The smells that newborn mice are exposed to affect many social behaviours later in life. How this 'imprinting' occurs has been a mystery.
Scientists from Japan have now discovered the molecules necessary for imprinting. Their new study sheds light on the decision-making process and neurodevelopmental disorders such as autism spectrum disorders. It also proposes a more effective use of oxytocin therapy for such disorders at an early age.
Imprinting is a popularly known phenomenon, wherein certain animals and birds become fixated on sights and smell they see immediately after being born. In ducklings, this can be the first moving object, usually the mother duck. In migrating fish like salmon and trout, it is the smells they knew as neonates that guides them back to their home river as adults. How does this happen?
Exposure to environmental input during a critical period early in life is important for forming sensory maps and neural circuits in the brain. In mammals, early exposure to environmental inputs, as in the case of imprinting, is known to affect perception and social behaviour later in life. Visual imprinting has been widely studied, but the neurological workings of smell-based or "olfactory" imprinting remain a mystery.
To find out more, scientists from Japan, including Drs. Nobuko Inoue, Hirofumi Nishizumi, and Hitoshi Sakano at University of Fukui and Drs. Kazutaka Mogi and Takefumi Kikusui at Azabu University worked on understanding the mechanism of olfactory imprinting during the critical period in mice. Their study, published in eLife, offers fascinating results.
The study adds valuable new insights to our understanding of decision making and mental struggle in humans and reveals new research paths in the neuroscience of all types of imprinting.
"We discovered three molecules involved in this process," reports Dr Nishizumi, "Semaphorin 7A (Sema7A), a signalling molecule produced in olfactory sensory neurons, Plexin C1 (PlxnC1), a receptor for Sema7A expressed in the dendrites of mitral/tufted cells, and oxytocin, a brain peptide known as the love hormone."
During the critical period, when a newborn mouse pup is exposed to an odour, the signalling molecule Sema7A initiates the imprinting response to the odour by interacting with the receptor PlxnC1. As this receptor is only localized in the dendrites in the first week after birth, it sets the narrow time limitation of the critical period. The hormone oxytocin released in the nursed infants imposes the positive quality of the odour memory.
It is previously known that male mice normally show strong curiosity toward unfamiliar mouse scents of both genders. "Blocking" Sema7A signalling during the critical period results in the mice not responding in their usual manner; they display avoidance response to the stranger mice.
An interesting result of this study is the conflicting response to aversive odours. Let's say, a pup is exposed to an innately aversive odour during the critical period; this imprinted odour will now induce a positive response against the innate natural response towards the odour. Here, the hard-wired innate circuit and the imprinted memory circuit compete, and the imprinting circuit takes over. To solve this dilemma and reach a conclusion, the brain must have detailed a mechanism of crosstalk between the positive and negative responses, which opens a variety of research questions in the human context.
So, what do these results say about the human brain?
First, the results of the study open many research questions for the functioning of the human brain and behaviour. Like the critical period in the mouse olfactory system, can we find such a period in humans, possibly in other sensory systems? The way the mouse brain chooses imprinted memory over innate response, do we humans also follow similar decision-making processes?
Secondly, this study also suggests that improper sensory inputs may cause neurodevelopmental disorders, such as autism spectrum disorders (ASD) and attachment disorders (AD).
Oxytocin is widely used for treating ASD symptoms in adults. However, Dr Nishizumi says, "our study indicates that oxytocin treatment in early neonates is more effective than after the critical period in improving the impairment of social behaviour. Thus, oxytocin treatment of infants will help prevent the ASD and AD, which may open a new therapeutic procedure for neurodevelopmental disorders."
