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Repetitive sensory input induces long-term potentiation of pyramidal cell synapses in mouse somatosensory cortex by activation of higher-order thalamic projections and disinhibition of local interneurons.
A study shows that application of spatiotemporally patterned epidural electrical stimulation alongside rehabilitation allowed individuals with spinal cord injury and severe locomotor deficits to walk with limited assistance.
Two studies show that tau pathology drives the expression of complement molecules that in turn promote the phagocytosis of synapses and neuroinflammation.
Dopamine released in the rodent prefrontal cortex increases the signal-to-noise ratio of responses to aversive stimuli that are transmitted to the periaqueductal grey.
In a genetic mouse model related to schizophrenia, restoring the excitability of parvalbumin-expressing interneurons in hippocampal CA1 ameliorates network dysfunction and behavioural deficits.
Vagal afferents projecting from the gut to the brainstem and then relayed on to the midbrain carry reward signals that trigger dopamine release in the dorsal striatum.
Study shows that population activity in the rat lateral entorhinal cortex can encode the passage of time, which may contribute to temporal aspects of episodic memory.
Hippocampal cannabinoid 1 receptors are shown to be involved in the formation of incidental associations between pairs of low-salience sensory stimuli, which can then become indirectly associated with certain cues and thus influence behaviour.
Mice receiving autoantibodies against the GluA2 AMPA receptor subunit from individuals with autoimmune encephalitis exhibit changes in AMPA receptor subunit composition and impaired synaptic plasticity and memory.
Spontaneous activity in the developing auditory system is maintained by a homeostatic mechanism and is important for cochlear neuron subtype specification.
Progressive hyperpolarization of ventricular zone progenitors regulates their sequential differentiation and migration in mouse primary sensory cortex.
A study shows that, in a mouse model of neuronopathic Gaucher disease, delivery of a gene therapy into the brains of fetal animals prevents neurodegeneration, ameliorates associated neuroinflammation and promotes survival.