Basic science

Authomatic Mood-Congruent Amygdala Responses to Masked Facial Expressions in Major Depression

In a recent study by Thomas Suslow et al (Biol Psychiatry 2010; 67:155-160), the authors studied the neurobiological substrates of automatic emotion processing in depression.

They compared 30 acutely depressed patients and 26 healthy control subjects regarding automatic amygdala responses to happy and sad facial expressions, using functional magnetic resonance imaging.

 A presentation paradigm using subliminal, backward-masked stimuli was used to examine amygdale automatic responses.

The authors observed a robust emotion by group interaction in the right amygdala. The healthy controls revealed stronger responses to happy faces and depressed patients showed the opposite.

Amygdala responsiveness to happy facial expression correlated negatively with severity of depression.

The authors concluded that depressed patients exhibit potentiated amygdala reactivity to masked negative stimuli and a reduced responsiveness to masked positive stimuli when compared to healthy controls.

The authors suggested that depression is characterized by mood-congruent processing of emotional stimuli in the amygdala already at an automatic level of processing.

The relationship between cigarette smoking and panic disorder according to a recent critical review of the literature.

In an online recent published paper we made a critical review of the literature on cigarette smoking and panic disorder. The background was that cigarette smoking and panic disorder, with or without agoraphobia, tend to co-occur at a rate that cannot be explained by chance. The more widely accepted hypotheses of the possible etiopathogenesis underlying such a comorbidity are that: 1) cigarette smoking promotes panic by inducing respiratory abnormalities/lung disease or by increasing potentially fear-producing bodily sensations; 2) nicotine produces physiological effects characteristic of panic by releasing norepinephrine; 3) panic disorder promotes cigarette smoking as self-medication; and 4) a shared vulnerability promotes both conditions.

In the review we identified, via Medline, English language articles published from 1960 to 2008 using as key words: “nicotine and panic”, “tobacco and panic”, and “smoking and panic”. We selected 24 studies according to the following criteria: 1) panic disorder with or without agoraphobia and nicotine dependence, when used, diagnosed according to the DSM; 2) no additional co-morbidity or, if present, adjustment for it in the statistical analyses; 3) use of adult or adolescent samples; and 4) comparison with a non-clinical control group or application of a cross-over design.

On the basis of the critical evaluation of the 24 studies selected we found that panic disorder and cigarette smoking each appear to have the capacity to serve as a causal factor/facilitator in the development of the other. Although the temporal pattern and the etiopathogenetic explanations of such a co-occurrence seem still unclear, the review highlighted the evidence that cigarette smoking tends to precede the onset of panic, thus promoting it. We suggested, as concluding remarks, to encourage further studies in order to strengthen and confirm the observation that smoking tends to precede, thus facilitating, the onset of panic. We also pointed out the need to start using the diagnosis of nicotine dependence when studying cigarette smoking to achieve more comparable data results among different studies and awaken researchers and clinicians to use such a diagnosis since cigarette smoking is not an habit of life but a psychiatric disorder.

The article can bee found here .

Cannabidiol, a component of cannabis, inhibits drug-seeking behaviour

Effects of cannabidiol, a constituent of cannabis without psychotomimetic properties, were studied in rats using a drug (heroin) self-adminstration model in a study by  Ren and colleagues  on the Journal of Neuroscience.   The administration of cannabidiol reduced reinstatement of drug-seeking behaviour and relapse,  without causing any locomotor impairment. This effect was apparent 24 h after administration of cannabidiol and persisted for two weeks . This protracted behavioral effect implies a long-term impact on synaptic plasticity. This contrasts with the documented effects of THC  (the psychoactive constituent of cannabis), which is known to enhance heroin self-administration (Solinas et al., 2004). Of the over 1 million opiate-dependent subjects today, only less than a quarter of such individuals receive treatment, which have traditionally targeted µ-opioid receptors. Cannabidiol lacks hedonic properties on its own, is there a potential for it as a future treatment strategy to attenuate drug-seeking behaviour?

link to the article: http://www.jneurosci.org/cgi/content/abstract/29/47/14764