Search

Although adults have matured developments of general intelligence, brain structure and brain function, many people continue to be risk takers, despite the harm that can result. The neural basis underlying risk-taking behaviors has been studied extensively in adolescents, but less so in adults. Outcome expectancies are important factors influencing individuals’ risk behaviors, which comprise the expected risks (ER) and expected benefits (EB) associated with risk behaviors. In the current study, we systematically investigated inter-individual differences in adults’ outcome expectancies for risk behaviors, considering the general intelligence, brain function, and brain structure. At the intelligence level, individuals with higher intelligence scores showed lower ER but higher EB associated with risk behaviors. At the brain function level, resting-state functional connectivity (FC) between regions within the default mode network is negatively correlated with ER but positively correlated with EB associated with risk behaviors, while FC between the insula and motor cortex is negatively correlated with EB associated with the risk behaviors. At the brain structure level, gray matter volume in posterior cingulate cortex (PCC) and bilateral parahippocampus were negatively correlated with the ER associated with risk behaviors. Furthermore, the relationship between the outcome expectancy associated with risk behaviors and the FC between anterior cingulate cortex and PCC is partially mediated by the general intelligence. The current study provides new insight that furthers our understanding of how individual differences in adults’ risk attitudes and behaviors are modulated by general intelligence and reflected in resting-state FC and brain structures related to self-reference and inhibitory control processing.

Natriuretic peptides (NPs) have been shown to modulate neuronal activities. By immunohistochemistry and confocal microscopy, we examined expression of atrial NP (ANP), brain NP (BNP) and C-type NP (CNP) in rat retina. Our results showed that these peptides were differentially expressed in the neural retina. While strong ANP-, BNP- and CNP-immunoreactivity (IR) was clearly seen in the outer and inner plexiform layers and on numerous neurons in the inner nuclear layer, BNP- and CNP-, but not ANP-IR, was present in some ganglion cells. Furthermore, ANP, BNP and CNP were expressed in Müller cells with distinct profiles, as shown by double labeling of NPs and vimentin. Labeling for BNP was rather strong in the main trunks, major processes, but hardly detectable in the endfeet. The expression profile for ANP was similar, but with a much lower level. On the contrary, the endfeet and major processes in the inner retina were strongly CNP-positive, with the main trunks and other major processes in the outer retina much less labeled. These results raise a possibility that NPs, when released from Müller cells, may perform layer dependent functions.

The expression patterns of inwardly rectifying potassium (Kir) channel subunits (Kir 1.1, 2.1, 2.3, 3.1, 3.2, 3.3, 4.1, and 4.2) were studied in rat retina by immunohistochemistry, with special emphasis on neuronal expression. Except for Kir4.1, the subunits tested were all expressed on neurons in the inner nuclear and ganglion cell layers. While Kir2.1 was densely present in the cytoplasm, the staining for all other subunits was predominantly expressed on the cell membrane. Most subunits, but not Kir 2.1 and 2.3, were present in the outer and inner plexiform layers to different extents. Kir4.1-immunoreactivity was found in astrocytes wrapping retinal blood vessels, in addition to the Müller cell endfoot. The differential expression of the Kir subunits suggests the diversity of physiological roles these channels may play.

Modulation by melatonin of gamma-aminobutyric acid(A) (GABA(A)) receptor-mediated responses was studied in bipolar and amacrine-like cells acutely isolated from carp retina, using the whole-cell patch-clamp technique. Melatonin of 1 mM accelerated desensitization of the GABA(A) receptors at both bipolar and amacrine-like cells. In addition, 1 mM melatonin hardly changed the GABA(A) receptor-mediated response amplitude of bipolar cells, while it increased or decreased that of amacrine-like cells, depending on the concentration of GABA applied. These modulatory effects, which can not be blocked by luzindole, a melatonin receptor antagonist, may be due to the allosteric action caused by melatonin bound to a site of the GABA(A) receptors.

With the use of the whole-cell patch clamp technique, we examined effects of zinc on AMPA receptors of isolated carp retinal horizontal cells, predominantly consisting of flop splice variants. We found that zinc ranging from 30 microM to 1 mM failed to modulate glutamate-induced currents of these cells, which is clearly distinct from the results previously obtained in superior colliculus neurons and Xenopus ooctyes. Furthermore, glutamate responses remained unchanged when zinc was co-applied with PEPA, a flop variant-preferential AMPA receptor potentiator. With the co-application of cyclothiazide, a flip variant-preferential AMPA receptor potentiator, however, a dual effect could be observed: zinc potentiated glutamate responses at low concentrations, but inhibited them at higher concentrations. These results suggest that the action of zinc on AMPA receptors may be splice variant-relevant.

