TDK conference 2020

Signalling through the tyrosine receptor kinase-B (TrkB) is essential in neuronal development and synaptic plasticity, but the specific functions of TrkB on distinct neuronal subpopulations remains elusive. Somatostatin-expressing (SOM+) interneurons - a large ratio of which expresses TrkB - have been previously implicated in the modulation of several behavioural processes, particularly passive coping responses when facing a stressful challenge. Here, we aimed to assess the contribution of TrkB to SOM+-interneuron-mediated regulation of such coping responses in a wide-scale battery of behavioural testing procedures employing conditional knock out (CKO) mice lacking TrkB on SOM+ interneurons.

SOM-TrkB CKO mice were created from C57BL/6 mice using the cre-lox technique. First, a set of subjects underwent a wide range of tests assessing numerous behavioural domains (motor functions, anxiety, cognitive performance, social behaviour, fear memory). Then a separate set of subjects underwent a test battery directly assessing acute coping responses in stressful conditions.

While SOM-TrkB CKO mice showed no differences in motor activity, anxiety, social and cognitive behaviour, they consistently displayed a generally more active coping response in coping tests such as the backtest, tail suspension test and forced swim test characterized by decreased immobility when compared to wild type control subjects. Furthermore, during Pavlovian fear conditioning, subjects exhibited dampened acute fear responses and showed deficits in fear memory acquisition indicated by decreased freezing behaviour.

Our results demonstrate that deficient TrkB signalling on SOM+ interneurons promotes a behavioural shift towards more active coping responses when facing stressful challenges, suggesting that TrkB signalling is involved in the SOM+-interneuron-dependent modulation of passive coping responses.