House of Mind

"Biology gives you a brain. Life turns it into a mind" - Jeffrey Eugenides

  • 16th October
    2012
  • 16
Does the future of antidepressants lie in anesthetics? 
Mood disorders like depression are among the leading causes of mental disability in the U.S. Because the therapeutic effects of traditional interventions and pharmacological treatments have shown to be limited in terms of efficacy, new therapies that are rapid acting and have increased efficacy in treatment-resistant populations are actively being sought out. Today, I was surprised to learn that the volatile anesthetic isoflurane has been shown to have antidepressant effects in humans since 1985 (Langer et al.) Given that I use isoflurane to knock my rats out while I implant cannulas and our lab studio the development of depressive-like behavior following early life abuse, I was floored. 
Although clinical literature has provided hints into the use of anesthetics, whether isoflurane could also exert antidepressant-like effects in conventional animal models of depression had not been determined until recently. Paul Shepard’s lab at the Maryland Psychiatric Research Center (MPRC) have behavioral evidence suggesting that a short period of acute isoflurane inhalation is sufficient to impede the development of depressive-likebehavior in rats. 
For this study, the group administered isoflurane (2% in 100% O2) to adult male Sprague Dawley rats continuously for two hours through a nose cone attached to a standard stereotaxic apparatus. Two weeks following exposure to isoflurane, rats entered a conventional two-day learned helplessness paradigm. Learned helplessness is a term that refers to the condition of an organism (human or animal) that has learned to behave helplessly and fails to respond even in the presence of opportunities for it to help itself.  Another way of thinking about it is as a perceived loss of control over the outcome of a situation on the organism’s part. Specifically, the group used the shuttle box avoidance task, in which an animal must move from one compartment to the other in order to gain either gain a reward or avoid an aversive stimulus such as a shock. 
As shown in the figure above, isoflurane-treated rats (n=12) had fewer failure trials (Fig. 1A) and a faster mean escape latency (Fig. 1B) in the shuttle box avoidance task compared to naïve-controls (n=12). To specify this effect, a separate group of rats was exposed to an equivalent dose (1.5% in 100% O2) of another anesthetic agent, halothane,  for two hours, and  evaluated in an identical learned helplessness paradigm after the same two week recovery period. Halothane-treated rats (n=12) performed similarly to naïve-controls (n=10; Fig. 1C-D), suggesting that the reduced expression of learned helplessness is specific to isoflurane rather than a general effect associated with exposure to volatile anesthetics. Importantly, these results support and extend on previous findings indicating that isoflurane has antidepressant effects in humans and provide new insights and opportunities regarding alternate targets for development of rapid pharmacological treatments for depression. 
Obviously, more work needs to be done in order to clarify the mechanism of action and the timing in which isoflurane inhalation could prove to be useful. For example, would isoflurane work if it were given during infancy or adolescence? Could it be sufficient to prevent the depressive-like behavior even in the face of early life adversity? Moreover, research designed at determining the minimum exposure of isoflurane necessary for this effect would also be useful. Would animals, like the clinical population exhibit individual differences in terms of what dose is effective?  We don’t know, but I certainly hope we find out. 
This work was presented on Tuesday, October 16th 2012 by L. Wang as a poster titled Isoflurane impedes the development of a depression-like phenotype in rats. 

Does the future of antidepressants lie in anesthetics? 

Mood disorders like depression are among the leading causes of mental disability in the U.S. Because the therapeutic effects of traditional interventions and pharmacological treatments have shown to be limited in terms of efficacy, new therapies that are rapid acting and have increased efficacy in treatment-resistant populations are actively being sought out. Today, I was surprised to learn that the volatile anesthetic isoflurane has been shown to have antidepressant effects in humans since 1985 (Langer et al.) Given that I use isoflurane to knock my rats out while I implant cannulas and our lab studio the development of depressive-like behavior following early life abuse, I was floored

Although clinical literature has provided hints into the use of anesthetics, whether isoflurane could also exert antidepressant-like effects in conventional animal models of depression had not been determined until recently. Paul Shepard’s lab at the Maryland Psychiatric Research Center (MPRC) have behavioral evidence suggesting that a short period of acute isoflurane inhalation is sufficient to impede the development of depressive-likebehavior in rats. 

For this study, the group administered isoflurane (2% in 100% O2) to adult male Sprague Dawley rats continuously for two hours through a nose cone attached to a standard stereotaxic apparatus. Two weeks following exposure to isoflurane, rats entered a conventional two-day learned helplessness paradigm. Learned helplessness is a term that refers to the condition of an organism (human or animal) that has learned to behave helplessly and fails to respond even in the presence of opportunities for it to help itself.  Another way of thinking about it is as a perceived loss of control over the outcome of a situation on the organism’s part. Specifically, the group used the shuttle box avoidance task, in which an animal must move from one compartment to the other in order to gain either gain a reward or avoid an aversive stimulus such as a shock. 

