Stress, anxiety and aggression

Question 1

Definition of stress

Answer 1

‘Physiological reaction caused by perception of aversive or threatening situations’ -Walter Cannon (1871-1945)

Question 2

Stress facts

Answer 2

• Change that causes physical, emotional, or psychological strain.
• Physiological responses help prepare for ‘fight-or-flight’ situations
• Episodic (single episode/ acutely) or continuous
• Adaptive (without stress, life is quite boring and you need it to keep life interesting), but also harmful.

Question 3

Physiology of the stress response-SAM system
1- what do threats require?
2- what does SAM stand for?
3- what do the hypothalamus and sympathetic nervous system stimulate?
4- what else is secreted in the brain during stress?

Answer 3

1- Threats require enhanced activity→ need to mobilise energy resources
2- Sympathetic-Adrenal-Medullary (SAM) system
3- Hypothalamus and sympathetic nervous system stimulate adrenal medulla (kidneys) to release the catecholamine transmitters epinephrine (adrenaline) (↑ blood glucose) and norepinephrine (↑ blood pressure)
4- Norepinephrine also secreted in brain during stress

Question 4

SAM system
- where does it start
- what is the process
- what doe sit aid?
- function of glucocorticoids

Answer 4

It starts in the hypothalamus which is going to stimulate the sympathetic system eventually.

It releases corticotrophin-releasing hormone (CRH) (or sometimes written as CRF). This acts on the anterior pituitary gland and that releases ACTH as well as glucocorticoids and the adrenal cortex.

This helps the kidneys release catecholamine transmitters epinephrine and norepinephrine.

Glucocorticoids mobilise energy stores by inducing the degradation of proteins to free amino acids in muscle, lipolysis in adipose tissue and gluconeogenesis in the liver.

Question 5

Physiology of the stress response-HPA axis
1- what does HPA stand for?
2- explain the processes that occur
3- where else is CRH secreted?
4- benefit of glucocorticoids?
5- what also decreases?

Answer 5

1- Hypothalamic-Pituitary-Adrenal (HPA) axis

2-
- Paraventricular nucleus of the hypothalamus (PVN) releases the peptide corticotropin-releasing hormone/factor (CRH/CRF)
- CRH stimulates anterior pituitary to release adrenocorticotropic hormone (ACTH)
- ACTH enters general circulation and stimulates adrenal cortex to secrete glucocorticoids (e.g. cortisol)→increases glucose, decrease pain sensitivity

3- CRH also secreted in brain during stress in limbic system

4- Glucocorticoids help the animal survive. Thus in an adrenalectomized rat, a stressful situation may be fatal.

5- pain sensitivity

Question 6

Stress effects on the brain:
1- what can stress be?
2- what is the hippocampus involved in?
3- impact of chronic exposure to glucocorticoids?
4- what does glutamate reuptake lead to?

Answer 6

1- Stress can be neurotoxic (Sapolsky)

2- Hippocampus= involved in learning and memory

3- Chronic exposure to glucocorticoids destroys hippocampal neurons via decreased glucose entry and

4- glutamate reuptake→ excessive Ca2+ influx and toxicity

Question 7

Process of glutamate synapses?

Answer 7

Glutamate synapse releases glutamate transmitters which stimulate the postsynaptic neuron. If you stimulate the postsynaptic neuron, you have these receptors that open up (such as AMPA receptors, NMDA receptors, voltage gated calcium channels ect.) and these excite the post synaptic neuron. This kind of excitation can cause an over excitation and cause neurons to pretty much die out. When we’re really stressed, the hippocampus is the area which is going to be affected easily.

Question 8

Evidence for stress-induced neurotoxicity: Diamond et al. (1999)

Answer 8

• Rat exposed to cat smell and presence for 75 min (this would be stressful for rat)
• Blood glucocorticoids increased compared to the controls in the home cage or in the chamber alone with no cat
• Impaired primed-burst potentiation (PBP; similar to LTP, synaptic strengthening) in hippocampus
• Impaired in spatial task

Question 9

Evidence for stress-induced neurotoxicity (in higher order primates): Uno et al. (1989)

Answer 9

• Vervet monkey colonies in Kenya
• Have a hierarchical society
• When bottom rank monkeys subjected to continuous stress by upper rank, the following happens:

→ enlarged adrenal glands (excessive (nor)epinipherine production)
→ hippocampal degeneration

Question 10

Post-traumatic stress disorder (PTSD)
1- meaning
2- when is PTSD likelihood increased?
3- symptoms?
4- triggered by?
5- what type of response?

