House of Mind

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

  • 1st August
    2014
  • 01
neurosciencenews:

Learning the Smell of Fear
Read the full article Learning the Smell of Fear at NeuroscienceNews.com.
Babies can learn what to fear in the first days of life just by smelling the odor of their distressed mothers, new research suggests. And not just “natural” fears: If a mother experienced something before pregnancy that made her fear something specific, her baby will quickly learn to fear it too — through the odor she gives off when she feels fear.
The research is in PNAS. (full access paywall)
Research: “Intergenerational transmission of emotional trauma through amygdala-dependent mother-to-infant transfer of specific fear” by Jacek Debiec and Regina Marie Sullivan in PNAS. doi:10.1073/pnas.1316740111
Image: Even when just the odor of the frightened mother was piped in to a chamber where baby rats were exposed to peppermint smell, the babies developed a fear of the same smell, and their blood cortisol levels rose when they smelled it. Credit University of Michigan.

Reblogging because it’s work coming out of the lab :) See below for abstract: 

Emotional trauma is transmitted across generations. For example, children witnessing their parent expressing fear to specific sounds or images begin to express fear to those cues. Within normal range, this is adaptive, although pathological fear, such as occurs in posttraumatic stress disorder or specific phobias, is also socially transmitted to children and is thus of clinical concern. Here, using a rodent model, we report a mother-to-infant transfer of fear to a novel peppermint odor, which is dependent on the mother expressing fear to that smell in pups’ presence. Examination of pups’ neural activity using c-Fos early gene expression and 14C 2-deoxyglucose autoradiography during mother-to-infant fear transmission revealed lateral and basal amygdala nuclei activity, with a causal role highlighted by pharmacological inactivation of pups’ amygdala preventing the fear transmission. Maternal presence was not needed for fear transmission, because an elevation of pups’ corticosterone induced by the odor of the frightened mother along with a novel peppermint odor was sufficient to produce pups’ subsequent aversion to that odor. Disruption of axonal tracts from the Grueneberg ganglion, a structure implicated in alarm chemosignaling, or blockade of pups’ alarm odor-induced corticosterone increase prevented transfer of fear. These memories are acquired at younger ages compared with amygdala-dependent odor-shock conditioning and are more enduring following minimal conditioning. Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity. Results are discussed within the context of caregiver emotional responses and adaptive vs. pathological fears social transmission.

neurosciencenews:

Learning the Smell of Fear

Read the full article Learning the Smell of Fear at NeuroscienceNews.com.

Babies can learn what to fear in the first days of life just by smelling the odor of their distressed mothers, new research suggests. And not just “natural” fears: If a mother experienced something before pregnancy that made her fear something specific, her baby will quickly learn to fear it too — through the odor she gives off when she feels fear.

The research is in PNAS. (full access paywall)

Research: “Intergenerational transmission of emotional trauma through amygdala-dependent mother-to-infant transfer of specific fear” by Jacek Debiec and Regina Marie Sullivan in PNAS. doi:10.1073/pnas.1316740111

Image: Even when just the odor of the frightened mother was piped in to a chamber where baby rats were exposed to peppermint smell, the babies developed a fear of the same smell, and their blood cortisol levels rose when they smelled it. Credit University of Michigan.

Reblogging because it’s work coming out of the lab :) See below for abstract: 

Emotional trauma is transmitted across generations. For example, children witnessing their parent expressing fear to specific sounds or images begin to express fear to those cues. Within normal range, this is adaptive, although pathological fear, such as occurs in posttraumatic stress disorder or specific phobias, is also socially transmitted to children and is thus of clinical concern. Here, using a rodent model, we report a mother-to-infant transfer of fear to a novel peppermint odor, which is dependent on the mother expressing fear to that smell in pups’ presence. Examination of pups’ neural activity using c-Fos early gene expression and 14C 2-deoxyglucose autoradiography during mother-to-infant fear transmission revealed lateral and basal amygdala nuclei activity, with a causal role highlighted by pharmacological inactivation of pups’ amygdala preventing the fear transmission. Maternal presence was not needed for fear transmission, because an elevation of pups’ corticosterone induced by the odor of the frightened mother along with a novel peppermint odor was sufficient to produce pups’ subsequent aversion to that odor. Disruption of axonal tracts from the Grueneberg ganglion, a structure implicated in alarm chemosignaling, or blockade of pups’ alarm odor-induced corticosterone increase prevented transfer of fear. These memories are acquired at younger ages compared with amygdala-dependent odor-shock conditioning and are more enduring following minimal conditioning. Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity. Results are discussed within the context of caregiver emotional responses and adaptive vs. pathological fears social transmission.

