Impairment of synaptic plasticity in the primary somatosensory cortex in a model of diabetic mice.

Type 1 and type 2 diabetic patients experience alterations in the Central Nervous System, leading to cognitive deficits. Cognitive deficits have been also observed in animal models of diabetes such as impaired sensory perception, as well as deficits in working and spatial memory functions. It has been suggested that a reduction of insulin-like growth factor-I (IGF-I) and/or insulin levels may induce these neurological disorders.

SIRT2 Inhibition Rescues Neurodegenerative Pathology but Increases Systemic Inflammation in a Transgenic Mouse Model of Alzheimer's Disease.

Sirtuin 2 (SIRT2) has been proposed to have a central role on aging, inflammation, cancer and neurodegenerative diseases; however, its specific function remains controversial. Recent studies propose SIRT2 pharmacological inhibition as a therapeutic strategy for several neurodegenerative diseases including Alzheimer's disease (AD). Surprisingly, none of these published studies regarding the potential interest of SIRT2 inhibition has assessed the peripheral adverse side consequences of this treatment.

Locus coeruleus inhibition of vibrissal responses in the trigeminal subnucleus caudalis are reduced in a diabetic mouse model.

Diabetic neuropathy is the loss of sensory function beginning distally in the lower extremities, which is also characterized by pain and substantial morbidity. Furthermore, the locus coeruleus (LC) nucleus has been proposed to play an important role in descending pain control through the activation of α2-noradrenergic (NA) receptors in the spinal dorsal horn. We studied, on control and diabetic mice, the effect of electrical stimulation of the LC nucleus on the tactile responses in the caudalis division of the spinal trigeminal nucleus (Sp5C), which is involved in the relay of orofacial nociceptive information.