Neuroscience
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Comparative Study
Differential neuronal activation in the hypothalamic paraventricular nucleus and autonomic/neuroendocrine responses to I.C.V. endotoxin.
The paraventricular nucleus (PVN) of the hypothalamus is a key site for regulating neuroendocrine and autonomic activities. To study the role of the PVN activation in brain inflammation-induced autonomic/endocrine responses, lipopolysaccharide (LPS; 0.5 or 5 microg) was administered i.c.v. and rats were killed 1, 3 or 6 h after the injection. I.c.v. ⋯ Activation of the PVN by i.c.v. LPS likely occurs through both central and systemic routes. Differential neuronal activation in the PVN is functionally related to autonomic/endocrine responses elicited by brain inflammation.
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Both endocannabinoids through cannabinoid receptor type I (CB1) receptors and dopamine through dopamine receptor type D1 receptors modulate postsynaptic inhibition in substantia nigra by changing GABA release from striatonigral terminals. By recording from visually identified pars compacta and pars reticulata neurons we searched for a possible co-release and interaction of endocannabinoids and dopamine. Depolarization of a neuron in pars reticulata or in pars compacta transiently suppressed evoked synaptic currents which were blocked by GABA(A) receptor antagonists (inhibitory postsynaptic currents [IPSCs]). ⋯ We conclude that endocannabinoids and dopamine can be co-released. Retrograde signaling through endocannabinoids and dopamine changes inhibition independently from each other. Activation of dopamine D1 receptors emphasizes extrinsic inhibition and activation of CB1 receptors promotes intrinsic inhibition.
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Comparative Study
Immune rejection of a facial nerve xenograft does not prevent regeneration and the return of function: an experimental study.
Nerve grafts may be used to repair damaged peripheral nerves and also to facilitate spinal cord regeneration after experimental trauma. Little is known, however, about the possible use of xenografts and the role of immune rejection in the outcome of repair. ⋯ With longer (15-20 mm) transplants, however, restoration of eye closure becomes dependent on cyclosporine administration. Thus, in a situation where nerve repair does not occur without a graft, a host immune attack has an attritional effect which is not sufficient to prevent repair over short distances, but becomes obvious when the regenerating fibres have to cross longer segments of transplanted tissue.
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In the present work we examined the involvement of selected P2X receptors for extracellular ATP in the onset of neuronal cell death caused by glucose/oxygen deprivation. The in vitro studies of organotypic cultures from hippocampus evidenced that P2X2 and P2X4 were up-regulated by glucose/oxygen deprivation. Moreover, we showed that ischemic conditions induced specific neuronal loss not only in hippocampal, but also in cortical and striatal organotypic cultures and the P2 receptor antagonists basilen blue and suramin prevented these detrimental effects. ⋯ P2X2 was expressed in neuronal cell bodies and fibers in the CA1 pyramidal cell layer and in the strata oriens and radiatum. Intense P2X4 immunofluorescence was localized to microglia cells. Our results indicate a direct involvement of P2X receptors in the mechanisms sustaining cell death evoked by metabolism impairment and suggest the use of selected P2 antagonists as effective neuroprotecting agents.
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To examine the role of GABA in the respiratory rhythm and pattern generation in neonatal mice, we analyzed the function of the respiratory control system of 67-kDa isoform of glutamic acid decarboxylase (GAD67)-deficient neonatal mice. In these mutant (GAD67-/-) mice, GABA levels in the brainstem were reduced to about 30% of those in wild-type (GAD67+/+) mice. In in vivo preparations, ventilatory parameters were analyzed by whole body plethysmography and electromyography of intercostal muscles. ⋯ Superfusion of the in vitro GAD67-/- preparation with 10 microM GABA prolonged C4 burst duration and partly restored a normal pattern of inspiration, although the restoration was limited. These results indicate that reduced GABA levels during the perinatal period induce malfunction in the respiratory control system. We suggest that GABAergic transmission is not essential for basic respiratory rhythm generation but plays an important role in the maintenance of regular respiratory rhythm and normal inspiratory pattern in neonatal mice.