Natriuretic peptides (NPs) may act as neuromodulators through activation of three specific receptor subtypes (NPRs). In the present study we examined the expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) on different subtypes of retinal amacrine cells (ACs) in rat by immunofluoresecence double labeling. All three NPs were moderately expressed in dopaminergic and cholinergic ACs, stained by tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT), respectively. The immunostaining appeared on the membrane, cytoplasm and somatodendritic compartments of these ACs. In AII glycinergic ACs, labeled by parvalbumin (PV), however, only faint punctate staining, if any, was seen. These results suggest that NPs could be produced in ACs and play a neuromodulatory role in the inner retina. Together with a previous immunocytochemical study, showing that NPR-B is present in cultured rat GABAergic ACs, our results further suggest that NPs produced in ACs may also modulate their own activity.

The expression of the glycine receptor (GlyR) alpha1, alpha2 and beta subunits and glycine transporter (GlyT) on Müller cells was studied in bullfrog retina using double immunofluorescence labeling and confocal scanning microscopy. Double labeling of glial fibrillary acidic protein (GFAP), a specific marker for Müller cells, and the GlyR subunits showed that almost all Müller cells moderately expressed GlyR alpha1 and weakly GlyR beta, whereas no immunoreactivity for GlyR alpha2 was observed. The labeling for GlyR alpha1 and GlyR beta appeared in somata, major processes, endfeet and branchlets of the Müller cells. Müller cells were also GlyT1-labeled. Consistent with previous electrophysiological results, these findings suggest that Müller cells may be involved in modulation of glycinergic transmission by reciprocal interactions with retinal neurons through GlyR and GlyT.

The expression patterns of different Ca(2+) channel alpha(1) subunits (alpha(1A-E)) were immunohistochemically studied in the rat retina. Intense immunoreactivity (IR) for alpha(1A) (P/Q-type) and alpha(1B) (N-type) Ca(2+) channels was observed in both the outer and inner plexiform layers (OPL and IPL). In addition, alpha(1B)-IR was found in the outer and inner nuclear layers. Staining for alpha(1E) (R-type) was diffusely distributed in all three nuclear layers and in the IPL. The alpha(1C) and alpha(1D), two L-type Ca(2+) channel subunits, exhibited distinct expression patterns, with alpha(1C) being almost exclusively expressed on bipolar cells, and alpha(1D) mainly on photoreceptor cell bodies and in the OPL. Staining for alpha(1D) was also observed on Muller cells. The differential expression pattern of the alpha(1) subunits suggests that these Ca(2+) channel subtypes may be associated with different retinal functions.

Subcellular localization and properties of glycine receptors on bipolar cells (BCs) were studied using whole-cell recordings and non-stationary noise analysis (NSNA) in bullfrog retinal slices. The currents elicited by focally applied glycine were of comparable amplitudes at the dendrites and axon terminals of both OFF and ON BCs. Moreover, glycine receptors were also expressed at the axons of some BCs. NSNA revealed that the weighted mean single-channel conductance of the glycine receptors at the dendrites (18.2 pS) was significantly larger than that of those at the axon terminals (8.1 pS), thus implying that the glycine receptors on bullfrog retinal BCs may be heterogeneous at these two sites.

It was previously reported that strychnine-sensitive glycine receptors and GABA A receptors co-existed on carp retinal third-order neurons (amacrine/ganglion cells) (Li, P. and Yang, X.-L., Strong synergism between GABA A and glycine receptors on isolated carp third-order neurons. NeuroReport, 9 (1998) 2785–2789.). In this study, the effects of the divalent cation Zn 2+ on these two receptors were studied in amacrine/ganglion cells acutely isolated from carp, with the use of the whole-cell patch clamp recording technique. The glycine-induced currents were steadily potentiated by Zn 2+ of lower concentrations (0.1–10 μM), while being dose-dependently inhibited by Zn 2+ of higher concentrations (>100 μM). Both the effects involved changes in apparent glycine affinity of the glycine receptor. In contrast, Zn 2+ consistently suppressed the GABA A mediated currents of these cells, and did not show similar dual effect. The differential modulation by Zn 2+ of glycine receptors versus GABA A receptors provides a versatility for regulating inhibitory glycinergic and GABAergic inputs converging on most amacrine/ganglion cells.