Somatosensory Crossmodal Plasticity in Superior Colliculus of Visually Deafferented Rats

Terminal fields of a certain pathway result denervated if the regeneration after the lesion of the pathway fails. If the lesion happened in a young animal, terminal fields of other nervous pathways that are spatially coincident or are close to the denervated field, growth of axon collaterals or reactive synaptogenesis could take place and reinervate deafferented neurons. In that way these denervated neurons can be recruited for functional compensatory responses and can convey information to areas that result enriched with additional inputs to be processed. The present paper reviews the plastic reactions that take place in the superior colliculus, a mesencephalic layered structure, after the neonatal suppression of its visual afferents that terminate in its superficial layers. The postlesional reactive ascending growth of somatosensory afferents that in control animals innervate intermediate and deep collicular layers invade the superficial layers and connect with visually deafferented cells that result recruited for descendent collicular responses and to send sensory information to the visual cortex via the colliculo-geniculate payhway. In that way in neonatally deafferented animals, somatosensory information gains additional territory to be processed. Two somatosensory connections to the superior collicuus will be discussed in this review. One ascending from the cuneitorm nucleus and the other descending that originates in the barrel cortex.

Astrocytes promote peripheral nerve injury-induced reactive synaptogenesis in the neonatal CNS

Neonatal damage to the trigeminal nerve leads to “reactive synaptogenesis” in the brain stem sensory trigeminal nuclei. In vitro models of brain injury-induced synaptogenesis have implicated an important role for astrocytes. In this study we tested the role of astrocyte function in reactive synaptogenesis in the trigeminal principal nucleus (PrV) of neonatal rats following unilateral transection of the infraorbital (IO) branch of the trigeminal nerve. We used electrophysiological multiple input index analysis (MII) to estimate the number of central trigeminal afferent fibers that converge onto single barrelette neurons. In the developing PrV, about 30% of afferent connections are eliminated within 2 postnatal weeks. After neonatal IO nerve damage, multiple trigeminal inputs (2.7 times that of the normal inputs) converge on single barrelette cells within 3–5 days; they remain stable up to the second postnatal week. Astrocyte proliferation and upregulation of astrocyte-specific proteins (GFAP and ALDH1L1) accompany reactive synaptogenesis in the IO nerve projection zone of the PrV. Pharmacological blockade of astrocyte function, purinergic receptors, and thrombospondins significantly reduced or eliminated reactive synaptogenesis without changing the MII in the intact PrV. GFAP immunohistochemistry further supported these electrophysiological results. We conclude that immature astrocytes, purinergic receptors, and thrombospondins play an important role in reactive synaptogenesis in the peripherally deafferented neonatal PrV.

Protective and regenerative response endogenously induced in the ischemic brain

Neuronal cells are highly vulnerable to ischemic insult. Because adult neurons are highly differentiated and cannot self-propagate, loss of neurons often results in functional deficits in mammalian brains. However, it has recently been shown that neurons and neuronal circuits exhibit protective and regenerative responses in a rodent model of experimental ischemia. At first, neurons respond by producing several protective proteins such as heat shock proteins (HSPs) after sublethal ischemia and then acquire tolerance against a subsequent ischemic insult (ischemic tolerance). Once neurons suffer irreversible injury, two repair processes, neurogenesis and synaptogenesis, are endogenously induced. Neuronal stem and (or) progenitor cells can proliferate in two brain areas in adult animals: the subventricular zone and the subgranular zone in the dentate gyrus. After ischemic insult, these stem (progenitor) cells proliferate and differentiate into neurons in the dentate gyrus of the hippocampus. Reactive synaptogenesis has been also observed in the injured brain following a period of long-term infarction, but it is unclear if it can compensate for disconnected circuits. Understanding the molecular mechanism underlying these protective and regenerative responses will be important in developing a new strategy for aimed at the augmentation of resistance against ischemic insult and the replacement of injured neurons and neuronal circuits.Key words: ischemic tolerance, neurogenesis, synaptogenesis.