Biology subjects

Zelena, D.

Publications and source records attributed to Zelena, D..

3 recordsLinked to original sources

bioRxiv2022

Recruitment of Corticotropin-releasing Hormone CRH Neurons in response ton Categorically Distinct Stress Challenges in the Mouse Brain

1.Corticotropin-releasing hormone (CRH) neurons in the paraventricular hypothalamic nucleus (Pa) are in the position to integrate stress-related information and initiate adaptive neuroendocrine-, autonomic-, metabolic- and behavioral responses. In addition to hypophyseotropic cells, CRH is widely expressed in the CNS, however their involvement in organization of the stress response is not fully understood. In these experiments, we took the advantage of recently available Crh-IRES-Cre; Ai9 mouse line to study the recruitment of hypothalamic and extrahypothalamic CRH neurons in categorically distinct, acute stress reactions. Reporter mice were exposed to restraint, ether, high salt and lipopolisacharide stress. The induced activation of CRH neurons was detected by colocalization of immediate early gene c-Fos in Td tomato expressing cells. We found differential activation of CRH neurons in central amygdaloid nucleus (Ce), bed nucleus stria terminalis lateral division, ventral posterior (BSTLVP), medial preoptic nucleus (MPO), ventromedial hypothalamic nucleus (VMH), premammillary nucleus (PM) and prepositus hypoglossal nucleus (Pr) in response to physiological (ether, high salt and LPS) and psychological (restraint) stressors. CRH positive cells in Pa became activated, however in the Barringtons nucleus and locus coeruleus no actiovation could be observed due to most tested stressors. Furthermore no CRH neuron activation occured in dorsal (BSTLD) and posterior (BSTLP) region of lateral division of bed nucleus stria terminalis after restraint stress. In the inferior olive only ether exposition resulted in CRH neuron activation. These results confirm activation of CRH neurons in the Pa, reveals new subset of stress-related CRH cells through the mouse brain and disprove the recruitment of CRH cells in the SOL and in the Barringtons nucleus to acute psychological stress in mice.

neuroscience↗

bioRxiv2022

A thalamo-preoptic pathway promoting social touch

Social touch is an important form of communication, it is still unknown how it is processed. Here, we discovered a functional role for a neuronal pathway projecting from the posterior intralaminar thalamic nucleus (PIL) to the medial preoptic area (MPOA) in controlling social contact. Neurons in the PIL and the MPOA were activated by physical contact between female rodents and also by chemogenetic stimulation of PIL neurons. Chemogenetic stimulation of PIL neurons tagged by social contact experience increased direct physical interactions between familiar female rats without affecting other forms of social behavior. Furthermore, selective stimulation of the PIL-MPOA pathway, and the local activation of PIL terminals within the MPOA, elevated direct social contact between the animals suggesting the role of pathway-specific activated cell assemblies. Neurons projecting from the PIL to the MPOA contain the neuropeptide parathyroid hormone 2 (PTH2). The expression of the peptide was induced by social housing, the presence of PTH2 receptor was identified in MPOA neurons, and local injection of PTH2 increased the firing rate of identified preoptic area GABAergic neurons via the PTH2 receptor suggesting that PTH2 acts as a neurotransmitter in the PIL-MPOA pathway. We also found a homologous PIL to MPOA neuronal pathway in the human brain. Altogether, we discovered a direct thalamo-preoptic pathway, which bypasses the cerebral cortex and controls social touch. This pathway originates in neurons expressing PTH2, a neuropeptide recently shown in fish to respond to the social environment. These observations provide evidence for common evolutionary-conserved PTH2-containing social-touch specific engram circuits.

neuroscience↗

bioRxiv2020

Somatostatin neurons of the bed nucleus of stria terminalis enhance associative fear memory consolidation in mice

Excessive fear learning and extinction-resistant fear memories are core symptoms of anxiety and trauma-related disorders. Despite significant evidence from clinical studies reporting hyperactivity of the bed nucleus of stria terminalis (BNST) under these conditions, the role of BNST in fear learning and expression is still not clarified. Here, we tested how BNST modulates fear learning in mice using a chemogenetic approach. Activation of GABAergic neurons of BNST during fear acquisition, more specifically the consolidation phase, resulted in enhanced cued fear recall. Importantly, BNST activation had no acute impact on fear expression during conditioning or recalls, but it enhanced cued fear recall subsequently, potentially via altered activity of downstream regions as indicated by c-Fos. Enhanced fear memory consolidation could be replicated by selectively activating somatostatin neurons (but not corticotropin releasing factor neurons), suggesting significant modulation of fear memory strength by specific circuits of BNST.

neuroscience↗