Seasonal and diel changes in salinity, temperature, dissolved oxygen and sulphide at a station in the upper Derwent estuary, southeastern Tasmania.

Temperature, salinity, oxygen saturation and sulphide levels fluctuated widely both seasonally and with depth at a station on the upper Derwent estuary just downstream from a pulp and paper mill. In summer (February) oxygen saturation at the bottom reached a minimum of about 20% and sulphide levels peaked at 11 mg L- Conditions at this time would be expected to be lethal to a wide variety of organisms. Some of the possible causes for these changes are discussed

Method and means for dynamic measurement of rates of adsorption from solutions

A method and apparatus for dynamic measurement of rates of absorption from solutions. The method has the advantage of avoiding the use of solvent normally used to establish a baseline. The method involves pre-evacuating the adsorbent contained in an adsorbent cell and thereafter rapidly contacting the adsorbent with analytical solution, all without prior exposure of adsorbent to pure solvent. The result is a sharp characteristic adsorption line

Organization and maintenance of molecular domains in myelinated axons

Myelinated axons are segregated into molecular domains that are essential for action potential propagation. Each domain is characterized by clustering of specific molecular components and disruption of these domains, as seen in multiple sclerosis and ataxias, results in altered neuronal function. However, mechanisms responsible for domain organization remain elusive. We utilized mouse conditional knockouts to uncover mechanisms responsible for the organization and maintenance of the paranode, juxtaparanode, and axon initial segment (AIS). Paranode disruption results in mislocalization of juxtaparanodal proteins and disorganization of the axonal cytoskeleton. Caspr and Caspr2, which localize to the paranode and juxtaparanode, contain binding sites for the cytoskeletal adaptor protein 4.1B. We generated 4.1B null mice and showed that loss of 4.1B resulted in severe disorganization of the juxtaparanode in both the peripheral (PNS) and central nervous system (CNS). At P30 PNS paranodes, loss of 4.1B disrupted Caspr localization and AGSJs. Loss of 4.1B at CNS paranodes resulted in progressive disruption of Caspr and AGSJs. Thus, 4.1B plays a role in interactions between the paranodal AGSJs and axonal cytoskeleton and is required for long-term maintenance of axonal domains. The cerebellar Purkinje AIS is targeted by basket axon collaterals that form the pinceau, which is critical for cerebellar function. Mechanistic details of pinceau organization are poorly understood. Loss of cytoskeletal adaptor protein AnkyrinG results in mislocalization of the cell adhesion molecule Neurofascin (Nfasc) at the Purkinje AIS and abnormal organization of the pinceau. We generated cell type-specific Nfasc null mice and found that Purkinje Nfasc is required for AIS maturation and for maintaining stable contacts between basket axon terminals and the Purkinje AIS during pinceau organization, while basket neuron Nfasc is required for proper basket axon collateral outgrowth and targeting to Purkinje soma/AIS. Disruption of the AIS and pinceau from loss of Nfasc leads to Purkinje neuron degeneration and ataxia. Together, the results presented in this dissertation elucidate mechanisms responsible for organization of the paranode, juxtaparanode, AIS, and pinceau. This knowledge will be critical for designing future therapeutic strategies to treat pathologies where restoration of axonal domains will be required to restore neuronal function

The Evolved Function of Social Anxiety: Detecting High Stakes Social Interactions.

In three articles, I examine the evolved function of social anxiety. Social anxiety – like other responsive defenses – is useful only when the magnitude of the response is appropriate to the demands of situations that involve genuine social threats. In the first article, I review the literature on the ultimate function of social anxiety and argue that the computational systems that underlie social anxiety function to: 1) detect high stakes social interactions; and, 2) minimize the risk of subsequent negative evaluation. In the second article, I present the results of a series of studies in which participants from across the distribution of levels of trait social anxiety completed a threatening or non-threatening priming task, then were asked to identify the emotion displayed in a series of faces. Results revealed a curvilinear relationship between dispositional social anxiety scores and response time, suggesting that moderate social anxiety is advantageous in certain situations. The final article used content analysis to examine the characteristics of the interaction partners and types of situations that college-aged participants recall – as well as the vocabulary and pronouns used – when asked write about an anxiety-provoking situation.Ph.D.PsychologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/64716/1/buttermo_1.pd

