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Overt behavior

My answer always is that no one has yet done a detailed neurobehavioral study of these individuals and the deficit that they may have. It may be very subtle in nature, and 1 am not sure that we have the methods available to detect and quantify those deficits. The fact that these people are not walking in with overt behavioral disturbances as the people with MPTP did. 1 think, is related to the fact that, one, they may not have the kind of neurotoxicity we are suspecting, and two, if they do, the kind of functional consequences that you may get from serotonergic dysfunction may be much more subtle than the kind of functional consequences you get with dopamine dysfunction, where it is very easy to recognize the parkinsonian patient... [Pg.319]

Effects In Humans. Neither postmortem nor functional cerebrospinal fluid (CSF) studies in humans provide firm evidence for similar, long-term damages or alterations to monoaminergic neurons in chronic stimulant abusers. In part, the lack of demonstrable neurochemical changes may well be due to the obvious preclusion of well-controlled prospective experimentation in humans, as well as to variability in critical variables (e.g., individual sensitivity or pattern of abuse) encountered in clinical research. Possible relationship of the various complications of stimulant abuse including hyperpyrexia, seizure, anoxia, and metabolic exhaustion to neuronal chromatolysis, terminal destruction, and monoamine and enzymatic depletion have not been systematically explored in human autopsy eases. It should be also noted that, under nonperturbed conditions, overt behavioral deficits are rare in... [Pg.332]

COMMENT I think another matter to take into account is that, at least from the experienee of dopamine systems, in order to get overt behavioral dysfunetion you really need a pretty whopping lesion. In the primate, to get the kind of Parkinsonism that people talk about in animal models, that animal model actually turns out to be very difficult to produce in chronic Parkinsonism. The problem is developing an animal that has 90 to 95 percent depletion of dopamine on a chronic basis. As you know, it is a very narrow window, and it is very difficult to produce that kind of animal preparation. So I think you have to consider the possibility that lack of symptoms after serotonergic lesions could, perhaps, be related to the fact that we are dealing with preparations where there is a 50, 60, 70 percent depletion where we don t have enough of a lesion to produce an overt behavioral disturbance. [Pg.352]

The interaction of ketamine with each of the three anticonvulsant compounds was also tested. Ketamine, 15 mg/kg, a dose showing no anti-PTZ effect and causing no overt behavioral changes, potentiated the effect of phenobarbital (20 mg/kg) in delaying the clonic and tonic convulsive responses and lethality (figure 3). Ketamine also potentiated the ability of phenytoin (20 mg/kg) to delay... [Pg.82]

The results demonstrate anticonvulsant properties of PCP and ketamine in two quite different seizure models. On the one hand, ketamine was effective in antagonizing several components of PTZ activity. Others have previously reported anti-PTZ effects of ketamine. However, the present results demonstrate that the anticonvulsant effects of ketamine against PTZ seizures closely resembled the effects of phenobarbital in that both compounds delayed clonic convulsions and prevented tonic extension. Moreover, a low dose of ketamine, which alone showed no anticonvulsant effect or overt behavioral changes, potentiated the anti-PTZ effects of phenobarbita 1. These findings suggest that ketamine possesses selective anticonvulsant properties. The anticonvulsant mechanism of action for phenobarbital is not known. However, the similarities between ketamine and phenobarbital, and the interaction between the two compounds, suggest a common mechanism or site of acti on. [Pg.89]

FIGURE 4. Dose-response-curves for the effects of phencyclinoids on (A) locomotion (B) stereotypy and (C) ataxia. Overt behaviors were scored using the behavioral rating scales of Sturgeon et al. (1979). [Pg.115]

