Neuroscience
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In the present study, multielectrode array (MEA) recording was used to illustrate the spatial-temporal progression of anterior cingulate cortex (ACC) activity following stimulation of the thalamus in a thalamocingulate pathway-preserved slice. The MEA was placed under the slice that contained the ACC, and 60 channels of extracellular local field potentials evoked by bipolar electrical stimulation within the thalamus were analyzed. Several distinct thalamic-evoked responses were identified. ⋯ The thalamus-evoked responses were activated and progressed along a deep surface-deep trajectory loop across the ACC layers. Glutamatergic neurotransmitters were crucially involved in information processing. Opioid interneurons may play a modulatory role in regulating the signal flows in the cingulate cortex.
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In heterozygous mice, attenuation of G-protein-coupled receptor kinase 2 (GRK2) level in nociceptors is associated with enhanced and prolonged inflammatory hyperalgesia. To further elucidate the role of GRK2 in nociceptor function we reversibly decreased GRK2 expression using intrathecal antisense oligodeoxynucleotide (AS-ODN). GRK2 AS-ODN administration led to an enhanced and prolonged hyperalgesia induced by prostaglandin E(2), epinephrine and carrageenan. ⋯ Unlike hyperalgesic priming induced by transient activation of protein kinase C epsilon (PKCε), (Aley et al., 2000; Parada et al., 2003b), the enhanced and prolonged hyperalgesia following attenuation of GRK2 is PKCε- and cytoplasmic polyadenylation element binding protein (CPEB)-independent and is protein kinase A (PKA)- and Src tyrosine kinase (Src)-dependent. Finally, rats treated with GRK2 AS-ODN exhibited enhanced and prolonged hyperalgesia induced by direct activation of second messengers, adenyl cyclase, Epac or PKA, suggesting changes downstream of G-protein-coupled receptors. Because inflammation can produce a decrease in GRK2, such a mechanism could help explain a predilection to develop chronic pain, after resolution of acute inflammation.
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Comparative Study
Strain differences in the effects of chronic corticosterone exposure in the hippocampus.
Stress hormones are thought to be involved in the etiology of depression, in part, because animal models show they cause morphological damage to the brain, an effect that can be reversed by chronic antidepressant treatment. The current study examined two mouse strains selected for naturalistic variation of tissue regeneration after injury for resistance to the effects of chronic corticosterone (CORT) exposure on cell proliferation and neurotrophin mobilization. The wound healer MRL/MpJ and control C57BL/6J mice were implanted subcutaneously with pellets that released CORT for 7 days. ⋯ Strain differences were found in the N-methyl-D-aspartate (NMDA) receptor, and BDNF I and IV promoters. Strain and CORT exposure interacted to alter tropomyosine-receptor-kinase B (TrkB) expression and this may be a potential mechanism protecting MRL/MpJ mice. In addition, differences in the inflammatory response of matrix metalloproteinases (MMPs) may also contribute to these strain differences in resistance to the deleterious effects of CORT to the brain.
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The distribution of low-threshold tetrodotoxin-resistant (TTX-r) Na(+) current and its co-expression with high-threshold TTX-r Na(+) current were studied in randomly selected acutely dissociated rat trigeminal ganglion (non-identified TG cells) and TG cells serving the temporomandibular joint (TMJ-TG cells). Conditions previously shown to enhance Na(V)1.9 channel-mediated currents (holding potential (HP) -80 mV, 130-mM fluoride internally) were employed to amplify the low-threshold Na(+) current. Under these conditions, detectable low-threshold Na(+) current was exhibited by 16 out of 21 non-identified TG cells (average, 1810 ± 358 pA), and by nine of 14 TMJ-TG cells (average, 959 ± 525 pA). ⋯ In TG cells expressing prominent low-threshold Na(+) currents, changing the external solution to one containing 0 mM Na(+) reduced the amount of current required to hold the cells at -80 mV through -50 mV, the peak effect being observed at HP -60 mV. TG cells recorded from with a more physiological pipette solution containing chloride instead of fluoride exhibited small low-threshold Na(+) currents, which were greatly increased upon superfusion of the TG cells with the adenylyl cyclase (AC) activator forskolin. These data suggest two hypotheses: (1) low- and high-threshold Na(V)1.9 and Na(V)1.8 channels, respectively, are frequently co-expressed in TG neurons serving the TMJ and other structures, and (2), Na(V)1.9 channel-mediated currents are small under physiological conditions, but may be enhanced by inflammatory mediators that increase AC activity, and may mediate an inward leak that depolarizes TG neurons, increasing their excitability.
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Case Reports
Focal electrical intracerebral stimulation of a face-sensitive area causes transient prosopagnosia.
Face perception is subtended by a large set of areas in the human ventral occipito-temporal cortex. However, the role of these areas and their importance for face recognition remain largely unclear. ⋯ A face-sensitive intracerebral N170 was also recorded in this area, supporting its contribution as a source of the well-known N170 component typically recorded on the scalp. Altogether, these observations indicate that face recognition can be selectively impaired by local disruption of a single face-sensitive area of the network subtending this function, the right OFA.