  • 11th November
    2013
  • 11

Entrainment of circadian rhythms by stressful stimuli: Evidence from a rodent model


Circadian rhythms in humans and animals are sensitive to stressors and changes in the emotional state. However, whether circadian rhythms can be entrained by fear stimuli had not been directly investigated until now. To test this, circadian behaviors of male Long Evan rats maintained on an LD (12-h light/12-h dark) cycle were monitored in a live-in chamber comprised of safe nesting and risky foraging areas. Initially, animals pressed a lever to procure food pellets in the foraging area and were entrained to the environmental conditions for a week. 

Then, animals were subjected to (i) 14 days of ‘Unsignaled’ footshocks (0.8 mA; pseudo-random 2 shocks/hr) which were delivered only during the dark phase of the LD cycle, and (ii) 14 days of ‘Signaled’ footshocks (a 9-sec light cue preceding the footshock) also during the dark cycle (counterbalanced orders). During the unsignaled footshock, rats reversed their normal circadian feeding behavior, meaning that they exhibited more feeding behavior during the light phase than the dark phase, and showed arrhythmic locomotor activity. During the signaled footshock, however, rats returned to or conserved their normal circadian feeding (i.e., the feeding behavior was observed mostly during the dark phase) and rhythmic locomotor activity. In sum, rats exposed the unpredictable stressor (i.e. unsignaled shock) quickly learned to adapt their behavior by shifting their meal time earlier so that there was a lesser possibility of the feeding coinciding with the shock. Furthermore, lesioning the amygdala in these animals prevented the reversal of the feeding time, suggesting that amygdala function is causal in producing this effect and postulating a new role for amygdala function. 

These results suggest that amygdala-dependent fear, associated with environmental threats limited to the naturally active phase (i.e. dark), can act as a non-photic entraining stimulus and lead to circadian activity during the naturally inactive phase (i.e. light). Importantly, there is growing evidence suggesting  a link between mood disorders such as depression and anxiety and disturbances in circadian rhythm, which makes determining the mechanism underlying the entrainment of circadian rhythm by fearful or stressful stimuli of clinical relevance. Moreover, if aversive conditioning is able to induce changes in circadian rhythm, can appetitive conditioning do the same? 

Source: 

E.E. S. Kim, J. Kashima, O. Motch, H.O. de la Iglesia, J.J. Kim. Entrainment of circadian rhythms by fear. Program No. 189.04/HHH29.2013. Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2013. 

 

  • 6th March
    2012
  • 06
WiredScience: A pill that can erase painful memories forever?

Even though PTSD is triggered by a stressful incident, it is really a disease of memory. The problem isn’t the trauma—it’s that the trauma can’t be forgotten. Most memories, and their associated emotions, fade with time. But PTSD memories remain horribly intense, bleeding into the present and ruining the future. So, in theory, the act of sharing those memories is an act of forgetting them. 

In the past decade, scientists have come to realize that our memories are not inert packets of data and they don’t remain constant. Even though every memory feels like an honest representation, that sense of authenticity is the biggest lie of all.

Every memory begins as a changed set of connections among cells in the brain. If you happen to remember this moment—the content of this sentence—it’s because a network of neurons has been altered, woven more tightly together within a vast electrical fabric. This linkage is literal: For a memory to exist, these scattered cells must become more sensitive to the activity of the others, so that if one cell fires, the rest of the circuit lights up as well. Scientists refer to this process as long-term potentiation, and it involves an intricate cascade of gene activations and protein synthesis that makes it easier for these neurons to pass along their electrical excitement. Sometimes this requires the addition of new receptors at the dendritic end of a neuron, or an increase in the release of the chemical neurotransmitters that nerve cells use to communicate. Neurons will actually sprout new ion channels along their length, allowing them to generate more voltage. Collectively this creation of long-term potentiation is called the consolidation phase, when the circuit of cells representing a memory is first linked together. Regardless of the molecular details, it’s clear that even minor memories require major work. The past has to be wired into your hardware.

I just found this online and could not be more proud that I know and am professionally associated to these people. I’ve actually had the pleasure of meeting Dr. Karim Nader (he’s the coolest) at a GRC conference and hearing all he has to say about memory reconsolidation and zeta. And as for Joe Le Doux, well he’s the director for our institute (EBI). 

Anyhow, the link above is a strongly encouraged read, as it explains the persistence of PTSD (and traumatic memories) as well as memory mechanisms like reconsolidation. The molecular player in question, PKMzeta, is actually at the centerpiece of one of our current collaborations. 

In short, read read read!

  • 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.


  • 9th June
    2010
  • 09
  • 28th March
    2010
  • 28