illuminated the ways in which brain circuits develop and are controlled by several kinases. At present I am particularly interested in auditory circuits of chicken at first order nuclei, electrophysiological properties of neural populations, such as the nucleus magnocellularis and nucleus laminaris that plays primary role in auditory signal processing received directly from vestibular nerve eight. I believe that this information can be leveraged to improve our understanding of hearing disorders and to develop better treatment options, especially at the higher auditory nuclei. We are interested in exploring the pathophysiology of auditory circuits in the CNS and potential risk factors at molecular level. As we know, the brainstem relies on adequate blood supply, and the same risk factors that contribute to cardiovascular disease can also affect blood flow to the brainstem, leading to reduced auditory processing ability. There is an urgent need to understand how metabolic disorders lead to compromised blood flow and the availability of neurotrophins that play an essential role in shaping the development and function of auditory circuits in the brainstem. My current research is investigating the regulation of Kv and HCN channels in the nucleus magnocellularis and laminaris through neurotrophins, a family of proteins critical to the development and survival of neurons. Our group has published several articles in high-impact factor journals that shed light on the role of neurotrophins, for eg. how brain-derived neurotrophic factor (BDNF) regulates dendritic pruning and the development of ipsilateral vs. contralateral connections in the auditory brainstem.
Apart from the unique neuronal properties involving Kv and HCN channels, my research group has also focused on the expression of Kv channels in the NM, which are tonotopically organized. This means that they have a higher density in the caudal region, where neurons respond to low frequency sounds our group has identified this area as NMc. This allows for precise regulation of the firing rates of these neurons in response to low-frequency sounds. In contrast, HCN channels are more densely expressed in the rostral region of the NM, where neurons respond to high-frequency sounds. This reflects the need for precise temporal coding of high-frequency sounds, which is accomplished through the activity of HCN channels. The activity of HCN channels can also modulate the activity of Kv channels. HCN channels can generate a depolarizing current that can counteract the hyperpolarizing current generated by Kv channels, leading to an overall increase in neuronal excitability. This interaction between Kv and HCN channels can shape the firing patterns of NM neurons. Spontaneous firing rate could be a guiding factor for the development of these circuits whereas phosphorylation of specific residues on Kv and HCN channels to either enhance or reduce their activity shaping tonotopy. Our knowledge is subtle, but we know that phosphorylation of specific residues on Kv1.1 channels by PKC and PKA has been shown to increase their activity in the NM. Similarly, phosphorylation of specific residues on HCN channels by PKG and other protein kinases can modulate their activity. How these kinases are governed by neurotrophins and play an important role in developing tonotopic auditory circuits, I am trying to solve the clues.
I am very much open to discuss my latest research in auditory neuroscience, exchange ideas with other researchers, and explore potential collaborations that may lead to new findings and advances in the field.
ORCID