Muscle spindles provide flexible sensory feedback for movement sequences.

Sensory feedback is essential for motor performance and must adapt to task demands. Muscle spindle afferents (MSAs) are a major primary source of feedback about movement, and their responses are readily modulated online by gain-controller fusimotor neurons and other mechanisms. They are therefore a powerful site for implementing flexible sensorimotor control.

Calcitonin Related Polypeptide Alpha Mediates Oral Cancer Pain.

Oral cancer patients suffer pain at the site of the cancer. Calcitonin gene related polypeptide (CGRP), a neuropeptide expressed by a subset of primary afferent neurons, promotes oral cancer growth. CGRP also mediates trigeminal pain (migraine) and neurogenic inflammation.

Naturalistic Spike Trains Drive State-Dependent Homeostatic Plasticity in Superficial Layers of Visual Cortex.

The history of neural activity determines the synaptic plasticity mechanisms employed in the brain. Previous studies report a rapid reduction in the strength of excitatory synapses onto layer 2/3 (L2/3) pyramidal neurons of the primary visual cortex (V1) following two days of dark exposure and subsequent re-exposure to light. The abrupt increase in visually driven activity is predicted to drive homeostatic plasticity, however, the parameters of neural activity that trigger these changes are unknown.

Locus coeruleus-norepinephrine: basic functions and insights into Parkinson's disease.

The locus coeruleus is a pontine nucleus that produces much of the brain's norepinephrine. Despite its small size, the locus coeruleus is critical for a myriad of functions and is involved in many neurodegenerative and neuropsychiatric disorders. In this review, we discuss the physiology and anatomy of the locus coeruleus system and focus on norepinephrine's role in synaptic plasticity.

Input-Specific Metaplasticity in the Visual Cortex Requires Homer1a-Mediated mGluR5 Signaling.

Effective sensory processing depends on sensory experience-dependent metaplasticity, which allows homeostatic maintenance of neural network activity and preserves feature selectivity. Following a strong increase in sensory drive, plasticity mechanisms that decrease the strength of excitatory synapses are preferentially engaged to maintain stability in neural networks. Such adaptation has been demonstrated in various model systems, including mouse primary visual cortex (V1), where excitatory synapses on layer 2/3 (L2/3) neurons undergo rapid reduction in strength when visually deprived mice are reexposed to light.

Homer1a Is Required for Establishment of Contralateral Bias and Maintenance of Ocular Dominance in Mouse Visual Cortex.

It is well established across many species that neurons in the primary visual cortex (V1) display preference for visual input from one eye or the other, which is termed ocular dominance (OD). In rodents, V1 neurons exhibit a strong bias toward the contralateral eye. Molecular mechanisms of how OD is established and later maintained by plastic changes are largely unknown.

Rebound potentiation of inhibition in juvenile visual cortex requires vision-induced BDNF expression.

The developmental increase in the strength of inhibitory synaptic circuits defines the time window of the critical period for plasticity in sensory cortices. Conceptually, plasticity of inhibitory synapses is an attractive mechanism to allow for homeostatic adaptation to the sensory environment. However, a brief duration of visual deprivation that causes maximal change in excitatory synapses produces minimal change in inhibitory synaptic transmission.