应激易化成瘾及复吸的生物学机制

自从1946年Ｂａｌｅｓ开创性地研究社会心理应激与成瘾物质滥用的关系,至今50余年,无论是基于人群的临床流行病学研究,还是动物实验,均证明应激与成瘾及复吸间存在着肯定的正相关关系[1]。动物自身给药(ＳＡ)模型及动物ＳＡ复发模型的建立更是极大地推动了应激与成瘾关系?..     

Histoire du concept d’anxiété : de la théorie des humeurs à la biologie moléculaire

If the study of the anxiety seems to have known an eclipse during years 1930–1960, the works of D. Klein [32] (1964) [32] have labeled a renewal of interest in the study of the anxiety at the same time on the experimental, pharmacological, epidemiological but also clinical plan. From the 1970s, the modification of the classification of anxiety disorders at the instigation of the criteria of the DSM in a purpose of clinical researches and pharmacological allowed to distinguish various forms of anxiety the biological origins of which seem better established today at the price of a dismemberment of the classification of the neurosis's. If the anxiety neurosis as the specific entity was separated in generalized anxiety disorder and panic disorder, the phobic disorder was fragmented in social phobia, agoraphobia and simple phobia. The neurosis of constraint is a part from now on obsessive compulsive disorders and the hysteria became a somatoform disorder. The place of the central anxiety in the mental illness and which formerly rolled out in the form of anxiety of castration, separation or division in the psychodynamic model became otherwise a secondary phenomenon, the sign of an adjustment disorder. The development of the pharmacological treatments of the anxiety since the discovery of the benzodiazepines (1957) but also the antidepressants shows us that we changed gradually paradigm and it seems from now on that through a better knowledge of the neurobiological mechanisms of the anxiety we can relieve patients’ largest number even if at the same time we attend an overconsumption of anxiolytics. The paradox of the human being seems to know better its fear to master her (it) and its research for the property–to be seems often short-lived.     

Neurobiological basis of chemotherapy-induced cognitive impairment: A review of rodent research

For some cancer survivors chemotherapy treatment is associated with lasting cognitive impairment, long after treatment cessation. Several candidate mechanisms have been suggested, yet clinical research has been unable to clearly tease apart these hypotheses. Rodent research has allowed a systematic study of these underlying mechanisms in the absence of potential patient confounds. Herein, this research is reviewed with emphasis on the role of the blood-brain barrier, neurogenesis, oxidative stress, white matter, immune system/(neuro) inflammation, HPA axis, blood flow, and cancer in chemotherapy-induced cognitive impairment. Furthermore, potential pharmacotherapy and behavioral intervention strategies are reviewed. This paper ends with methodological considerations in study of chemotherapy and cognition.     

Alpha absolute power measurement in panic disorder with agoraphobia patients

Background

Panic attacks are thought to be a result from a dysfunctional coordination of cortical and brainstem sensory information leading to heightened amygdala activity with subsequent neuroendocrine, autonomic and behavioral activation. Prefrontal areas may be responsible for inhibitory top-down control processes and alpha synchronization seems to reflect this modulation. The objective of this study was to measure frontal absolute alpha-power with qEEG in 24 subjects with panic disorder and agoraphobia (PDA) compared to 21 healthy controls.

Methods

qEEG data were acquired while participants watched a computer simulation, consisting of moments classified as “high anxiety”(HAM) and “low anxiety” (LAM). qEEG data were also acquired during two rest conditions, before and after the computer simulation display.

Results

We observed a higher absolute alpha-power in controls when compared to the PDA patients while watching the computer simulation. The main finding was an interaction between the moment and group factors on frontal cortex. Our findings suggest that the decreased alpha-power in the frontal cortex for the PDA group may reflect a state of high excitability.

Conclusions

Our results suggest a possible deficiency in top-down control processes of anxiety reflected by a low absolute alpha-power in the PDA group while watching the computer simulation and they highlight that prefrontal regions and frontal region nearby the temporal area are recruited during the exposure to anxiogenic stimuli.     

Parler du harcèlement (stalking)