Having attacked the thinking of others on emotion, I am obligated to suggest my own list of basic emotions. Since I prefer to think primarily in terms of affects, I like to use affective terms for the emotions. Each emotional modality in such a list should be species-wide and hence adaptive, and include a basic, distinct affect and adaptive (if nonspecific) overt behavioral tendency. The list is also based on evidence for specific neural mediation, presence in other primates, specific situational elicitors, specific emotional expressions, and specific visceral adjustments, but space does not permit systematic review of these data. Taken together, the list is intended to comprise the inventory of whole-body behaviors exhibited by normal adults throughout the world. For each emotional modality, I will mention some of its characteristic features. [Pg.32]

This emotion protects us from toxins (Rozin et al., 1993), and may be the main emotional explanation for hygienic practices. It is present from birth (Steiner, 1979). The overt behaviors range from avoidance of the stimulus to ejecting it from the mouth, throat or stomach. Associations between a stimulus that elicits disgust are easy to acquire and hard to extinguish (Rozin et al., 1993). Nature seems to protect us indefinitely from any stimulus that was potentially harmful in the past. [Pg.34]

Emotions are sometimes said to be physiologically arousing, but sleep is an exception. It is a true motivated behavior because drowsy animals will seek a suitable place to sleep rather than simply collapsing on the spot. Drowsiness can be distinguished from fatigue by its overt behavior. Drowsiness prompts sleep fatigue prompts rest. But the function of sleep seems to be rest also. [Pg.34]

Studies in mice with a targeted inactivation of other 5-HT receptor sub-types, such as the S-HTsa and 5-HT7, or a transgenic line that overexpresses 5-HT3, demonstrate that these receptors modulate the activity of neural circuits involved specifically in exploratory and reward-related behavior. When exposed to novel environments, KO mice lacking the S-HTsa exhibit increased exploratory activity and an attenuated stimulatory effect of lysergic acid diethylamide (LSD) on exploratory activity but no change in anxiety-related behavior (Grailhe et al. 1999), whereas S-HTy KO mice do not express any overt behavioral phenotype at all (Hedlund et al. 2003). [Pg.84]

Tannock, R., Schachar, R.J., Carr, R.P. and Logan, G.D. (1989) Dose-response effects of methylphenidate on academic petfot-mance and overt behavior in hyperactive children. Pediatrics 84 648-657. [Pg.465]

It is possible that psi information flows directly from the psi receptor to the brain and then results in overt behavior. An everyday example of this would be your reaction if someone sneaks up behind you and makes a loud noise. You jump We would then talk about the reception and conversion of the sound waves into a barrage of neural impulses from the ear and their direct effect on various startle reflex mechanisms within the nervous system and brain, resulting in your behavior-jumping. The whole thing happens before consciousness has time to get involved. [Pg.56]

Psi information may flow from receptor to conscious mind to brain to behavior. This possibility gives importance to the mental processes of the percipient, even though they eventually affect the brain processes and overt behavior and so have the same final manifestations found in the behavioristic approach but in this case, the percipient is at least partially conscious of what is going on. [Pg.58]

The following section describes protocols for evaluating both dependence and abuse. For reasons of homogeneity with the other procedures presented above, only protocols in the rat will be presented. Although results in the rat are generally similar to those obtained in non-human primates, the regulatory authorities, in particular the FDA, prefer primate studies for abuse evaluation because of a presumed increased predictability to man. The active doses and pharmacokinetics are likely to be closer between human and non-human primates, as are the kinds of overt behavioral effects observed. [Pg.49]

This was totally non-verbal, unrelated to his overt behavior (which by then was quite civil), and was experienced by me as a palpable force which attacked my solar plexus -- sort of like psychically having the wind kicked out of me. Any Shamanic warrior" would have understood how to protect himself from this, but I was wide open and totally ignorant that such forces actually existed outside of Carlos Castaneda books. [Pg.31]

Adams MD, Earnhardt JT, Martin BR, Harris LS, Dewey WL, Razdan RK (1977) A cannabinoid with cardiovascular activity but no overt behavioral effects. Experientia 33 1204-1205... [Pg.619]

Besides straightforward observations of overt behavior, the wear of... [Pg.363]


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See also in sourсe #XX -- [ Pg.81 ]




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