Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression.

Reconciling the role of central serotonin neurons in human and animal behavior

http://europepmc.org/articles/PMC3915298?pdf=render

Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting.

The possibility of using polysorbate 80-coated polybutylcyanoacrylate nanoparticles to deliver low molecular polar hydrophilic drugs to the CNS has been studied. Tubocurarine (a quaternary ammonium salt) does not penetrate the normal intact blood-brain barrier. However, the injection of this drug directly into the cerebral ventricles of the brain provokes the development of epileptiform seizures as assessed by electroencephalogram (EEG). An in situ perfused rat brain technique was used as an experimental technique together with a simultaneous recording of the EEG. Nanoparticles were prepared by butylcyanoacrylate polymerization in an acidic medium. Fifteen minutes after the introduction of tubocurarine-loaded polysorbate 80-coated nanoparticles into the perfusate, epileptiform spikes in the EEG appeared. Intraventricular injection of tubocurarine caused the appearance of the EEG seizures 5 min after administration. Neither tubocurarine solution nor tubocurarine-loaded nanoparticles without polysorbate 80 or a mixture of polysorbate 80 and tubocurarine were able to influence the EEG. Thus only the loading of tubocurarine onto the polysorbate 80-coated nanoparticles appears to enable the transport of this quaternary ammonium compound through the blood-brain barrier.

Significant entry of tubocurarine into the brain of rats by adsorption to polysorbate 80–coated polybutylcyanoacrylate nanoparticles: An in situ brain perfusion study

Publisher Summary This chapter discusses the interplay between the laboratory and the clinic in analyzing the biological bases of parkinsonism arid formulating a rational approach to its treatment. There is a discussion regarding the syndrome, its accompanying neuropathology, and the current modes of treatments. Two animal models of parkinsonism are reviewed. Models involving 6HDA and MPTP represent a considerable advantage over previous pharmacological and surgical models of parkinsonism. Lesions can be made that are neurochemically specific; they can be restricted to the brain or even to individual dopamine (DA) projections; and they are permanent. Most important, they result in a collection of neurological impairments that parallel the clinical syndrome to a remarkable degree. Destruction of the nigrostriatal bundle (NSB) in adult animals produces akinesia, rigidity, and sensory neglect, large lesions are required before these neurological deficits occur, such deficits do not occur when comparable lesions are made in very young animals. Instead, a quite different syndrome emerges and after exposure to stressors, adult preclinical animals with moderate DA depletions show behavioral dysfunctions that are similar to those seen after more extensive lesions.

Animal models of parkinsonism using selective neurotoxins: clinical and basic implications.

Catecholaminergic involvement in the control of aggression: Hormones, the peripheral sympathetic, and central noradrenergic systems

The role of α-adrenergic mechanisms within the area postrema in dopamine-induced emesis

Effects of parachlorophenylalanine and 5,6-dihydroxytryptamine on aggressive behaviour evoked by cholinomimetics and anticholinesterases injected into the cerebral ventricles of conscious cats.

Emotional behaviour, especially aggression, evoked by cholinomimetics, anticholinesterases, nicotinic, and muscarinic ganglionic stimulants injected into the cerebral ventricles of unanesthetized cats was studied and compared. Aggressive behaviour was obtained after intraventricular carbachol, muscarine, arecoline, eserine, neostigmine, and 4-m-chlorophenylcarbamoyloxy-2-butynyl-trimethylammonium chloride (McN-A-343). The aggressive behaviour and the autonomic and motor phenomena of various single doses of cholinomimetics and anticholinesterases were dose-dependent and long-lasting. Neostigmine produced aggressive behaviour only in about one-fourth of the experiments, while arecoline and McN-A-343 induced aggression of slightest intensity. The type of aggressive behaviour caused by carbachol, arecoline, eserine, neostigmine, and McN-A-343 was classified as irritable-type aggressive behaviour, while muscarine induced fear-type aggressive behaviour. Intraventricular administration of nicotine, dimethylphenylpiperazinium, tetramethylammonium, and N-benzyl-3-pyrrolidyl acetate methobromide (AHR-602) did not evoke aggressive behaviour, but they induced fleeting autonomic and motor phenomena. The ability of single intraventricular injections of cholinomimetics and anticholinesterases to trigger and to maintain long-lasting aggressive behavioural phenomena cannot be ascribed to a rapid ‘detonator’ transmission, but rather to an action that differs from the conventional transmitter function. In addition, we advance a hypothesis that the cholinoceptive neurons sensitive to cholinomimetics and anticholinesterases behave as a biologic generator that when activated produces long-lasting aggression with autonomic and motor phenomena.

Comparative study of aggressive behaviour after injection of cholinomimetics, anticholinesterases, nicotinic, and muscarinic ganglionic stimulants into the cerebral ventricles of conscious cats: failure of nicotinic drugs to evoke aggression.

The emetic action of dopmaine, norepinephrine, epinephrine, nicotine, dimethylphenyl-piperazinium (DMPP), and 4-m-chlorophenylcarbamoyloxy-2-butynyltrimefhylammonium (McN-A-343) injected intracerebroventricularly (i.c.v.) to the unanesthetized cat was investigated and compared. ED50 values (mg) were as follows: nicotine, 0.011; epinephrine, 0.047; norepinephrine, 0.57; DMPP, 0.9; dopamine, 1.66; and McN-A-343, 4.42. The most potent was nicotine, whereas the least active McN-A-343. On the other hand, DMPP produced the longest emetic response, about 30 min, while McN-A-343-induced emesis lasted up to 1 min. The ablation of the area postrema abolished the emetic response to i.c.v. dopamine, norepinephrine, epinephrine, nicotine, and DMPP. However, the emetic response to i.c.v. McN-A-343 was significantly reduced in cats with an ablated area postrema. Taken together, the results obtained show that the area postrema is almost always involved in the central regulation of emesis and that the area postrema represents, in most cats, a common site of confluence of different inputs subserving the emesis.

Ablation of the area postrema and emesis.

In unanesthetized cats, defecation produced by thyrotropin-releasing hormone (TRH) was investigated after its injection into the cerebral ventricle (ICV) through chronically implanted cannulae. TRH injected in doses from 0.1 to 1.0 mg into the cerebral ventricle evoked defecation which was not dose-dependent. The antimuscarinic drug, atropine, the ganglionic blocker, mecamylamine, the alpha and beta adrenergic blocking agents, yohimbine and propranolol, the dopamine antagonist, chlorpromazine, the 5-hydroxytryptamine antagonist, methysergide, and the antihistamine, antazoline, all injected into the cerebral ventricle had virtually no effect on the defecation evoked by TRH injected similarly. In cats pretreated with ICV reserpine, 5,6-dihydroxytryptamine and hemicholinium-3, the defecation induced by ICV TRH was not significantly changed. On the other hand, in cats pretreated with ICV 6-hydroxydopamine, the defecation caused by ICV TRH was potentiated. Therefore, it is concluded that TRH-induced defecation could not be related to central catecholaminergic, 5-hydroxytryptaminergic and cholinergic receptors, but rather to central TRH sites in the cat.

Studies of thyrotropin-releasing hormone (TRH)-induced defecation in cats.

Popular Tasks used by Researchers

How can I help with your research?

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

We encountered an error while loading the panel. Please try refreshing the page.

Something went wrong

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

Anyone with the link can view this chat. You can switch it back to private anytime.

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

D.B. Beleslin

Author Tools

Chat about Author