5. Reaction of microglia to deafferentation. Deafferentation induces an increase in the number, size of cell body, and processes of microglia in the PrV. This reaction is no longer present after recovery of ION function [38]. Although the effects of microglia reaction on synaptic plasticity in the PrV are still unknown, sensory afferents from whiskers do modify microglia function without a critical period.

6. Receptive fields of PrV cells. Receptive field properties of the PrV cells are investigated with in vivo recording techniques. In the first in vivo recordings of the rat PrV [49] the recorded cell types were not identified. Later studies [50] identified barrelette (relay) cells of the PrV by antidromic activation from thalamic stimulation, …show more content…
Presynaptic transmitter release probability of trigeminal afferent terminals. PrV cells receive whisker-sensory afferents via the trigeminal tract (TrV) formed by the central axonal branches of the TG cells. A paired-pulse protocol was used to reveal transmitter release probability (Pr) of TG central terminals. The Pr varied from low to high as shown by a Gaussian distribution of paired-pulse-ratio (PPR)[59]. This presynaptic property may facilitate the transmission of continuous TG responses[60] to the PrV neurons. Thus, the PrV is different from thalamic VPM and barrel cortex that receive exclusively high Pr presynaptic afferent terminals[61-70]. Neonatal ION transection induces death of 9-10% TG cells [25, 26]. The central terminals of surviving TG cells are still functional, although their peripheral branches are transected. The distribution of PPRs also fits to similar Gaussian function in the deafferented PrV [59], thus the broad spectrum of presynaptic transmitter release probability is not sensory …show more content…
Formation of inhibitory circuits. In neonatal brainstem slices, containing the PrV, stimulation of the trigeminal afferent fibers induces both postsynaptic excitatory and inhibitory responses in barrelette cells, suggesting that postsynaptic circuits have formed by birth. Latency analyses show that a monosynaptic circuit mediates the excitatory response, while a di-synaptic circuit mediates the inhibitory response [58]. Neonatal ION transection results in cell death in both TG [23-26] and PrV [27-29] and strengthening of excitatory synaptic connections as described above. The inhibitory response is still present in surviving barrelette cells, suggesting that formation and stabilization of inhibitory circuits in the PrV does not depend on sensory