Answer 10

1- Long-lasting psychological symptoms after traumatic event (e.g. natural disaster, experience of violence) is over
2- PTSD likelihood is increased if the traumatic event involves danger or violence from other people (assault, war)
3- Symptoms= flashbacks, hypervigilance, irritability, heightened reactions to sudden noises, detachment from social activities
4- Often triggered by cues (e.g. helicopter sound) related to traumatic event (e.g. war)
5- Learned, conditioned response

Question 11

PTSD and brain changes:
- what brain change occurs in combat veterans and police officers with PTSD
- possible risk factor for PTSD?
- possible reason for hippocampus and PTSD?

Answer 11

• Reduced size of hippocampus in combat veterans and police officers with PTSD (Bremner et al. 1995; Gurvits et al., 1996; Lindauer et al., 2005)
• Possible risk factor for PTSD
  – Monozygotic twin study from Vietnam war (Gilbertson et al. 2002)
  – For the twin that fought in the war (those with PTSD) compared to the one who did not had a smaller hippocampus
• Possible reason for hippocampus and PTSD
  – Hippocampus plays a role in distinguishing contexts
  – Inability in PTSD from detecting threatening vs safe contexts, ‘threat generalisation’

Question 12

What other brain regions are altered due to PTSD? + explain

Answer 12

Amygdala and medial prefrontal cortex

• Prefrontal cortex (PFC) involved in impulse control and thought to normally inhibit amygdala, involved in emotional expression (Rauch et al. 2006)
• PTSD associated with greater amygdala activation for fearful and happy face compared to controls.
• PTSD associated with reduced mPFC activation for fearful face and higher for happy face compared to controls.
• PTSD-related changes may indicate excessive emotional response and reduced inhibitory control

Shin et al. (2005)

Question 13

List two PTSD treatments and what brain alterations occur?

Answer 13

Psychotherapy:
eg.
- discuss experience of traumatic event, emotional pain, losses suffered in combat, etc.
- come to terms with the trauma, identify any unhelpful or destructive thoughts (e.g. blaming yourself wrongly)
- come up with action plan (e.g. how to establish positive relationships with others)

Associated with decreased amygdala activity and increased PFC, increased hippocampus activity (Thomaes et al., 2014)

Antidepressants (SSRIs):
Increased hippocampal volume (Bossini et al., 2007; Vermetten et al., 2003)

Question 14

What is another PTSD treatment?

Answer 14

Exposure therapy

Question 15

PTSD treatment: exposure therapy
Explain

Answer 15

• Learned associations (cue–stress) play a role in PTSD
• Cue alone induces a fear response conditioned (conditioned because its a learned cue that provokes it)
• If present cue alone, you get conditioned memory response because that memory of the cue and the stress comes back.

Question 16

What did Pavlov find?

Answer 16

Extinction learning reduces cue responding

conditioning= cue + salient experience (association is being made) → salivating

after conditioning= bell alone → salivating

during extinction= present bell multiple times in the absence of food → eventually salivation lowers/ stops

Question 17

PTSD treatment: exposure therapy-
1- what does cue exposure therapy borrow principles from?
2- how does exposure therapy work?
3- what can is also be done with?

Answer 17

1- Extinction learning- same idea of present cue in absence of salient experience (stressful experience)

2- Repeated cue presentation over weeks in safe therapy context reduces response to cue (learning of non-threat, reduction of fear/anxiety) - present cue (eg. helicopter) in safe context.You do this multiple times and the conditioned response which is a fearful stressful response is reduced over time.

4- can also be done with phobias/ drug addiction

Question 18

• definition of anxiety
• elaborate
• definition of anxiety disorder

Answer 18

• Anxiety= apprehensive uneasiness or nervousness over an impending or anticipated ill (Merriam-Webster)
• Normal part of life, unlike stress may not have an identifiable trigger, but some similar responses (faster heartbeat, breathing)
• Anxiety disorder= more intense fear/anxiety inappropriate for circumstance.

example: graduation and uneasiness about the future

Question 19

Anxiety disorders:
- definition
- due to?
- difference in experiencing between genders
- types?

Answer 19

• Anxiety disorder=more intense fear/anxiety inappropriate for circumstance, more than a temporary worry
• Likely due to cumulative effects of stress, contributes to depressive and substance abuse disorders
• Women more likely than men to experience
• Many types, but panic disorder, agoraphobia, generalised anxiety disorder (GAD), social anxiety disorder have known biological component

Question 20

Panic disorder:
- meaning
- symptoms
- what factors play a role
- coping?