Localization of the paranodal protein Caspr in the mammalian retina

Purpose: The retina has the demanding task of encoding all aspects of the visual scene within the space of one fixation period lasting only a few hundred milliseconds. To accomplish this feat, information is encoded in specialized parallel channels and passed on to numerous central nuclei via the optic nerve. These parallel channels achieve specialization in at least three ways: the synaptic networks in which they participate, the neurotransmitter receptors expressed and the types and locations of ion channels or transporters used. Subcellular localization of receptors, channels and transporters is made yet more complex in the retina by the double duty many retinal processes serve. In the present work, we show that the protein Caspr (Contactin Associated Protein), best known for its critical role in the localization of voltage-gated ion channels at the nodes of Ranvier, is present in several types of retinal neurons including amacrine, bipolar, horizontal, and ganglion cells. Methods: Using standard double label immunofluorescence protocols, we characterized the pattern of Caspr expression in the rodent retina. Results: Caspr labeling was observed through much of the retina, including horizontal, bipolar, amacrine, and ganglion cells. Among amacrine cells, Caspr was observed in AII amacrine cells through co-localization with Parvalbumin and Disabled-1 in rat and mouse retinas, respectively. An additional amacrine cell type containing Calretinin also co-localized with Caspr, but did not co-localize with choline-acetyltransferase. Nearly all cells in the ganglion cell layer contain Caspr, including both displaced amacrine and ganglion cells. In the outer retina, Caspr was co-localized with PKC labeling in rod bipolar cell dendrites. In addition, Caspr labeling was found inside syntaxin-4 'sandwiches' in the outer plexiform layer, most likely indicating its presence in cone bipolar cell dendrites. Finally, Caspr was co-localized in segments of horizontal cell dendrites labeled with Calbindin-D28k. Conclusions: Caspr is best known for its role in organizing the localization of different voltage-gated ion channels in and around nodes of Ranvier. As neuronal processes in the retina often play a dual role involving both input and output, it is possible that the localization of Caspr in the retina will help us decipher the way retinal cells localize ion channels in their processes to increase computational capacity

Organization and maintenance of molecular domains in myelinated axons

Over a century ago, Ramon y Cajal first proposed the idea of a directionality involved in nerve conduction and neuronal communication. Decades later, it was discovered that myelin, produced by glial cells, insulated axons with periodic breaks where nodes of Ranvier (nodes) form to allow for saltatory conduction. In the peripheral nervous system (PNS), Schwann cells are the glia that can either individually myelinate the axon from one neuron or ensheath axons of many neurons. In the central nervous system (CNS), oligodendrocytes are the glia that myelinate axons from different neurons. Review of more recent studies revealed that this myelination created polarized domains adjacent to the nodes. However, the molecular mechanisms responsible for the organization of axonal domains are only now beginning to be elucidated. The molecular domains in myelinated axons include the axon initial segment (AIS), where various ion channels are clustered and action potentials are initiated; the node, where sodium channels are clustered and action potentials are propagated; the paranode, where myelin loops contact with the axolemma; the juxtaparanode (JXP), where delayed-rectifier potassium channels are clustered; and the internode, where myelin is compactly wrapped. Each domain contains a unique subset of proteins critical for the domain’s function. However, the roles of these proteins in axonal domain organization are not fully understood. In this review, we highlight recent advances on the molecular nature and functions of some of the components of each axonal domain and their roles in axonal domain organization and maintenance for proper neuronal communication

Effects of mosquitofish (Gambusia affinis) cues on wood frog (Lithobates sylvaticus) tadpole activity

We examined the changes in activity of wood frog (Lithobates sylvaticus) tadpoles exposed to combinations of visual, chemical, and mechanical cues of the invasive mosquitofish (Gambusia affinis). We also examined whether the responses of the tadpoles to the predator cues were influenced by the short-term accumulation of chemical cues in the experimental container. In our experiment, the activity of wood frog (L. sylvaticus) tadpoles was not affected by the presence of various cues from mosquitofish. Our experiment demonstrated that the repeated use of trial water can influence the activity level of tadpoles, regardless of the predator cue treatment used. Tadpoles in the first trial tended to be less active than tadpoles in subsequent trials. This effect does not appear to be mediated by the accumulation of predator cues since there was no significant interaction term. Our results suggest that short-term accumulation of predator chemical cues do not affect the behavior of wood frog tadpoles: however, our results suggest that the repeated use of the same water in consecutive trials may affect tadpole behavior, perhaps through the accumulation of conspecific chemical cues

The Cytoskeletal Adaptor Protein Band 4.1B Is Required for the Maintenance of Paranodal Axoglial Septate Junctions in Myelinated Axons

Precise targeting and maintenance of axonal domains in myelinated axons is essential for saltatory conduction. Caspr and Caspr2, which localize at paranodal and juxtaparanodal domains, contain binding sites for the cytoskeletal adaptor protein 4.1B. The exact role of 4.1B in the organization and maintenance of axonal domains is still not clear. Here we report the generation and characterization of 4.1B null mice. We show that loss of 4.1B in the PNS results in mislocalization of Caspr at paranodes and destabilization of paranodal axo-glial septate junctions (AGSJs) as early as postnatal day 30. In the CNS, Caspr localization is progressively disrupted and ultrastructural analysis showed paranodal regions that were completely devoid of AGSJs, with axolemma separated from the myelin loops, and loops coming off the axolemma. Most importantly, our phenotypic analysis of previously generated 4.1B mutants, used in Horresh et al. (2010), showed that Caspr localization was not affected in the PNS, even after one year; and 4.1R was neither expressed, nor enriched at the paranodes. Furthermore, ultrastructural analysis of these 4.1B mutants showed destabilization of CNS AGSJs at about one year. We also discovered that the 4.1B locus is differentially expressed in the PNS and CNS, and generates multiple splice isoforms in the PNS, suggesting 4.1B may function differently in the PNS versus CNS. Together, our studies provide direct evidence that 4.1B plays a pivotal role in interactions between the paranodal AGSJs and axonal cytoskeleton, and that 4.1B is critically required for long-term maintenance of axonal domains in myelinated axons