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Combined one-color laser-photolysis/laser-induced fluorescence methods have been applied to photodissociate nitrobenzene (NB) molecules and to detect the resulting nitric oxide (NO) photofragments. A one-color laser is used to induce photodissociation and detection of NO via the A(v‘= 0)–X(v”= 0–4) transitions. A strongly wavelength-dependent signature is obtained due to the population of v”= 0–3 of NO. The ratios of the peak heights of the P12bandhead are (v”= 0):(v”= 1):(v”= 2):(v”= 3) = 1:0.3:0.1:0.02. A detection limit of ∼500 ppb by weight of NB in air at pressures of 10 and 100 Torr is achieved by monitoring NO X(v”= 2). This is the first attempt to use an excited NO vibrational level for NB detection, and the method can be extended to detection of other nitro compounds. It has the advantage that background of ambient ground-state NO is precluded.

The effect of insertion of plasma membrane components from lymphocytes responding to mitogens into the membranes of nonresponding cells using Sendai virus envelopes as vehicles was examined. T cells modified by B membranes were stimulated by lipopolysaccharide (LPS) to proliferate as well as to produce interleukin-2 activity. B cells modified by T membranes were stimulated by concanavalin A to proliferate and to produce interleukin-2 activity. B cells derived from C3H/HeJ LPS-nonresponder strain of mice, when modified by B membranes derived from the LPS-responder C3H/eb strain, acquired LPS responsiveness. These findings indicate that the inability of either T or B cells to respond to specific mitogens is due to the lack of suitable plasma membrane constituents and that by changing the membrane composition the lymphocytes can be endowed with new functions.

We determined whether primed and unprimed B cells in the spleen of (BALB/c × C57BL/Ka)F(1) mice contain subpopulations that express a predominant surface Ig isotype. Spleen cells were stained for surface isotypes and sorted on the fluorescence-activated cell sorter (FACS) in order to obtain B cells bearing predominantly IgM (μp cells), IgD (δp cells), or IgG (γp cells). Each population was assayed for its capacity to restore the adoptive primary and secondary anti-bovine serum albumin (BSA) antibody response in irradiated syngeneic recipients. In addition, the adoptive response restored by isotype-predominant cells was compared to that restored by isotype- positive cells (B cells bearing a given surface isotype alone or in combination with others). The experimental results show that μp cells restore the adoptive primary and secondary IgM and IgG responses to BSA, and γP cells restore only the primary and secondary IgG response. Δp Cells restored the adoptive secondary IgG response, but failed to restore the adoptive primary response at the cell doses tested. ΓP Cells but not δp cells suppressed the IgM response of the μ(+) and δ(+) cells. The contribution of isotype-predominant cells to both the adoptive primary and secondary anti-BSA response was smaller than that of B cells bearing a combination of surface isotypes. Differences in the Ig isotype pattern expressed on the surface of primed and unprimed B cells are discussed.

We investigated the ability of IgM-, IgD-, and IgG-bearing cells from the spleens of unprimed (BALB/c x C57BL/Ka)F1 mice to restore the adoptive primary anti-BSA and anti-DNP antibody responses. Purified populations of isotype-specific cells were prepared by immunofluorescent staining and sorting on the fluorescence activated cell sorter. Bright or dull cells were transferred to irradiated syngeneic recipients which were challenged with DNP-BSA in complete Freund's adjuvant. Unfractionated spleen cells as well as IgM- and IgD-bearing cells restored the adoptive primary IgM and IgG antibody response. IgG-bearing cells restored a vigorous adoptive response which was all IgG (2-mercaptoethanol resistant). Depletion of IgG-bearing cells markedly increased the adoptive IgM response, and depletion of IgM-bearing cells markedly increased the IgG response. However, depletion of IgD-bearing cells resulted in a considerable reduction in the IgG response. The latter finding indicates that there is a subpopulation of IgD-bearing cells which express little or no surface IgM and which make a considerable contribution to the adoptive primary IgG response.

We investigated the ability of IgM-, IgD-, and IgG-bearing cells from the spleens of (BALB/c x C57BL/Ka)F1 mice primed to dinitrophenyl-bovine serum albumin (DNP-BSA) to restore the adoptive secondary anti-BSA and anti-DNP antibody responses. A rabbit anti-mouse IgD antiserum was prepared and the specificity documented by radioimmunoprecipitation, and cell surface staining. Purified populations of IgM-, IgD-, and IgG-bearing cells were prepared by immunofluorescent staining with isotype-specific reagents, and sorting on the fluorescence activated cell sorter. Bright or dull cells were transferred to irradiated syngeneic recipients which were challenged with DNP-BSA in saline. Unfractionated spleen cells restored an adoptive secondary serum antibody response which was all IgG (2-mercaptoethanol resistant). Purified IgM- or IgD-bearing cells restored both the secondary IgM and IgG antibody response. IgG-bearing cells restored only the IgG response. In addition, the IgG-bearing cells appear to suppress the adoptive secondary IgM response, since depletion of IgG-bearing cells from transferred spleen cells results in a marked increase in the adoptive IgM response.

In order to label dopamine D2 receptors selectively we tritiated the potent benzamide neuroleptic, YM-09151-2 (26.7 Ci/mmol). The binding of [3H]-YM-09151-2 to canine striatal membranes was saturable and specific with a KD of 57 pmol/l and Bmax of 36 pmol/g tissue as determined by Scatchard analysis. The KD, but not the Bmax, of [3H]-YM-09151-2 increased 6-fold in the absence of sodium chloride. [3H]-YM-09151-2 labeled 40% more sites than [3H]-spiperone in the same tissue homogenate. [3H]-YM-09151-2 binding was inhibited by dopaminergic drugs in a concentration and stereoselective manner with the appropriate dopamine D2 receptor profile. Thus, dopamine agonists inhibited [3H]-YM-09151-2 binding to canine striatal membranes with the following rank order of potency: (-)-N-n-propylnorapomorphine > apomorphine > (±)-6,7-dihydroxy-2-aminotetralin > (+)-N-n-propylnorapomorphine > dopamine > (-)-noradrenaline > serotonin > (-)-isoprenaline. Dopaminergic antagonists competed for [3H]-YM-09151-2 binding with the following order of potency: spiperone > (+)-butaclamol > haloperidol > clebopride > (-)-sulpiride > SCH-23390 > (-)-butaclamol. Furthermore, dopamine agonists recognized 2 states of the receptor labeled by [3H]-YM-09151-2, D2highand D2low. The D2highstate of the receptor could be converted to D2lowby guanine nucleotides and sodium ions as is the case for [3H]-spiperone binding to D2 receptors. [3H]-YM-09151-2 appears to be a more selective ligand for dopamine D2 receptors than [3H]-spiperone, since YM-09151-2 displays approximately 9-fold lower affinity than spiperone for cortical serotonergic (S2) receptors. [3H]-YM-09151-2 may become a useful tool for the selective characterization of dopamine D2 receptors.