Download Brain Plasticity and Emotional Regulation

Brain Plasticity and Emotional
Regulation
Second Session
What is Brain Plasticity?
 Term is in vogue, but what do we really mean?
 Pliable and changeable. It’s really been several
“Decades of the Brain”.
 Dalai Lama has held numerous conferences in
India to discuss breakthroughs in Neuroscience.
 The brain isn’t fully formed (especially, PFC) until
the mid-20’s, but remains plastic throughout life.
 We can’t forget what a revolutionary discovery it is
that the human brain can change itself.
Hebb’s Axiom
 Neurons the fire together wire together!
Localization is NOT fixed
 Most neuroscientists believed that the brain
was “hard-wired” and specialized to the
point that one area could never do the work
of another (cf. Doidge, Schwartz)
 Michael Merzninich and Fast Forward
 Eduard Taub and the Silver Spring Monkeys
(de-afferented their arms) and forced them
to learn to eat.
But Plasticity is Competitive
 And therefore, can be positive or negative.
 Even, individual neurons get more specific
with training.
 Then when they are trained and become
efficient, they become faster.
 Concert violinists have more neurons for the
tips of their fingers than the average person.
Hormonal Assist
 Levi-Montalcini discovered NGF (nerve
growth factor).
 One caught Merzenich’s attention: brainderived neurotrophic factor (BDNF) which
plays a crucial role in reinforcing plastic
changes.
 It also promotes the growth of the thin fatty
coat around every neuron that speeds up
the transmission of electrical signals.
Down Regulation of Emotion
 1) Emotions arise when an individual attends to a
situation and sees it as relevant to his or her
goals.
 2) Emotions are multifaceted, whole-body
phenomena that involve loosely-coupled changes
in the domains of subjective experience, behavior,
and central and peripheral physiology.
 3) They can interrupt what we are doing and force
themselves on our awareness. It is this third
element that is most crucial for an analysis of
emotion regulation.
The Modal Model of Emotion
Situation
Attention
Appraisal Response
O--------------O--------------O------------O
Emotion Regulation Strategies
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1) Situation Selection
2) Situation Modification
3) Attentional Deployment
4) Cognitive Change
5)Response Modulation
Situation Selection
 Taking actions that make it more (or less)
likely that we will end up in a situation we
expect will give rise to desirable (or
undesirable) emotions.
Situation Modification
 Sometimes, efforts to modify a situation will
bring a new situation into being.
 A related issue becomes the social
consequences of emotion expression.
Attentional Deployment
 Refers to how individuals direct their attention
within a given situation in order to influence their
emotions.
 “Distraction” focuses attention away from the
situation and “Concentration” draws attention to
emotional features of a situation.
 When this occurs repetitively, it is referred to as
rumination, i.e. ruminating on sad events leads to
longer and more severe depressive symptoms.
Cognitive Change
 Refers to changing how we “appraise” the
situation we are in to alter its emotional
significance, either by changing how we think
about a situation or about our capacity to manage
the demands it poses.
 Is physiological arousal prior to a sports event
competence enhancing (“getting pumped up”) or
debilitating (“stage fright”)
 Reappraisal- changing a situation’s meaning in a
way that alters its emotional impact. (cf. research
in Post-Traumatic Growth).
Response Modulation
 Though this occurs late in the emotion-generative
process, it refers to influencing physiological,
experiential, or behavioral responding as directly
as possible.
 Exercise and relaxation can decrease
physiological aspects of negative emotion (but
alcohol, drugs, cigarettes, and even food can
modify emotion experience.
 One key seems to be finding ways of expressing
the emotions in adaptive rather than maladaptive
ways.
Prefrontal-Amygdala Interactions in
the Regulation of Fear
 The nervous system of every living thing is but a
bundle of predispositions to react in particular
ways upon the contact of particular features of the
environment (James, 1884)
 The study of emotion regulation is intimately
associate with the concept of inhibition, namely,
higher cortical functions are responsible for
inhibiting subcortical areas.