As shown in the figure above, isoflurane-treated rats (n=12) had fewer failure trials (Fig. 1A) and a faster mean escape latency (Fig. 1B) in the shuttle box avoidance task compared to naïve-controls (n=12). To specify this effect, a separate group of rats was exposed to an equivalent dose (1.5% in 100% O2) of another anesthetic agent, halothane,  for two hours, and  evaluated in an identical learned helplessness paradigm after the same two week recovery period. Halothane-treated rats (n=12) performed similarly to naïve-controls (n=10; Fig. 1C-D), suggesting that the reduced expression of learned helplessness is specific to isoflurane rather than a general effect associated with exposure to volatile anesthetics. Importantly, these results support and extend on previous findings indicating that isoflurane has antidepressant effects in humans and provide new insights and opportunities regarding alternate targets for development of rapid pharmacological treatments for depression. 

Obviously, more work needs to be done in order to clarify the mechanism of action and the timing in which isoflurane inhalation could prove to be useful. For example, would isoflurane work if it were given during infancy or adolescence? Could it be sufficient to prevent the depressive-like behavior even in the face of early life adversity? Moreover, research designed at determining the minimum exposure of isoflurane necessary for this effect would also be useful. Would animals, like the clinical population exhibit individual differences in terms of what dose is effective?  We don’t know, but I certainly hope we find out. 

This work was presented on Tuesday, October 16th 2012 by L. Wang as a poster titled Isoflurane impedes the development of a depression-like phenotype in rats. 

  • 27th September
    2011
  • 27

This is your brain on stress and city living

Although city life offers many advantages and even some health benefits, meta-analyses indicate that city living is a substantial risk factor for mood and anxiety disorders. Basically, people who live in cities have a higher incidence for these disorders. Also, genetically predisposed individuals are at an even greater risk if they are brought up in cities. In schizophrenia, for example, the incidence is nearly doubled in subjects that were born, raised and currently lived in the city. And let’s not forget that, usually, with city life comes a more stressful social environment, a factor known to exacerbate many psychiatric disorders, particularly the ones mentioned above. 

So how is it that being from/living in a certain place can affect how your brain works? 

In order to understand this question, Lederborgen et al (2011) used functional magnetic resonance imaging (fMRI) to study the neural responses of subjects taking a social stressor task that consisted of solving math problems under time pressure while also receiving negative feedback from the experimenter. The subjects differed in terms of their living conditions, as they were from urban (+100,000 people), town (+10,000) or rural areas.

The task was an effective stressor as it successfully induced stress, indexed by increases in heart rate, blood pressure, and salivary cortisol (stress hormone) levels. In addition, there was significant activity in brain areas implicated in the stress response, emotion, and social behavior. Of these, 2 major areas exhibited the most robust changes: 

  • Amygdala: Current city living was associated with increased amygdala activity. Activation positively correlated with the size of the city that the individual currently lived in, with city dwellers having the highest levels of amygdala activation.
  • Anterior cingulate cortex: Activation correlated with the upbringing (or how long) a person had lived in a city. Individuals that were entirely brought up in cities showed the greatest perigenual anterior cingulate cortex (pACC) activation. This region is important due to its role in the regulation of amygdala activity during negative affect and stress. 

Moreover, the authors show evidence suggesting that there is reduced functional connectivity between the amygdala and specifically, the perigenual anterior cingulate cortex of those participants that were born and raised in cities. Considering that weakened coupling of these areas has also been linked to genetic risk for psychiatric disorders, these findings have important clinical relevance. Now let’s stretch our thinking- with urbanization increasingly becoming the way of life and the very real risk of overcrowding, what does this mean for brain development?

The authors state that the results were not explained by demographic/clinical factors or a number of other variables. They have also been able to replicate their findings in a larger and better distributed sample. However, they recognize that limitations of their work include that their study was purely correlational and they discuss the need for a larger scale study that has ways of identifying and measuring more variables that may be related to city living. 

For those of you that live (or were brought up) in cities, cheer up. There are a variety of reasons for choosing to live (and enjoy) the city life. In a way, the city has its way of forcing you into developing coping strategies- which is a good thing, right? Now here’s something to think about: psychologists have even found that one of the factors accounting for the preference of city living is the degree of control that people have (and feel they have) over their lives. 

