Effects of disease salience and xenophobia on support for humanitarian aid.

This article examines how disease salience influences attitudes toward two types of humanitarian aid: sending foreign aid and housing refugees. Some have argued that disease salience increases levels of out-group prejudice through what is referred to as the behavioral immune system (BIS), and this increase in out-group prejudice works to shape policy attitudes. However, an alternative mechanism that may explain the effects of disease salience is contamination fear, which would suggest there is no group bias in the effects of disease threat. Existing work largely interprets opposition to policies that assist out-groups as evidence of out-group prejudice. We suggest it is necessary to separate measures of out-group animosity from opinions toward specific policies to determine whether increased out-group prejudice rather than fear of contamination is the mechanism by which disease salience impacts policy attitudes. Across two experiments, disease salience is shown to significantly decrease support for humanitarian aid, but only in the form of refugee support. Furthermore, there is converging evidence to suggest that any influence of disease salience on aid attitudes is not caused by a corresponding increase in xenophobia. We suggest that the mechanism by which disease threat influences policy attitudes is a general fear of contamination rather than xenophobia. These findings go against an important hypothesized mechanism of the BIS and have critical implications for the relationship between disease salience and attitudes toward transnational policies involving humanitarian aid.

Multiple T-type Ca2+ current subtypes in electrophysiologically characterized hamster dorsal horn neurons: possible role in spinal sensory integration.

Whole cell patch-clamp recordings were used to investigate the contribution of transient, low-threshold calcium currents (I(T)) to firing properties of hamster spinal dorsal horn neurons. I(T) was widely, though not uniformly, expressed by cells in Rexed's laminae I-IV and correlated with the pattern of action potential discharge evoked under current-clamp conditions: I(T) in neurons responding to constant membrane depolarization with one or two action potentials was nearly threefold larger than I(T) in cells responding to the same activation with continuous firing. I(T) was evoked by depolarizing voltage ramps exceeding 46 mV/s and increased with ramp slope (240-2,400 mV/s). Bath application of 200 µM Ni(2+) depressed ramp-activated I(T). Phasic firing recorded in current clamp could only be activated by membrane depolarizations exceeding ∼43-46 mV/s and was blocked by Ni(2+) and mibefradil, suggesting I(T) as an underlying mechanism. Two components of I(T), "fast" and "slow," were isolated based on a difference in time constant of inactivation (12 ms and 177 ms, respectively). The amplitude of the fast subtype depended on the slope of membrane depolarization and was twice as great in burst-firing cells than in cells having a tonic discharge. Post hoc single-cell RT-PCR analyses suggested that the fast component is associated with the Ca(V)3.1 channel subtype. I(T) may enhance responses of phasic-firing dorsal horn neurons to rapid membrane depolarizations and contribute to an ability to discriminate between afferent sensory inputs that encode high- and low-frequency stimulus information.

Local circuit connections between hamster laminae III and IV dorsal horn neurons.

To better understand the role of intrinsic spinal cord circuits in the integration of mechanosensory information, we studied synaptic transmission between neurons in Rexed's laminae III-IV, a major termination zone for cutaneous mechanoreceptor afferents, using dual, simultaneous whole cell electrophysiological recordings in young hamsters. Synaptic connections were detected between 32 of 106 cell pairs (linkage probability of 0.3) and were predominantly unidirectional (91%). Inhibitory connections outnumbered excitatory connections by 2:1. Amplitude of single-axon postsynaptic potentials (PSPs) was independent of postsynaptic cell input resistance. Intracellular labeling suggested that recordings were obtained from local axon interneurons. In connected cell pairs, the percentage of presynaptic action potentials that failed to evoke a postsynaptic response was 44 +/- 29%. Shape indices of PSPs suggested that synaptic contacts were widely distributed along the postsynaptic membrane. Linkage probability was unrelated to intrinsic firing properties, laminar position of the cells or the distance (<160 mum) separating them. However, PSPs in target cells following action potentials in neurons with phasic firing patterns had longer duration and lower failure rates than PSPs activated by neurons with tonic firing patterns. Thus transmission reliability at synapses between lamina III/IV interneurons overall is low, and efficacy of these connections is related to firing properties of the presynaptic cells. The observations also suggest that synaptic organization in LIII-IV is fundamentally different from the superficial dorsal horn (LI-II) where neural circuits may be composed of stereotyped units made from connections between a few functional types of neurons.

Morphology and electrophysiological properties of hamster spinal dorsal horn neurons that express VGLUT2 and enkephalin.

