Topic: Designer receptors exclusively activated by designer drugs

Designer receptors exclusively activated by designer drugs (DREADD) are chemogenetic tools that enable the selective activation or silencing of neurons in a given brain area. According to classical findings on the role of the lateral hypothalamic area (LHA) in hunger, we hypothesized that selective silencing of the LHA may decrease food intake.We bilaterally injected adeno-associated viral (AAV) vectors carrying the gene of a modified M4 muscarinic acetylcholine receptor into the LHA of rats. Later, rats were treated with DREADD actuator agents and food intake was measured in a 30 min time-win

The balance between excitatory and inhibitory systems is crucial for the normal functioning of the brain, and dysfunction in the inhibitory system may be a potential mechanism for psychosis. Current studies emphasize parvalbumin-positive (PV+) GABAergic interneurons as a key component in the development of schizophrenia symptoms, with reduced PV protein levels found in cortical PV+ interneurons in individuals with schizophrenia. Rodent models of schizophrenia indicate that the medial prefrontal cortex (mPFC) is the main structure where PV neurons exhibit aberrant function. However, it is still

Communication between neurons and glial cells are crucial to establish and maintain brain function. Some of these interactions are activity-dependent, yet it remains unexplored how acute changes in neuronal activity affect neuron-to-glial dynamics.Here, we used excitatory and inhibitory designer receptors exclusively activated by designer drugs (DREADD) based chemogenetic methods to study the effects of acute manipulations of a subpopulation of layer 5 cortical projection and dentate gyrus neurons in adult (Rbp4Cre) mouse brain after 90 minutes. We validated changes in activity with in vitro p

Disturbances in the neuronal activity of the hippocampal CA2 subregion have been shown to result in impaired social memory in rodents. However, the current assessment of behavioural role of CA2 within the circuit of cognition relies on classical tests, presenting only a snapshot of the behaviour of subjects. As both clinical and preclinical data have revealed a relevance for CA2 in psychiatric disorders such as schizophrenia, it is crucial to uncover the effects of CA2 E/I imbalance in more natural social environments over longer periods of time. Furthermore, gaining a deeper understanding of

Neurons in the centromedial amygdala (CeM) are activated during fear memory formation. We designed a new viral vector, AAV9-pfos-hM4Di:mCherry:PEST expressing Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) under a c-fos promoter, enabling the specific manipulation of activated neurons. We use this viral vector to temporarily inactivate the neurons involved during cued-fear learning in the CeM and to uncover their molecular profile.Male and female wildtype C57BL/6J mice are injected with the viral vector in the CeM, exposing one group to the shocks paired with the tones (f