Brain research
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This study addresses the spatial relation between local Na(+) and K(+) imbalances in the ischemic core in a rat model of focal ischemic stroke. Quantitative [Na(+)] and [K(+)] brain maps were obtained by (23)Na MRI and histochemical K(+) staining, respectively, and calibrated by emission flame photometry of the micropunch brain samples. Stroke location was verified by diffusion MRI, by changes in tissue surface reflectivity and by immunohistochemistry with microtubule-associated protein 2 antibody. ⋯ Some residual mismatch between the sites of maximum Na(+) and K(+) imbalances was attributed to the different channels and pathways involved in transport of the two ions. A linear regression of the [Na(+)]br vs. [K(+)]br in the samples of ischemic brain indicates that for each K(+) equivalent leaving ischemic tissue, 0.8±0.1 Eq, on average, of Na(+) enter the tissue. Better understanding of the mechanistic link between the Na(+) influx and K(+) egress would validate the (23)Na MRI slope as a candidate biomarker and a complementary tool for assessing ischemic damage and treatment planning.
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We recently found that hydrogen sulfide (H2S) participates in inhibitory regulation of rhythmic respiration by acting on the parafacial respiratory group (pFRG) in medullary slices of neonatal rats. The present study investigated whether ATP-sensitive potassium (KATP) channels are expressed in neurons of the pFRG, and, if so, whether they play a role in central regulation of respiratory activity, in particular the H2S-mediated central inhibition of respiratory rhythm in medullary slices of neonatal rats. Immunohistochemical techniques revealed that KATP channels are expressed in neurons of the pFRG region. ⋯ Micro-injection of the H2S donor sodium hydrosulfide (NaHS) into the pFRG region produced identical inhibitory responses to those induced by pinacidil. However, combined micro-injection of Gl and NaHS eliminated inhibitory effects of NaHS and converted to minor excitatory effects on the respiratory rhythm. It can be concluded that KATP channels of pFRG neurons are involved in the central regulation of respiratory rhythm and H2S-mediated inhibitory actions on respiratory rhythm in medullary slices of neonatal rats.
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Spreading depression (SD) is a profound depolarization of neurons and glia that propagates in a wave-like manner across susceptible brain regions, and can develop during periods of compromised cellular energy such as ischemia, when it influences the severity of acute neuronal damage. Although SD has been well characterized in the cerebral cortex and hippocampus, little is known of this event in the Substantia Nigra (SN), a brainstem nucleus engaged in motor control and reward-related behavior. Transverse brain slices (250 μm; P21-23 rats) containing the SN were subject to oxygen and glucose deprivation (OGD) tests, modeling brain ischemia. ⋯ In the hippocampus, SD also developed during anoxia or aglycemia alone (associated with less profound ΔΨm than OGD), while these conditions rarely led to SD in the SNr. Our results demonstrate that OGD consistently evokes SD in the SN, and that this phenomenon only involves the SNr. It remains to be established whether nigral SD contributes to neuronal damage associated with a sudden-onset form of Parkinson's disease known as 'vascular parkinsonism'.
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This study was done in urethane anesthetized, ovariectomized (OVX) female rats that were either implanted or not implanted with silastic capsules containing17β-estradiol (E2) to investigate the effect of systemic changes in E2 on the discharge rate of subfornical organ (SFO) neurons that projected to supraoptic nucleus (SON) and responded to changes in plasma levels of angiotensin II (ANG II) or hypernatremia. Extracellular single unit recordings were made from 146 histologically verified single units in SFO. Intra-carotid infusions of ANG II excited ~57% of these neurons, whereas ~23% were excited by hypertonic NaCl. ⋯ In all cases this inhibitory effect of E2 was blocked by an intra-carotid injection of the E2 receptor antagonist ICI-182780, although ICI-182780 did not alter the neuron's response to ANG II or hypertonic NaCl. Additionally, ICI-182780 in the OVX+E2 animals significantly raised the basal discharge of SFO neurons and their response to ANG II or hypertonic NaCl. These data indicate that E2 alters the response of SFO neurons to ANG II or NaCl that project to SON, and suggest that E2 functions in the female to regulate neurohypophyseal function in response to circulating ANG II and plasma hypernatremia.
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How general anaesthetic drugs cause unconsciousness is a topic of ongoing clinical and scientific interest. It is becoming increasingly apparent that they disrupt cortical information processing, but the effects appear to depend on the spatial scale under investigation. In this study we investigated whether the intravenous anaesthetic etomidate synchronises neuronal activity on a sub-millimetre scale in mouse neocortical slices. ⋯ When recorded from the region of the slice initiating SLE activity, etomidate consistently increased both population event amplitude (median(range) 85(24-350) to 101(30-427) µV) and slope 16.6(1.5-106.2) to 20.2(1.7-111.1) µV/ms (p=0.016 and p=0.0013, respectively). The results are consistent with an increase in neuronal synchrony within the receptive field of the recording electrode, estimated to be a circle diameter of 300µm. In conclusion, the neocortical slice preparation supports in vivo data showing that general anaesthetics increase neuronal synchrony on a local scale and provides an ideal model for investigating underlying mechanisms.