Experimental neurology
-
Experimental neurology · May 2009
Quantitative T2 mapping as a potential marker for the initial assessment of the severity of damage after traumatic brain injury in rat.
Severity of traumatic brain injury (TBI) positively correlates with the risk of post-traumatic epilepsy (PTE). Studies on post-traumatic epileptogenesis would greatly benefit from markers that at acute phase would reliably predict the extent and severity of histologic brain damage caused by TBI in individual subjects. Currently in experimental models, severity of TBI is determined by the pressure of applied load that does not directly reflect the extent of inflicted brain injury, mortality within experimental population, or impairment in behavioral tests that are laborious to perform. ⋯ Histological evaluation of lesion volume (Fluoro-Jade B) was used as the reference outcome measure, and was performed 2 weeks after TBI. From MRI parameters studied, quantitative T2 values of cortical lesion not only correlated with histologic lesion volume (P<0.001, r=0.6, N=34), as well as NS (P<0.01, r=-0.5, N=34) and BB (P<0.01, r=-0.5, N=34) results, but also successfully differentiated animals with mTBI from those with sTBI 70.6 +/- 6.2 6.2 ms vs. 75.9 +/- 2.6 ms, P<0.001). Quantitative T2 of the lesion early after TBI can serve as an indicator of the severity of post-traumatic cortical damage and neuro-motor impairment, and has a potential as a clinical marker for identification of individuals with elevated risk of PTE.
-
Experimental neurology · May 2009
Sex differences in the response to activation of the poly (ADP-ribose) polymerase pathway after experimental stroke.
It is increasingly recognized that histological and functional outcomes after stroke are shaped by biologic sex. Emerging data suggests that ischemic cell death pathways are sexually dimorphic (Hurn, P., Vannucci, S., Hagberg, H. (2005) Adult or perinatal brain injury: does sex matter?. Stroke 36, 193-195 ; Lang, J. ⋯ In contrast, female Harlequin mice had no neuroprotective effect of gene deletion despite robust reductions in PAR formation and AIF translocation. Although equivalent activation of this cell death pathway occurs in both sexes after ischemia, detrimental effects are only present in males. AIF translocation and PAR formation do not mediate ischemic injury in the female brain, therefore agents designed to reduce PARP1 activation are unlikely to benefit females.
-
Experimental neurology · May 2009
Nociceptive responses and spinal plastic changes of afferent C-fibers in three neuropathic pain models induced by sciatic nerve injury in the rat.
Peripheral nerve injuries induce plastic changes on primary afferent fibers and on the spinal circuitry, which are related to the emergence of neuropathic pain. In this study we compared three models of sciatic nerve injury in the rat with different degrees of damage and impact on regeneration capability: crush nerve injury, chronic constriction injury (CCI) and spared nerve injury (SNI). All three models were characterized by means of nerve histology, in order to describe the degenerative and regenerative process of injured axons. ⋯ After CCI, changes on SP-immunoreactivity were not observed, and IB4-immunoreactive area decreased initially but recovered to normal levels on the second week post-injury. Thus, nociceptive responses depend on the type of injury, and the immunoreactivity pattern of afferent fibers at the spinal cord display changes less pronounced after partial than complete sciatic nerve injury. Although signs of neuropathic pain appear in all three lesion models, nociceptive responses and central plasticity patterns differ between them.
-
Experimental neurology · May 2009
Daily intermittent hypoxia augments spinal BDNF levels, ERK phosphorylation and respiratory long-term facilitation.
Acute intermittent hypoxia (AIH) elicits a form of respiratory plasticity known as long-term facilitation (LTF). We hypothesized that: 1) daily AIH (dAIH) preconditioning enhances phrenic and hypoglossal (XII) LTF in a rat strain with low constitutive LTF expression; 2) dAIH induces brain-derived neurotrophic factor (BDNF), a critical protein for phrenic LTF (pLTF) in the cervical spinal cord; and 3) dAIH increases post-AIH extracellular regulated kinase (ERK) activation. Phrenic and XII motor output were monitored in anesthetized dAIH- or sham-treated Brown Norway rats with and without acute AIH. pLTF was observed in both sham (18+/-9% baseline; 60 min post-hypoxia; p<0.05; n=18) and dAIH treated rats (37+/-8%; p<0.05; n=14), but these values were not significantly different (p=0.13). ⋯ AIH increased BDNF in sham (25+/-8%; p<0.05), but not dAIH-pretreated rats (-7+/-4%), and had complex effects on ERK phosphorylation (ERK2 increased in shams whereas ERK1 increased in dAIH-treated rats). Thus, dAIH elicits metaplasticity in LTF, revealing XII LTF in a rat strain with no constitutive XII LTF expression. Increased BDNF synthesis may no longer be necessary for phrenic LTF following dAIH preconditioning since BDNF concentration is already elevated.
-
Experimental neurology · Apr 2009
Enhanced recovery of human spinothalamic function is associated with central neuropathic pain after SCI.
Spinothalamic tract (STT) dysfunction seems to be crucially involved in the development of central neuropathic pain (NP) after spinal cord injury (SCI). However, previous attempts to identify differences in the extent or location of STT damage between subjects with and without NP failed. ⋯ Furthermore, the correlation between current pain intensity (assessed on average 5 years after SCI) and extent of functional recovery substantiates the close relationship between recovery of STT function and the occurrence of NP. These findings contribute to a better understanding of mechanisms involved in the generation of NP after SCI.