Basic science
Astrocyte´s new role in controlling breathing
Jul 20th
A recent study published in Science highlights the role of astrocytes, star-shaped cells found in the brain and spinal cord, in regulating respiration by ’sensing’ changes in the concentration of carbon dioxide in the blood and stimulating neurons to regulate respiration.
Astrocytes have been traditionally thought to just provide structural and metabolic support for other cells, so this new information adds an unexpected role in controlling breathing.
Find a link to the paper abstract here
Find a comment on Nature news about this topic here
Feb 9th
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.
Metabolic Changes in Schizophrenia and Human Brain Evolution
Feb 2nd
Khaitovich et al. – Genome Biology 2008, 9:R124
In this study, authors aim to identify molecular mechanisms involved in the evolution of human-specific cognitive abilities by combining biological data from two research directions:
- Identifying the molecular changes that took place in the human evolutionary lineage, presumably due to positive selection
- Considering the molecular changes observed in schizophrenia, a psychiatric disorder believed to affect such human cognitive functions as the capacity for complex social relations and language
They assume that schizophrenia affects recently evolved biological processes underlying human-specific cognitive abilities, so they expect a significant overlap between the recent evolutionary and the pathological changes.
Authors directly study brain metabolism in prefrontal cortex of humans (schizophrenic patients and controls) and non-human primates (chimpanzees and rhesus macaques) by using 1H NMR spectroscopy. They realize that metabolites linked to energy metabolism, neurotransmission and lipid/cell membrane metabolism are different between schizophrenic patients and controls. In addition, they realize that the different metabolites found in schizophrenic patients and controls have as well evolved rapidly in the evolutionary lineage, when performing an analysis including chimpanzees and rhesus macaques. Finally, using linkage disequilibrium analysis, authors conclude that these differences are explained by positive selection instead of relaxation of selective constraint.
In the discussion, authors argue that is conceivable that human brain is running very close to the limit of its metabolic capacities, so, as a consequence, any perturbation of normal energy metabolism levels may be expected to adversely affect brain function, leading to human cognitive disfunctions, such as schizophrenia.
Authors finally conclude that, taken together, findings indicate that changes in human brain metabolism may have been an important step in the evolution of human cognitive abilities and remark that results are consistent with the theory that schizophrenia is a costly by-product of human brain evolution.
You can find a direct link to the full-text article here:
The relationship between cigarette smoking and panic disorder according to a recent critical review of the literature.
Jan 19th
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
Jan 4th
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
The Suffocating Amygdala
Dec 29th
Neurons in the amydgala can directly sense an increased concentration of carbon dioxide, an article published on “Cell” reported. Exposure to CO2 triggers fearful and anxiety responses, both in humans and in animals. In fact, it is well known that inhalation of high doses of CO2 can evoke panic attacks. More >

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