 Thus, the term: “down regulation”
Amygdala
 The lateral amygdala (LA) projects to the central
nucleus of the Amygdala (Ce) directly and via the
basal amygdala nuclei. The Ce is the origin of
amygdala outputs to fear generating structures in
the hypothalamus and brainstem. (LeDoux et al
1988).
 LA is seen as the site of fear memory, while Ce is
seen as the site of fear expression (LeDoux,
2000).
Relationship to Anxiety
 In this paradigm, it has been suggested that
anxiety disorders may result from a lack of
balance between fear and safety memories
(Quirk & Gehlert, 2003).
 Therefore, modulation of amygdala plasticity
and/or output would be an efficient way of
regulating fear expression.
Our friend “GABA”
 Situated between the BLA (Basal Lateral
Amygdala) and Ce are islands of GABA (gammaamnobutyric aced)-ergic “intercalated” (ITC) cells.
These cells receive input from BLA and project to
Ce output neurons, thereby acting as an inhibitory
interface between centers of fear learning and fear
expression. Thus, the amygdala is capable of
learning fear associations and fear inhibition.
PFC and the Amygdala
 Recent studies point to the medial prefrontal
cortex (mPFC) as a possible inhibitor of fear in
extinction (Quirk, 2006).
 Early studies implicated the primate ventromedial
prefrontal cortex (vmPFC) in extinction of
appetitive conditioning.
 It is connected to the infralimbic (IL) and prelimibic
(PL) sub-regions. IL is therefore well situated to
inhibit the expression of fear either via the
amygdala or by acting directly on lower centers.
The hippocampus
 Inactivation of the hippocampus prior to
extinction training leads to impaired recall of
extinction (fear) (Corcoran et al, 2005).
 Direct projections from the hippocampus to
the amygdala are sufficient for contextual
extinction.
Preliminary applications to PTSD
 Long after the probability of danger has decreased, the
person is unable to inhibit the expression of the latent fear
associations.
 This may be associated with pathology in the prefrontalamygdala system. Specifically, inhibition of the amygdala
by the vmPFC has been associated with anxiety and mood
disorders.
 These individuals also show impairments in a functional
network involving the amygdala and anterior cingulate
cortex (ACC).
 Thus, they exhibit a negative correlation between vmPFC
activity (underactive) and amygdala activity (overactive).
 These same ventral prefrontal area are also
compromised in major depression…(Pesawas et
al.,2005).
 Rats exposed to an early life stressor related to
maternal care develop permanent alterations in
GABA-ergic function in vmPFC and amygdala
(Caldji et al. 2003).
 Daily chronic restraint decreases dendritic
branching and reduces the density of synaptic
spines in vmPFC. In the amygdala, chronic
restraint has the opposite effect, causing
increased dendritic branching and reduces density
of synaptic spines in vmPFC.
 These findings suggest that chronic stress
increases the ability of the amygdala to
learn and express fear associations, while at
the same time reducing the ability of the
prefrontal cortex to reduce fear.
 This situation (the vicious cycle in with
increased fear and anxiety leads to more
stress, which leads to further dysregulation)
has been termed “allostatic load”.
 Prefrontal changes appear reversible, but
amygdala changes do not (Radley et al.,
2005)
Treatment Implications
 High-frequency stimulation of the IL directly or
indirectly via its thalamic afferent, improves longterm extinction (Quirk et al. 2006).
 Extinction learning can also be augmented with
systemic drugs including dopamine agonists,
noradrenergic agonists, and cannabinoid agonists(
Chhatwal et al., 2005)
 Additional approaches to activating the PFC
include repetitive Transcranial Magnetic
Stimulation (Cohen et al., 2004), deep brain
stimulation (Abelson et al.,2005) or even
meditation (Lasar et al., 2000)