The presence of μ-, δ- and κ-binding sites in homogenates of guinea-pig brain was demonstrated by the use of selective labelling techniques. In saturation experiments, the tritiated ligands [^3H]-[D-Ala^2, MePhe^4, Gly-ol^5]enkephalin, [^3H]-dihydromorphine, [^3H]-morphine and [^3H]-dihydronormorphine labelled only the μ-binding site. The δ-binding site could be labelled selectively with [^3H]-[D-Pen^2, D-Pen^5]enkephalin. However, the less selective δ-ligand, [³H]-[D-Ala², D-Leu⁵] enkephalin, could only be used when its μ-binding was blocked with the unlabelled μ-ligand [D-Ala², MePhe⁴, Gly-ol⁵]enkephalin. Selective labelling of the κ-binding site was more of a problem since the non-selective ligands [^3H]-etorphine, [^3H]-(±)-ethylketazocine and [³H]-(-)-bremazocine bind to the μ-, δ- and κ-sites. Therefore, the κ-binding site could only be labelled selectively when the binding of the tritiated ligands to the μ- and δ-sites was prevented by addition of the unlabelled μ-ligand [D-Ala^2, MePhe^4, Gly-ol^5]enkephalin and the unlabelled δ-ligand [D-Ala², D-Leu⁵]enkephalin. By analysis of the saturation curves obtained using these selective labelling techniques, the proportion of binding sites in homogenates of guinea-pig brain at 25°C was 24% μ-sites; 32% δ-sites and 44% κ-sites. The selective labelling techniques were also used to label the μ, δ- and κ-sites in displacement assays. The compounds with the highest degree of preference for each binding site were: for the μ-site, [D-Ala^2, MePhe^4, Gly-ol^5]enkephalin and Tyr-Pro-MePhe-D-Pro-NH_2; for the δ-site, [D-Pen², L-Pen⁵]enkephalin, [D-Pen², D-Pen⁵]enkephalin and ICI 174864 and for the κ-site, U-50,488H and U-69,593. As far as antagonists were concerned, naloxone displayed the highest preference for the μ-binding site and Mr 2266 had a preference for the κ-binding site but neither compound was highly selective unlike the δ-antagonist ICI 174864. The effect of pre-incubation with β-funaltrexamine on opioid binding was investigated in homogenates of guinea-pig brain and myenteric plexus-longitudinal muscle.

No description available.

In this study the effects of repeated antigen injections on total complement (C') and C'4 of guinea pig serum were investigated to determine if constant antigenic stimulation would show changes in the C' and C'4 titers. Attempts were also made to correlate any changes with variations in antibody titers during the repeated antigen injections.

The purpose of this paper is to report the results of studies on the aerobic, mesophilic intestinal flora of guinea pigs subjected to conditions similar to those encountered by man in spacecraft.

The principal purpose of this work was to determine the effect of immunized guinea pig serum upon the survival time of tumor infected mice, and to make a correlation between this effect and the complement titer.

Electrophysiological studies of myenteric neurons in the guinea-pig antrum suggest that different neuroactive compounds are involved in synaptic transmission. It is not known what neurotransmitters and neuropeptides are present and to what extent they colocalize. Immunohistochemical stainings were performed on whole-mount preparations of the guinea-pig antrum. Immunoreactivity for neuron-specific enolase was used as a general marker and was set at 100%. There was no overlap between cholinergic and nitrergic neurons, resulting in two separate subpopulations. The presence of choline acetyltransferase immunoreactivity was used to identify the cholinergic subset, which accounted for 56% of the cells. Immunoreactivity for nitric oxide synthase, on the other hand, was displayed in 40.7% of the neurons. Substance-P immunoreactivity was present in 37.4% of the cells and vasoactive intestinal peptide and neuropeptide Y in 21.7% and 28.6%, respectively. Small subsets of neurons had immunoreactivity for serotonin (3.9%), calretinin (6.8%) and calbindin (0.5%). Colocalization studies revealed several subgroups of neurons, containing one or more of the screened markers. Though some similarity is found in the chemical coding of the antrum compared to that of the small intestine and the corpus, remarkable differences can be seen in the occurrence of some subpopulations. Cholinergic neurons are not as predominant as in other parts of the gut, serotonin presence is doubled and some vasointestinal-peptide-positive neurons express substance P. These differences might reflect the highly specialized function of the antrum; however, the exact role of these classes remains to be established.

