The powerful placebo: doubting the doubters.
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Controlled Clinical Trials as Topic↗
Biomedical subjects
W A Weiger
Publications and source records attributed to W A Weiger.
Serotonergic modulation of behaviour: a phylogenetic overview.
Serotonergic neurons are present in all phyla that possess nervous systems. In most of these phyla, serotonin modulates important behaviours, including feeding, sexual and aggressive behaviour. Serotonin exerts its effects by acting in three basic modes: as a classical neurotransmitter, as a neuromodulator, or as a neurohormone. In a number of invertebrate species, the neural circuitry underlying the effects of serotonin has been well characterized, whereas in vertebrates, the mechanisms by which serotonin affects behaviour are currently less fully understood. The following review examines the role played by serotonin in the generation and modulation of behaviour in successively more complex species, ranging from coelenterates to humans.
Animals↗
Excitation of identified serotonergic neurons by escape command neurons in lobsters.
Serotonin-containing neurosecretory neurons in the first abdominal ganglion (A1 5-HT cells) of the lobster (Homarus americanus) ventral nerve cord have been shown previously to function as 'gain setters' in postural, slow muscle, command neuron circuitries. Here we show that these same amine neurons receive excitatory input from lateral (LG) and medial (MG) giant axons, which are major interneurons in phasic, fast muscle systems. Activation of either LG or MG axons elicits short-latency, non-fatiguing, long-lasting excitatory postsynaptic potentials (EPSPs) in A1 5-HT cells which follow stimulus frequencies of up to 100 Hz in a 1:1 fashion. Single spikes triggered in either giant axon can produce EPSPs in the A1 5-HT cells of sufficient magnitude to cause the cells to spike and to fire additional action potentials after variable latencies; action potentials elicited in this way reset the endogenous spontaneous spiking rhythm of the A1 5-HT neurons. The giant-axon-evoked EPSP amplitudes show substantial variation from animal to animal. In individual preparations, the variation of EPSP size from stimulus to stimulus was small over the first 25 ms of the response, but increased considerably in the later, plateau phase of each response. When tested in the same preparation, EPSPs in A1 5-HT cells evoked by firing the LG axons were larger, longer-lasting and more variable than those triggered by firing the MGs. Firing A1 5-HT cells through an intracellular electrode, prior to activation of the giant fiber pathway, significantly reduced the size of LG-evoked EPSPs in A1 5-HT cells. Finally, morphological and physiological results suggest that similarities exist between giant fiber pathways in lobsters and crayfish. The possible functional significance of an involvement of these large amine-containing neurosecretory neurons in both tonic and phasic muscle circuitries will be discussed.
Animals↗
Serotonin-containing neurons in lobsters: origins and characterization of inhibitory postsynaptic potentials.
1. The serotonin-containing neurons in the A1 ganglion of the lobster have been shown to act as "gain setters" in neuronal circuits that control the adoption of behaviorally relevant postures. These neurons are subject to tonic inhibition, which has been proposed as an important regulator of their activity. This study explores the pharmacological nature and anatomic location of the neurons responsible for inhibition of these A1 cells; the role played by inhibitory inputs in controlling the firing rates of these neurons is also examined. 2. Three classes of inhibitory postsynaptic potentials (IPSPs) are distinguished in the somata of A1 serotonin-containing neurons. The most common (type I) has amplitudes ranging from 0.4 to 1.5 mV; types II (2-5 mV) and III (< 0.4 mV) are less often seen. 3. Type I IPSPs are reversibly blocked by picrotoxin, a gamma-aminobutyric acid antagonist, but not by serotonin or octopamine antagonists known to act at other lobster synapses. 4. Elimination of type I IPSPs by reversible or irreversible blockage of conduction from the A3 ganglion results in a firing rate increase of approximately 50% in A1 serotonin-containing neurons; IPSP recovery results in a firing rate decrease of corresponding magnitude. Connective transections that do not affect IPSPs do not cause a firing rate increase. 5. Lesions studies suggest that type I IPSPs originate in neurons whose somata are located near the midline of the A3 ganglion; a cell impaled in this region showed action potentials that correlated with IPSPs in an A1 serotonin-containing neuron.
Aggression↗
Serotonin-containing neurons in lobsters: the actions of gamma-aminobutyric acid, octopamine, serotonin, and proctolin on activity of a pair of identified neurons in the first abdominal ganglion.
1. Serotonin has been shown to be an important neurohormone that modulates behavioral output in lobsters. This study explores the neurochemical identity of excitatory and inhibitory inputs to a pair of identified serotonin-containing neurons in the first abdominal ganglion (A1) of the lobster that also contain the pentapeptide proctolin. These neurons are spontaneously active, appear to be driven by an endogenous pacemaking mechanism, and have been shown to play a role in circuits that control behaviorally relevant postures. 2. To explore the exogenous control of neuronal activity, a number of putative neuroactive compounds were superfused over the A1 serotonin-containing neurons in isolated ventral nerve cords. Three amines, gamma-aminobutyric acid (GABA), octopamine, and serotonin, were found to be potent inhibitors in a dose-dependent manner. GABA inhibition had a rapid onset and termination and yielded a transient postinhibitory rebound activity immediately after amine washout; activity eventually returned to the preinhibition level. Octopamine inhibition had a less rapid onset and termination, and the steady-state activity after inhibition was higher than preinhibition firing in most cells (22% of which were statistically significantly increased). Serotonin inhibition had a relatively slow onset and termination, and the steady-state activity after inhibition remained low in most cells (19% significantly decreased). 3. Repeated or prolonged exposure to these three amines reduced the efficacy of inhibition. Three types of desensitization have been empirically defined: 1) rapid desensitization, which tended to dampen the initial inhibition; this was particularly strong for GABA inhibition; 2) low-dose desensitization, in which the A1 serotonin containing neurons became less sensitive to inhibition by a particular concentration of amine after prior exposure to a lower concentration, although the lower concentration may not by itself have had inhibitory effects; this was seen with octopamine inhibition; and 3) long-term desensitization, in which the efficacy of inhibition of a particular amine concentration dwindled with repeated applications (even with up to 160 min washout between applications); this was seen with octopamine and serotonin inhibition, although not for every A1 serotonin-containing neuron analyzed. 4. Bath application of these three amines was still capable of inhibiting the A1 serotonin-containing neurons when inhibitory synaptic transmission was blocked by use of low Ca2+/high Mg2+ solutions. 5. The pentapeptide proctolin excited the A1 serotonin-containing neurons: it activated silent neurons and increased the firing rate of spontaneously active neurons. The excitatory effect outlasted the presence of the peptide.(ABSTRACT TRUNCATED AT 400 WORDS)
Abdomen↗
Chronic fatigue syndrome.
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Fatigue Syndrome, Chronic↗
An approach to the neurology of aggression.
Aggressive behavior is controlled at multiple anatomical levels within the human brain. To illustrate hierarchical neural controls over aggression, we compare and contrast the roles of the hypothalamus, amygdaloid complex, and orbital prefrontal cortex in terms of their distinctive sensory inputs, effector channels, and principles of integration as deduced from observations in animals and man. We illustrate characteristic syndromes of human aggression resulting from hypothalamic, temporolimbic, or frontal cortical lesions. The application of this perspective to research on criminal violence is discussed.
Aggression↗