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At least 217 records · Page 12Linked to original sources
PubMed1980

Enhancement by progesterone of lysergic acid diethylamide inhibition of the copulatory response in the female rat.

Copulatory behavior in the ovariectomized rat, the lordosis response (L.R.) was induced by either estrogen alone or estrogen followed by progesterone. L.R. has been shown to be inhibited dose-dependently by lysergic acid diethylamide (LSD). The effects of various hormone treatments on the LSD-induced inhibition were tested in the present study. Progesterone but not estrogen was found to significantly enhance the LSD effect in a dose-dependent manner. In contrast, the effect of LSD on spontaneous behaviors in an exploratory situation was not influenced by progesterone treatment. This phenomenon of increased L.R. inhibitor effect by LSD was probably not due to a steroid-induced change in LSD metabolism. The data show instead that progesterone specifically influences monoaminergic mechanisms, which are related to the action of LSD. This has important implications for the possibility that progesterone induces the L.R. by acting on monoaminergic mechanisms.

Animals↗
PubMed1974

Serotonin-sensitive adenylate cyclase in neural tissue and its similarity to the serotonin receptor: a possible site of action of lysergic acid diethylamide.

An adenylate cyclase (EC 4.6.1.1) that is activated specifically by low concentrations of serotonin has been identified in homogenates of the thoracic ganglia of an insect nervous system. The activation of this enzyme by serotonin was selectively inhibited by extremely low concentrations of D-lysergic acid diethylamide (LSD), 2-bromo-LSD, and cyproheptadine, agents which are known to block certain serotonin receptors in vivo. The inhibition was competitive with respect to serotonin, and the calculated inhibitory constant of LSD for this serotonin-sensitive adenylate cyclase was 5 nM. The data are consistent with a model in which the serotonin receptor of neural tissue is intimately associated with a serotonin-sensitive adenylate cyclase which mediates serotonergic neurotransmission. The results are also compatible with the possibility that some of the physiological effects of LSD may be mediated through interaction with serotonin-sensitive adenylate cyclase.

Adenylyl Cyclases↗
PubMed1986

5-Hydroxytryptamine and (+)-lysergic acid diethylamide displace [3H]thyrotropin-releasing hormone at its binding sites in the rat limbic forebrain.

Binding of [3H]thyrotropin-releasing hormone (TRH) to its receptors in the rat limbic forebrain was partially displaced by 5-hydroxytryptamine (5-HT, ligand for 5-HT1 receptors) and (+)-lysergic acid diethylamide ((+)-LSD, ligand for 5-HT1 and 5-HT2 receptors) at nanomolar concentrations. Spiperone (ligand for 5-HT2 receptors) displaced [3H]TRH in a dose-dependent manner at micromolar concentrations. These results suggest that some TRH receptors are related to 5-HT1 receptors, probably adjoining them on the membrane. This type of TRH receptor is shown to be among the high-affinity receptors which we reported previously. The significance of the receptor-coexistence is such that TRH facilitates serotonergic transmission by increasing the density of 5-HT1 receptors. This finding seems to support a pharmacological observation of other investigators that TRH potentiates 5-HT-induced hyperactivity in mice, probably by affecting postsynaptic 5-HT receptors.

Animals↗
PubMed1983

Behaviorally inactive doses of mianserin antagonize the suppressant effect of lysergic acid diethylamide on a fixed-ratio operant.

Male Sprague-Dawley rats were trained to respond for food reinforcement on a fixed-ratio 15 schedule. Low, behaviorally inactive, doses of mianserin (0.1-1.0 mg/kg) administered 30 min before the operant session antagonized the behavioral suppression induced by lysergic acid diethylamide (LSD; 50 micrograms/kg) administered immediately before the session. Mianserin (0.5-1.0 mg/kg) also partially antagonized the behavioral suppressant effects of higher doses of LSD. At a dose which suppressed behavior to 70% of control when administered alone, mianserin (10 mg/kg) did not antagonize the behavioral suppression induced by LSD (100-200 micrograms/kg). The data suggest that the suppression of operant behavior produced by mianserin may be the result of nonselective or multiple actions, or possibly the emergence of an LSD-type partial agonist property. Specificity of drug action as an antagonist apparently occurs at the behaviorally inactive, low doses of mianserin which may act through a selective blockade of serotonin receptors stimulated by LSD.

Animals↗
PubMed1981

The effect of d-lysergic acid diethylamide (LSD), 2,5-dimethoxy-4-methylamphetamine (DOM), pentobarbital and methaqualone on punished responding in control and 5,7-dihydroxytryptamine-treated rats.

The purpose of the present study was to determine the role of central 5-hydroxytryptamine (5-HT) neuronal systems in the effects of d-lysergic acid diethylamide (LSD), 2,5-methoxy-4-methylamphetamine (DOM), pentobarbital (PB) and methaqualone (MQ) on punished responding in rats. Water-deprived rats were trained to drink from a tube that was electrified at intervals (variable interval 21 sec; 0.03 mA current intensity), electrification being signalled by a tone. In daily 10-min control sessions, these animals accepted a relatively constant number of shocks; water consumption was also quite stable. At maximally effective doses PB, and to a lesser extent MQ, produced large (400-600 percent of control) increases in punished responding with little decrease in water intake. Higher doses of these agents produced a significant depression of unpunished responding (water intake). The hallucinogens, on the other hand, produced only moderate (125-175 percent of control) increases in the number of shock received, yet a similar depression of unpunished responding. Selective destruction of 5-HT neurons by intracerebroventricular administration of the neurotoxin 5,7-dihydroxytryptamine per se produced little change in the number of shocks received or water consumed in controls sessions. This destruction of 5-HT neurons failed to alter the effects of PB or MQ on punished or unpunished responding. The increase in punished responding produced by the hallucinogens, however, was blocked by this destruction of 5-HT neurons. Furthermore, the capacity of the hallucinogens to decrease water intake was significantly potentiated by the neurotoxin pretreatment. These data demonstrate that the effects of the hallucinogens LSD and DOM on conditioned suppression are quite different from those of PB and MQ, and that this difference may be due to the extent of 5-HT involvement in the effects of these agents.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