Topic: chemogenetic inactivation

Cholinergic activity is thought to play an important role in learning and the control of brain state. Multiple studies have shown that pairing external phasic stimulation of the cholinergic basal forebrain (CBF) with a sensory stimulus drives long-lasting sensory cortical plasticity, implicating the CBF as a potential substrate for associative learning. For this to be ecologically valid, we hypothesized that CBF projections to the sensory cortex should exhibit phasic signaling that is temporally-synchronous with sensory-evoked responses in cortical neurons. Intrinsic sensory-evoked responses h

The hippocampal formation is a crucial region in the encoding and retrieval of memory, thought to be mediated through ensemble formation and recruitment or intrinsic attractor dynamics. Additionally, it has been shown that overall hippocampal population activity reflects environmental novelty. However, a common neural basis supporting these two processes remains unknown. Furthermore, many memories contain overlapping features, and it remains to be established how specific memories are retrieved without interference in the hippocampus. We propose that both engram and attractor models hinge on l

Memory consolidation is an essential process for our everyday lives. Memory representations are initially encoded in the hippocampus before being consolidated in the neocortex by synaptic plasticity processes that depend on protein synthesis. Within prefrontal cortex (PFC), inhibitory interneurons are critical in gating incoming hippocampal inputs and shaping pyramidal neuron responses. However, how molecular pathways affect synaptic signaling during memory consolidation is unclear. We hypothesize that mechanistic Target Of Rapamycin Complex 1 (mTORC1), a central regulator of protein synthesis

The loss of memories is the earliest and often most detrimental symptom in the course of Alzheimer’s disease (AD), the most common form of dementia. The loss of neuronal cells, which are assumed to carry mnemonic information, suggests itself to be the leading cause of memory loss. Besides, the question of alternative mechanisms has been raised. Our lab recently showed that an additional cell ensemble, so-called novelty-like cells, interfered with the engram and thus, impaired memory recall. This suggests a novel mechanism of memory impairment. However, the exact circuit that leads to the evoca