Loading…
Neuroscientists at the Indian Institute of Science, Bengaluru, identified the brain circuit that produces cold allodynia — pain triggered by ordinarily harmless cold — a common side effect of chemotherapy.
The study, published online in Cell Reports on 25 June 2026, traced inputs from the lateral parabrachial nuclei in the brainstem to the parafascicular nuclei of the medial thalamus in mice.
Those thalamic neurons were nociceptive, sensitised by peripheral neuropathy and acutely aversive, driving both the sensory and the affective-motivational responses to cold pain.
The work was done at IISc's Centre for Neuroscience in the laboratory of Arnab Barik, using intersectional viral genetics, in vivo imaging and ex vivo physiology.
Pain produced by a stimulus that does not normally hurt — a cool breeze, a light touch. It arises when injured nerves or sensitised central circuits misread harmless input as damage, which is why ordinary painkillers often fail.
Simple Analogy: A smoke alarm that shrieks when you boil a kettle.
The brain's main relay station: almost all sensory signals except smell pass through it before reaching the cerebral cortex. The parafascicular and centromedian nuclei belong to its intralaminar group.
Ion channels that sense cold in peripheral nerve endings; they are the classic molecular explanation for cold allodynia, while this study addresses the central circuit.
Cold allodynia is managed with pregabalin, gabapentin or duloxetine, topical lidocaine or capsaicin, and warmth — all symptomatic, none targeting the circuit.
GS Paper 3 > Science and Technology > Developments in biotechnology and health
General Awareness > Science and Indian research institutions
A neuropathic condition in which mildly cold temperatures produce burning or freezing pain.
Chemotherapy-induced peripheral neuropathy — nerve damage caused by anti-cancer drugs, especially platinum agents such as oxaliplatin.
A nucleus of the intralaminar group of the medial thalamus, shown here to receive brainstem pain inputs.