Sources: 

Kennedy, DP & Adolphs R. 2011. Stress and the city. Comment on: Nature. 474: 452-3. doi: 10.1038/474452a

Lederborgen et al. 2011. City living and urban upbringing affect neural social stress processing in humans. Nature. 474: 498-500. oi: 10.1038/nature10190

  • 31st January
    2011
  • 31
The structure above represents norepinephrine (NE), also known as noradrenaline. Like dopamine, NE is a catecholamine. Catecholamines are also referred to as fight or flight hormones because they are released in response to stress. Thus, NE is a powerful chemical substance that triggers an involuntary nervous system response in face of a stressor and has been implicated in anxiety disorders like post-traumatic stress disorder (PTSD). 
Dopamine is the precursor for norepinephrine and norepinephrine is the precursor for epinephrine.
Along with acetylcholine, NE is one of the primary neurotransmitters found in the peripheral nervous system, particularly the sympathetic nervous system.
The central adrenergic system has 2 main projections: neurons originating from noradrenergic cells in the ventrolateral tegmental area that are involved in sexual and feeding behavior and feed into the forebrain; and, neurons that originate in the locus coeruleus (LC) and area associated with cognitive functions. 
The brain’s main source of NE is the locus coeruleus, a structure located in the midbrain that has been implicated in arousal/activation (fight or flight response) in response to stress (stress increases NE release). However, NE is released principally from the adrenal medulla. 
NE release in the LC is also implicated in the regulation of agitation, anxiety, sleep-wake cycles as well as vigilance and emotion.
Noradrenergic neurons have axons that branch out extensively and innervate many regulatory structures like the hypothalamus, cerebellum and midbrain. 
Treatment for anxiety disorders often targets noradrenergic neurotransmission in key structures. Propanolol is a beta-adrenergic blocker that is frequently used to treat anxiety. Antidepressants are also frequently used (they inhibit re-uptake). 
NE interacts with other neurotransmitters in the brain. It is modulated and modulates other neurochemicals. These interactions affect behavior. 
In Alzheimer’s disease, there is a deficiency in the noradrenergic system, as indexed by a major loss of neurons in the LC. Of course, the pathogenesis of AD also depends upon the interaction of complex factors including other neurotransmitter systems…
In addition to AD, LC and NE dysregulation has been implicated in many psychiatric/neurodegenerative conditions including: Parkinson’s disease, depression, and schizophrenia. 
Sources:
Best, Ben. Chapter 10: Brain Neurotransmitters. 
Hermann, Nathan, et. al. 2004. The Role of Norepinephrine in Behavioral and Psychological Symptoms of Dementia. J Neuropsychiatry Clin Neurosci 16:261-276.

The structure above represents norepinephrine (NE), also known as noradrenaline. Like dopamine, NE is a catecholamine. Catecholamines are also referred to as fight or flight hormones because they are released in response to stress. Thus, NE is a powerful chemical substance that triggers an involuntary nervous system response in face of a stressor and has been implicated in anxiety disorders like post-traumatic stress disorder (PTSD). 

  • Dopamine is the precursor for norepinephrine and norepinephrine is the precursor for epinephrine.
  • Along with acetylcholine, NE is one of the primary neurotransmitters found in the peripheral nervous system, particularly the sympathetic nervous system.
  • The central adrenergic system has 2 main projections: neurons originating from noradrenergic cells in the ventrolateral tegmental area that are involved in sexual and feeding behavior and feed into the forebrain; and, neurons that originate in the locus coeruleus (LC) and area associated with cognitive functions. 
  • The brain’s main source of NE is the locus coeruleus, a structure located in the midbrain that has been implicated in arousal/activation (fight or flight response) in response to stress (stress increases NE release). However, NE is released principally from the adrenal medulla. 
  • NE release in the LC is also implicated in the regulation of agitation, anxiety, sleep-wake cycles as well as vigilance and emotion.
  • Noradrenergic neurons have axons that branch out extensively and innervate many regulatory structures like the hypothalamus, cerebellum and midbrain. 
  • Treatment for anxiety disorders often targets noradrenergic neurotransmission in key structures. Propanolol is a beta-adrenergic blocker that is frequently used to treat anxiety. Antidepressants are also frequently used (they inhibit re-uptake). 
  • NE interacts with other neurotransmitters in the brain. It is modulated and modulates other neurochemicals. These interactions affect behavior. 
  • In Alzheimer’s disease, there is a deficiency in the noradrenergic system, as indexed by a major loss of neurons in the LC. Of course, the pathogenesis of AD also depends upon the interaction of complex factors including other neurotransmitter systems…
  • In addition to AD, LC and NE dysregulation has been implicated in many psychiatric/neurodegenerative conditions including: Parkinson’s disease, depression, and schizophrenia. 

Sources:

Best, Ben. Chapter 10: Brain Neurotransmitters. 

Hermann, Nathan, et. al. 2004. The Role of Norepinephrine in Behavioral and Psychological Symptoms of Dementia. J Neuropsychiatry Clin Neurosci 16:261-276.