Answer 20

• Episodic attacks of acute (seconds to hours) anxiety, terror
• Symptoms: hyperventilation- increased breathing (low CO2), irregular heart-beat, dizziness, faintness, fear of losing control and dying
• Cultural factors play a role as Asian, African, and Latin American Countries have lower rates than e.g. USA (American Psychiatric Association)
• Coping with hyperventilation by breathing into a bag (raises CO2)

Question 21

Agoraphobia:
- meaning
- how do people cope with it?

Answer 21

• Intense fear or anxiety about leaving home, being in open/public areas, being in lines/crowds, etc.
• Coping through avoidance of those situations due to disproportionate fear or anxiety
  – Staying home for years, fear of panic attack

Question 22

Generalised Anxiety Disorder (GAD)
- meaning
- symptoms
- gender prevalence
- culture

Answer 22

• Excessive, uncontrollable worrying and anxiety from a wide range of situations and difficulties controlling these symptoms
• Sense of impending danger, sweating, trembling, difficulty concentrating
• More prevalent in women than men
• Cultural component (more prevalent in people of European descent than e.g. Asian, Latino, African descent)

Question 23

Social anxiety disorder/phobia
- meaning
- symptoms
- gender prevalence
- culture

Answer 23

• Persistent, excessive fear of being exposed to the scrutiny of others (e.g. public speaking, group conversations), appearing incompetent
• Sweating, blushing
• Equally likely in men and women
• Cultural component (more prevalent in people of European descent than e.g. Asian, Latino, African descent)

Question 24

Brain changes linked to anxiety disorders
- general brain areas affected
- linked to panic attack
- linked to SAD
- linked to GAD

Answer 24

• Functional imaging using PET and fMRI show changes in the prefrontal cortex, anterior cingulate cortex, and amygdala.
• Increased amygdala activity during panic attack (Pfleiderer et al., 2007) and in response to presentations of faces with anger, disgust, and fear in social anxiety disorder (Phan et al., 2005)
  – Activation correlates with symptoms (more activity in amygdala= more likely to have these symptoms)
• Adolescents with GAD exhibit increased amygdala and decreased ventrolateral prefrontal cortex activation (Monk et al., 2008)
• Lack of suppression of amygdala activation via ventromedial prefrontal cortex (vmPFC)
  – vmPFC plays a role in inhibition of fear

Question 25

What are treatments for anxiety disorders?

Answer 25

• GABAergic drugs
• neurosteroid synthesis
• compounds that affect the serotonin and glutamate system

Question 26

Treatments for anxiety disorders: GABAergic drugs
- what drug reduces anxiety + implication for animals
- what does this bind to + implications

Answer 26

• Benzodiazepines (BDZ) reduces anxiety and anxiety-like behaviours in animals.
  – Less time spent on the ‘anxiogenic’ open arm on the elevated plus maze (EPM). If you give Bz or similar compounds, these animals like rats and mice spend more time on the open arm, they show less anxiogenic behaviours.
• Bz binds to the inhibitory GABAA receptor as ‘agonist’.
  – Increases Cl- influx
  – hyperpolarisation (become more negative, less active and as a result you feel more relaxed)

Question 27

Treatments for anxiety disorders:
- what does BDZ administration do?
- what does Flumazenil (antagonist) do? + treat
- disadvantage
- what is needed

Answer 27

• BDZ administration reduces amygdala activity when looking at emotional faces (Paulus et al., 2005)
• Flumazenil (antagonist) disinhibits action at GABAA receptor and produces panic in panic disorder patients.
  – Treats BDZ overdose, acute alcohol intoxication
• Abuse potential, withdrawal, sedation.
• Better compounds are needed with fewer side effects.

Question 28

Treating anxiety by increasing neurosteroid synthesis:
1- what are neurosteroids and where are they synthesised
2- what do neurosteroids increase
3- what happens to neurosteroid synthesis during anxiety attacks
4- what drug type is ideal?

Answer 28

• Neuroactive steroids ‘neurosteroids’ (e.g. allpregnaolone) synthesized in periphery and CNS
• Neurosteroids increase activity of GABAA receptor.
• During anxiety attacks, neurosteroid synthesis is suppressed (blocked), resulting in suppression of GABAA receptor function.
• You want a drug like XBD173 which enhances neurosteroid synthesis and reduces panic, in absence of sedation and withdrawal symptoms (Nothdufter et al., 2011)

Question 29

Treatment for anxiety: compounds that affect the serotonin and glutamate system:
1- what reduces panic attacks?
2- similar findings for…?
3- extinguishing fear responses?
4- what does DCS do?

