Decreased motoneuron survival in Igf2 null mice after sciatic nerve transection.

The search for therapeutic targets to prevent neurons from dying is ongoing and involves the exploration of a long list of neurotrophic factors. Insulin-like growth factor 2 (IGF2) is a member of the insulin family with known neurotrophic properties. In this study, we used Igf2 knockout (Igf2) neonate mice to determine whether Igf2 deficiency is detrimental to motor neuron survival after axonal injury.

Placental glycogen stores are increased in mice with H19 null mutations but not in those with insulin or IGF type 1 receptor mutations.

The function of glycogen in the placenta remains controversial. Whether it is used as a source of fuel for placental consumption or by the fetus in times of need has yet to be determined. Two imprinted genes, insulin-like growth factor 2 (Igf2) and H19 are highly expressed in the placenta.

IGF2 knockout mice are resistant to kainic acid-induced seizures and neurodegeneration.

Insulin-like growth factor 2 (Igf2), a member of the insulin gene family, is important for brain development and has known neurotrophic properties. Though Igf2, its receptors, and binding proteins, are expressed in the adult CNS, their role in the adult brain is less well-understood. Here we studied how Igf2 deficiency affects brains of adult Igf2 knockout (Igf2(-/-)) mice following neurotoxic insult produced by the glutamate analog kainic acid (KA).

Effect of kainic acid treatment on insulin-like growth factor-2 receptors in the IGF2-deficient adult mouse brain.

Insulin-like growth factor-2 (IGF2) is a member of the insulin gene family with known neurotrophic properties. The actions of IGF2 are mediated via the IGF type 1 and type 2 receptors as well as through the insulin receptors, all of which are widely expressed throughout the brain. Since IGF2 is up-regulated in the brain after injury, we wanted to determine whether the absence of IGF2 can lead to any alteration on brain morphology and/or in the response of its receptor binding sites following a neurotoxic insult.

Urocortin III, a brain neuropeptide of the corticotropin-releasing hormone family: modulation by stress and attenuation of some anxiety-like behaviours.

Following its discovery 20 years ago, corticotropin-releasing hormone (CRH) has been postulated to mediate both hormonal and behavioural responses to stressors. Here, we characterize and describe a behavioural role for the murine gene, UcnIII, which encodes a recently discovered CRH-related neuropeptide, urocortin III. We found that mouse UcnIII is expressed predominantly in regions of the brain known to be involved in stress-related behaviours, and its expression in the hypothalamus increases following restraint.