Stalking is a common social problem often driven by psychiatric disorder in its perpetrators and productive of psychological and social damage in its victims. Unfortunately, it is not formally acknowledged in current classificatory systems (DSM-5 and ICD-10). Here, authors provide an overview of stalking through a clinical prism of general and forensic psychiatry. Stalking is a chronic behaviour consisting of willful, malicious and, repeated following and harassing of another person. Stalking can take its toll on victim's mental status. Sequelae are legion including depression (with suicidality), anxiety (panic and PTSD), catagelophobia, worsening of medical conditions, personality changes/paranoia, and, substance abuse. A total of 90 % of stalkers are men. A total of 80 % of victims are women. Stalking acts can express a range of motivations including anger, jealousy, rage over abandonment, striving for power, or, a need to control the victim. Evidence from fMRI studies demonstrated a heightened activity of subcortical dopaminergic pathways of reward system and possible low activity of central serotonin. Generally speaking, stalkers mostly do not become violent (associated homicide in 2 %). The Stalking and Harassement Behaviour Scale is commonly deployed in clinical and forensic settings. Types of stakers include erotomanic, love obsessional (including intimacy seekers and incompetent suiters), simple obsessional (including rejected and resentful categories), and false victimiztaion syndrome. Anti-stalking laws were borne out as a result of public concerns that community members were powerless to protect themselves against harassing behaviours. Stalkers are most likely to be found among the diagnostic classes of psychotic disorders or (severe) personality disorders. Treatment of these behavioural problems should target the specific underlying psychopathological mechanisms, which require careful diagnostic assessment. Both stalkers and victims are in urgent need of the development of specific treatments.     

Opioids and the developing organism: A comprehensive bibliography, 1984–1988

A comprehensive bibliography of the literature concerned with opioids and the developing organism for 1984-1988 is presented. Utilized with companion papers (Neurosci. Biobehav. Rev. 6:439-479; 1982; 8:387-403; 1984), these articles cover the clinical and laboratory references beginning in 1875. For the years 1984, 1985, 1986, 1987, and 1988, a total of 877 citations were recorded. A series of indexes accompanies the citations in order to make the literature more accessible. These indexes are divided into clinical and laboratory topics, and subdivided into such topics as the type of opioid explored and the general area of biological interest (e.g., physiology).     

Chronic subanesthetic halothane exposure causes selective alterations in neurotransmitter systems in discrete brain regions

The effects of prolonged exposure to subanesthetic concentrations of halothane on dopaminergic, noradrenergic, cholinergic, and GABAergic neuronal systems were studied in discrete regions of the rat brain. Exposures to 0.25% halothane in air were for 8 h/day, 5 days/week during an 8-week period; control rats received only air at an equivalent flow rate. Twenty-four hours after the last exposure the animals were killed and brain, liver, muscle, and serum samples were taken for analyses. Discrete brain regions were removed by microdissection and assayed for norepinephrine, dopamine, glutamate decarboxylase, choline acetyltransferase, and proteins. The remaining tissues and serum were analyzed for halothane content; however, halothane was not detected in any sample tested. Rats which were exposed to halothane exhibited a marked reduction in body weight gain and their urine volume was significantly greater than in the controls. Significant changes were observed in regions associated with the limbic system, for example, dopamine was increased in the ventral tegmental area, choline acetyltransferase was increased in the nucleus accumbens, caudate, and globus pallidus and its activity decreased in the central gray. The activity of glutamate decarboxylase was decreased in the accumbens and in the medial preoptic nuclei but increased in the lateral preoptic nucleus. There was no apparent effect on norepinephrine concentrations. We suggest that these selective changes in limbic regions may cause behavioral deficits consequent to chronic subanesthetic halothane exposure.     

Synaptic transmission between rat spinal cord explants and dissociated superior cervical ganglion neurons in tissue culture.

Physiological properties of the synapses formed between explants of spinal cord and dissociated autonomic ganglion neurons in tissue culture were studied using intracellular and extracellular stimulation and recording techniques (as well as iontophoresis) with a culture perfusion system allowing continuous microscopic observation during repeated changes of the bathing medium. The principal neurons of the superior cervical ganglion (SCGN) were dissociated from perinatal rats and the spinal cord explants were obtained from 15-day rat fetuses; these were allowed to mature for 3-10 weeks in co-culture. Recordings from over 1000 SCGN established that: (a) spontaneous small depolarizations and action potentials occurred in 20% of the SCGN studied, (b) the EPSPs observed in SCGN after spinal cord stimulation were sensitive to decreased Ca2+ and increased Mg2+, as well as to D-tubocurare, hexamethonium and mecamylamine, but not to atropine (at 10(-6) M concentration) or to the alpha-adrenergic blocking agents phentolamine or phenoxybenzamine; no potentiation of the EPSPs was seen with neostigmate or eserine, (c) acetylcholine directly applied to the SCGN was seen to mimic the responses seen after spinal cord stimulation; tetrodotoxin blocked both direct and iontophoretically fired action potentials, with only a suprathreshold acetylcholine potential remaining. These synapses were not sensitive to alpha-bungarotoxin. It is concluded that the synapses formed by spinal cord neurites on principal SCGN in tissue culture are nicotinic cholinergic, and that the evoked EPSPs recorded in this study are thus similar to the orthodromic fast EPSPs observed in vivo. No slow synaptic responses were observed and no demonstrable effects were noted that could be attributed to adrenergic transmission.