Answer 29

• The anti-depressant fluvoxamine, a SSRI, reduces panic attacks (Asnis et al., 2001).
• Similar findings for D-cycloserine (DCS) an indirect agonist of NMDA receptor (doesn’t directly bind to receptor but stimulates receptor function → more excitation)
• Presumed action by facilitating ability of behavioural therapy to extinguish fear responses
• DCS facilitates extinction of conditioned fear in animals (Walker et al. 2002)

Question 30

Aggression:
- common across?
- related to?
- may involve behaviours related to ______?

Answer 30

• Common across many species (mice, rats, geese, gorillas)
• Related to species survival, such as gaining access to mates, protecting offspring
• May involve behaviours related to threat (warning), defensive (attack), submission (accept defeat).

Question 31

Brain circuits of aggression:
1- programmed by?
2- what did electrical stimulation of periaqueductal gray (PAG) elicit?
3- what behaviours do 2 areas of the hypothalamus lead to?
4- what control these pathways?
5- what are the 3 amygdala nuclei that excite PAG or inhibit PAG

Answer 31

1- Programmed by brain stem

2- Electrical stimulation of periaqueductal gray (PAG) elicited aggressive attack and predation in cats (ready to attack) (Gregg and Slegel 2001)

3-
- Medial Hypothalamus→Dorsal PAG: defensive rage
- Lateral Hypothamaus→Ventral PAG: Predatory attack

4- Amygdala nuclei control these pathways. So we see the amygdala playing a role in anxiety and aggression.

5- Amygdala nuclei that can excite PAG or inhibit the PAG:
- central nucleus
- basal nucleus
- medial nucleus

Question 32

What reduces and increases aggression

Answer 32

Increasing serotonin transmission reduces aggression (Audero et al., 2013)

Reducing serotonin transmission via destruction of serotonergic axons (Vergnes et al., 1988) or reducing serotonin synthesis increases aggression (Mosienko et al. 2012)

Question 33

Aggression and serotonin: animal studies
- what is found in rhesus monkeys in relation to serotonin and aggression
- examples of behaviours
- what does serotonin get converted to and what does this lead to?

Answer 33

• Low levels of serotonin metabolite (5-HIAA) in cerebrospinal fluid in rhesus monkeys linked with high levels of aggression (Howell et al., 2007)
  – Picking fights with bigger monkeys
  – High risk taking (dangerous leaps)
  – Suggests serotonin inhibits aggression and controls risky behaviours
• Some serotonin gets converted into the metabolite 5-HIAA, this makes way into the CSF. 5-HIAA levels tend to correlate with 5-HT levels
• If 5-HIAA concentrations are really high they’re more likely to survive because they tend to do less stupid things like pick fights

Question 34

Aggression and serotonin: human studies
1- what is there some evidence for?
2- what is linked with aggression and antisocial behaviour
3- what has shown to reduce aggressive behaviour in some cases

Answer 34

1- Some (mixed) evidence that serotonergic neurons play an inhibitory role (Duke et al., 2013) in aggression
2- Low 5-HIAA (serotonin metabolites) in CSF linked with aggression and antisocial behaviour
3- SSRI (fluoxetine) has shown to reduce aggressive behaviour in some cases

Question 35

Aggression as a reward
- reward definition
- example of aggression seen as rewarding

Answer 35

Reward: Objects, actions, experiences that attains a positive motivational property. (Increases the probability of actions that lead to these- repeat these actions)

Previous gang member
“The sight of yellow police tape gives me a rush. My heart is beating, my hands sweating. I am not scared – I’m excited. My mind starts running. I want back in the game.” (seeing police tape made them have excited rush and they want to be back in the game)

Question 36

Aggression as a reward:
1- what do some individuals exhibit- motivated by?
2- examples
3- thought to be…
4- what are the two ways animal models allow us to study this behaviour

Answer 36

1- Certain individuals exhibit ‘appetitive’ aggression, motivated by intrinsic reward (Elbert et al., 2010)

2- Can be seen in sports such as boxing

3- Thought to be an adaptation to violent environments (Crombach et al., 2013)
– Remaining more functional in violent settings (war afflicted communities, e.g. Ugandan Child soldiers)
– Elevated social status

4- Animal models allow us to study this behaviour (and brain mechanisms) under controlled conditions
– Conditioned place preference (CPP)
– Instrumental conditioning

Question 37

Conditioned Place Preference (CPP)
- used with?
- what happens before, during and after conditioning

Answer 37

• Typically used with drug, food, social reward in mice/rats.
• Before conditioning: all chambers are neutral stimuli.
• Conditioning: One chamber is paired with reward (drug) where as the other one is not. (eg. blue chamber associated with drug, green chamber neutral)
• After conditioning: After several reward-chamber pairings, reward-paired side acquires motivational significance and acts as a conditioned stimulus
• If you let mouse explore, the animal goes back to the rewarding location- you get this place preference because experience is rewarding
• If a substance/experience is ‘rewarding’ then animals will spend more time in that chamber paired with that substance/experience, i.e. develop a preference.

