Neuroscience
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The epithelial cells of the choroid plexuses secrete cerebrospinal fluid (CSF), by a process which involves the transport of Na(+), Cl(-) and HCO(3)(-) from the blood to the ventricles of the brain. The unidirectional transport of ions is achieved due to the polarity of the epithelium, i.e. the ion transport proteins in the blood-facing (basolateral) membrane are different to those in the ventricular (apical) membrane. The movement of ions creates an osmotic gradient which drives the secretion of H(2)O. ⋯ Aquaporin 1 mediates water transport at the apical membrane, but the route across the basolateral membrane is unknown. A model of CSF secretion by the mammalian choroid plexus is proposed which accommodates these proteins. The model also explains the mechanisms by which K(+) is transported from the CSF to the blood.
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Comparative Study
N-methyl-D-aspartate receptors in the amygdala are necessary for the acquisition and expression of conditioned defeat.
Here, we describe a biologically relevant model called conditioned defeat that is used to examine behavioral responses to social defeat in Syrian hamsters. In this model experimental animals that are normally aggressive experience social defeat and consequently display high levels of submissive/defensive behavior even in response to non-threatening conspecifics. N-methyl-D-aspartate (NMDA) receptors within the amygdala play an important role in conditioned fear; therefore, the purpose of this study was to examine whether NMDA receptors within the amygdala are necessary for the acquisition and expression of conditioned defeat. ⋯ Similarly, infusions of AP5 into the amygdala immediately before exposure to a non-aggressive intruder significantly attenuated the display of submissive/defensive behavior. These data demonstrate that NMDA receptors are necessary for both the acquisition and expression of conditioned defeat. We believe that conditioned defeat is a unique and valuable animal model with which to investigate the neurobiology of fear-related changes in social behavior.
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Aquaporin-4 (AQP4) is the predominant water channel in the neuropil of the central nervous system. It is expressed primarily in astrocytes, but also occurs in ependymocytes and endothelial cells. A striking feature of AQP4 expression is its polarized distribution in brain astrocytes and retinal Muller cells. ⋯ We propose that AQP4 works in concert with Kir4.1 and the electrogenic bicarbonate transporter NBC and that water flux through AQP4 contributes to the activity dependent volume changes of the extracellular space. Such volume changes are important as they affect the extracellular solute concentrations and electrical fields, and hence neuronal excitability. We conclude that AQP4-mediated water flux represents an integral element of brain volume and ion homeostasis.
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We previously measured the time courses of hydrogen peroxide (H2O2), hydroxyl radical (*OH), and catalytic iron increases following traumatic spinal cord injury (SCI). This study determines whether the SCI-elevated level of *OH causes cell death. OH was generated by administering H2O2 and Fe2+ at the concentrations attained following SCI, each through a separate microdialysis fiber inserted laterally into the gray matter of the cord. ⋯ It also reduced the numbers of TUNEL-positive neurons (P=0.01). Electron microscopy confirmed that generated *OH induced neuronal and glial death with characteristic features of both necrosis and apoptosis. We conclude that 1) SCI-elevated *OH is sufficient to induce both necrosis and apoptosis, criteria for identifying an endogenous secondary damaging agent; 2) MnTBAP reduces *OH-induced cell death, perhaps by removing H2O2 administered in the tissue, thereby blocking formation of *OH, and also by scavenging downstream reactive species.
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Comparative Study
Synaptic properties and postsynaptic opioid effects in rat central amygdala neurons.
An important output of amygdaloid nuclei, the central nucleus of the amygdala (CeA) not only mediates negative emotional behaviors, but also participates in the stimulus-reward learning and expression of motivational aspects of many drugs of abuse, and links environmentally stressful conditions such as fear to endogenous pain-inhibiting mechanisms. The endogenous opioid system in the CeA is crucial for both reward behaviors and environmental stress-induced analgesia. In this study using whole-cell voltage-clamp recordings, we investigated synaptic inputs and the postsynaptic effects of opioid agonists in CeA neurons. ⋯ In contrast, the kappa-opioid receptor agonist hyperpolarized only type B neurons. These results illustrate three types of CeA neurons with distinctive membrane properties and differential responses to opioid agonists. They may represent functionally distinct CeA cell groups for the integration and execution of CeA outputs in the aforementioned CeA functions.