The excitatory amino acid glutamate mediates transmission at spinal synapses, including those formed by sensory afferent fibers and by intrinsic interneurons. The identity and physiological properties of glutamatergic dorsal horn neurons are poorly characterized despite their importance in spinal sensory circuits. Moreover, many intrinsic spinal glutamatergic synapses colocalize the opioid peptide enkephalin (ENK), but the neurons to which they belong are yet to be identified. Therefore, we used immunohistochemistry and confocal microscopy to investigate expression of the VGLUT2 vesicular glutamate transporter, an isoform reported in nonprimary afferent spinal synapses, and ENK in electrophysiologically identified neurons of hamster spinal dorsal horn. VGLUT2 immunoreactivity was localized in restricted fashion to axon varicosities of neurons recorded from laminae II-V, although the occurrence of immunolabeling in individual varicosities varied widely between cells (39 +/- 36%, n = 31 neurons). ENK colocalized with VGLUT2 in up to 77% of varicosities (17 +/- 21%, n = 21 neurons). The majority of neurons expressing VGLUT2 and/or ENK had axons with dense local terminations or projections consistent with propriospinal functions. VGLUT2 and ENK labeling were not correlated with cellular morphology, intrinsic membrane properties, firing patterns, or synaptic responses to sensory afferent stimulation. However, VGLUT2 expression was significantly higher in neurons with depolarized resting membrane potential. The results are new evidence for a population of dual-function dorsal horn interneurons that might provide another mechanism for limiting excitation within dorsal horn circuits during periods of strong sensory activation.

Mechanosensory afferent input and neuronal firing properties in rodent spinal laminae III-V: re-examination of relationships with analysis of responses to static and time-varying stimuli.

Relationships between neuronal firing pattern and mechanosensory input in the deep dorsal horn were investigated using whole-cell recordings from isolated hamster spinal cord with innervation from an attached skin patch. Neurons that fired repetitively to depolarizing current (tonic cells) responded to both moving and static stimulation of their cutaneous receptive fields, and discharged continuously for the duration of stimulus application. Neurons responding to depolarizing current with transient, rapidly adapting firing (phasic cells) were significantly more responsive to stimulus movement than to static skin contact. Phasic cells typically issued a brief discharge at the onset or termination of a stimulus; their responses during static skin contact were weaker than tonic cells. Tonic cells were activated during both ramp and steady-state skin indentations, whereas phasic cells responded with their strongest excitation to displacement velocities exceeding 8 microm/ms. Mechanosensory input to phasic cells originated primarily from low threshold receptors, whereas tonic cells demonstrated a mixture of inputs from both low and high threshold sources. A third class of neurons responded to depolarizing current with a pronounced firing delay and displayed a sensitivity to cutaneous stimuli that was similar to tonic cells except they showed a modest decrease in firing as skin indentation velocity increased. The results suggest a correlation between functional properties of mechanoreceptive afferent fibers and intrinsic discharge properties of laminae III-V neurons that may significantly influence integration of cutaneous mechanosensory information at the first spinal relay.

Vesicular glutamate transporters in the spinal cord, with special reference to sensory primary afferent synapses.

Spinal cord sensory synapses are glutamatergic, but previous studies have found a great diversity in synaptic vesicle structure and have suggested additional neurotransmitters. The identification of several vesicular glutamate transporters (VGLUTs) similarly revealed an unexpected molecular diversity among glutamate-containing terminals. Therefore, we quantitatively investigated VGLUT1 and VGLUT2 content in the central synapses of spinal sensory afferents by using confocal and electron microscopy immunocytochemistry. VGLUT1 localization (most abundant in LIII/LIV and medial LV) is consistent with an origin from cutaneous and muscle mechanoreceptors. Accordingly, most VGLUT1 immunoreactivity disappeared after rhizotomy and colocalized with markers of cutaneous (SSEA4) and muscle (parvalbumin) mechanoreceptors. With postembedding colloidal gold, intense VGLUT1 immunoreactivity was found in 88-95% (depending on the antibody used) of C(II) dorsal horn glomerular terminals and in large ventral horn synapses receiving axoaxonic contacts. VGLUT1 partially colocalized with CGRP in some large dense-core vesicles (LDCVs). However, immunostaining in neuropeptidergic afferents was inconsistent between VGLUT1 antibodies and rather weak with light microscopy. VGLUT2 immunoreactivity was widespread in all spinal cord laminae, with higher intensities in LII and lateral LV, complementing VGLUT1 distribution. VGLUT2 immunoreactivity did not change after rhizotomy, suggesting a preferential intrinsic origin. However, weak VGLUT2 immunoreactivity was detectable in primary sensory nociceptors expressing lectin (GSA-IB4) binding and in 83-90% of C(I) glomerular terminals in LII. Additional weak VGLUT2 immunoreactivity was found over the small clear vesicles of LDCV-containing afferents and in 50-60% of C(II) terminals in LIII. These results indicate a diversity of VGLUT isoform combinations expressed in different spinal primary afferents.