Four non-licking guinea pigs were reinforced with water for successive approximations to licking an operandum feeder. Once all subjects had obtained their total liquid intake for a three-week period by licking, an optimum deprivation schedule was determined. Fixed ratio and variable interval schedules were found to affect licking behavior of the guinea pigs being slightly lower than that of the rat. Precise control over the onset and offset of licking was demonstrated through discrimination training.

Coxiella burnetii is an intracellular pathogen that can cause both acute and chronic disease (Q fever) in humans and infects many animals with varying clinical illness and persistence. A guinea pig aerosol-challenge model of acute Q fever was developed using infection with C. burnetii across a 5-log range of challenge doses. Clinical signs included fever, weight loss, respiratory difficulty, and death, with degree and duration of response corresponding to dose of organism delivered. Histopathologic evaluation revealed coalescing panleukocytic bronchointerstitial pneumonia 7 days after a high-dose challenge, resolving to multifocal lymphohistiocytic interstitial pneumonia by 28 days. Clinical and pathologic changes noted in these guinea pigs were comparable to those seen in human acute Q fever, making this an accurate and valuable animal model. This model was used to compare the relative virulence of eight isolates from four different genotypic groups: I (RSA493, RSA334, and RSA270), IV (Q177 and Q173), V (Q212 and Q217), and VI (5J108-111). Guinea pigs infected with group I acute-diseaseassociated isolates had severe respiratory disease, while no to moderate clinical illness was observed in animals given group IV or V chronic-disease-associated isolates. 5J108- 111 appeared avirulent. These data suggest that C. burnetii isolates have a range of disease potentials and support a distinction in strain virulence between established genotypic groups, though isolates within the same genomic group cause similar pathologic responses. Heterologous protection was confirmed by cross vaccination and challenge with RSA493 and Q217. A marked non-specific suppression of lymphoproliferation was noted at 14 and 28 days post infection with RSA493; similar suppression was seen after infection with Q173 and Q212 but not 5J108-111. Proinflammatory cytokines IFN-γ and TNF-α were produced during early C. burnetii infection, at which time anti-inflammatory cytokines TGF-β and IL-10 were repressed. A vaccine made from phase I C. burnetii was found to be completely protective against lethal infection in the guinea pig model, while vaccination with killed phase II organisms conferred only partial protection, preventing death and reducing but not precluding fever and respiratory illness. Protective vaccination significantly stimulated cell-mediated immunity and elicited increases in IFN-γ, TNF-α, and IL-12p40 mRNA levels.

It is the aim of this work to study the role, if any, of C'4 in the immune response against Staphylococcus aureus infections.

Effects of neurokinin A (NKA) and substance P (SP) on coronary resistance vessels were studied in isolated guinea pig hearts perfused with isotonic buffer containing 20 mM KCl. Injections of NKA and SP caused dose-dependent reductions in perfusion pressure with ED50 values of 14.0 and 0.326 pmol, respectively. Blockade of nitric oxide synthesis or removal of the endothelium inhibited vasodilator responses to neurokinins. Infusions of NKA or SP caused tachyphylaxis and cross-desensitization to the other neurokinin but not to acetylcholine. Injections of 2.5 nmol NKA increased perfusion pressure by 31 ± 8% when given after tachyphylaxis developed to infused SP (2.5 nmol/100 μl/min). It was concluded that 1) neurokinins cause an endothelium-dependent relaxation of coronary resistance vessels by stimulating NK-1 receptors on endothelial cells, and 2) desensitization of the receptor mediating vasodilation unmasks a vasoconstrictor response to NKA.