Question 38

CPP with aggression reward (Golden et al., 2016)

Answer 38

• Resident (one that lives there) vs intruder males
• Male rodents are very territorial after sexual experience and will attack the unfamiliar intruder
• So what you can do with aggression reward is condition them.
• Get a resident animal (mouse) and they have an intruder mouse. The resident mouse will show an aggressive response
• During conditioning: Resident attacks the intruder in the ‘Paired’ side, no intruder on the ‘Unpaired’ side
• After conditioning: Resident mouse that exhibited aggression spends more time on the Paired side in the absence of the intruder mouse.
• Animal naturally goes back to the rewarding spot- where they attacked an intruder. This is how you can measure aggression.

Question 39

Operant/instrumental task for aggression reward
Food example

Answer 39

• Animals will learn to lever press for food reward in operant ‘Skinner’ chamber
• The reward sustains the lever press response or ‘reward self-administration’
• Once trained animals will press lever even in absence of reward or ‘reward seeking’

Question 40

Operant/instrumental task for aggression reward
Intruder example

Answer 40

• For agression- have intruder chamber
• Animals will learn to lever press for ‘intruder’ (aggression self-administration)
• Trained animals press lever even in absence (aggression-seeking)

sum- self-administration is done in presence of reward and seeking is done in the absence of it.

• As the training goes, they lever press more and more because they start to get a feel for the rewarding effects.
• For aggression seeking- they press way more on this active lever that used to get the intruder mouse.
• Theres an inactive lever which produces an inactive consequence and mice won’t press this.

Question 41

• role of the NAcc and VTA
• example
• activated by?
• measured by?
• artificial stimulation using?

Answer 41

• The nucleus accumbens (NAc) plays a key role in reward and motivated actions together with the VTA.
• e.g. food and drug-seeking
• Activated by rewarding experiences, e.g. drugs of abuse, food, water, and sex.
• Measured by the activity-sensitive protein ‘Fos’
• Artificial stimulation using ‘optogenetics’- you forcefully turn on these neurons involved in reward

Question 42

Immediate early genes (IEGs)
1- what is it?
2- what induces IEGs
3- sequence of IEGs
4- example of an IEG and what is its protein product
5- how is this detected
6- where is it translated and moved?

Answer 42

1- proxy marker of activity

2- Strong activity induces IEGs

3- which are rapidly transcribed to mRNA (20-45 min) and translated to protein product (90-120 min)

4- c-Fos or Fos is an IEG, it’s protein product ‘Fos’ is used often as a neuronal activity marker

5- Detect Fos protein post-mortem in prepared brain tissue slices via immunohistochemistry

6- Fos is translated in the cytoplasm but then moves back to nucleus.

Question 43

Explain Immediate early genes (IEGs)

Answer 43

• Excitatory glutamate synapse (glutame turns on neurons) so action potential arrives, glutamate is released and it binds to excitatory glutamate receptors- AMPA and NMDA.
• If glutamate binds to AMPA sodium comes in and it excites neurons.
• That excitation allows glutamate to bind to NMDA and open up NMDA receptors and calcium comes in.
• Then more of these ion channels called voltage gated calcium channels open up- more calcium comes in and this turns on genes. Because more activity equals more calcium and more calcium equals activation of these second messengers (kinases).
• These sense the elevation in calcium and they relay this activation message down the nucleus and within about 20-45 mins you have these activity sensitive genes called Fos or c-Fos which are transcribed.
• So this piece of DNA or the gene has something called the promoter for this molecule where the transcriptor factor binds.
• So these kinases tell the transcription factor ‘turn on, start reading this gene and go from left to right). You read it and you transcribe the message to mRNA.
• So if a neuron is strongly activated, you have a lot of mRNA for this gene called c-Fos and mRNA eventually becomes translated into protein.
• You want to detect it through some biochemical technique and that technique is called immunohistochemistry and this is tested post-mortum and often in animal tissue

Question 44

What does immunohistochemistry detection of Fos reveal?

Answer 44

Cocaine-activated neuronal ensemble

Question 45

Process of immunohistochemistry detection of Fos

Answer 45

• You need to take the brain after a particular rewarding experience in an animal.
• Once its euthanised it goes through a process called profusion fixation (the brain becomes harder)
• Its put on a machine called cryostat and it cuts slices from brain areas of interest on cryostat. You can do it from front to back of the whole brain
• then perform immunohistochemistry to detect fos and observe under microscope.

Question 46

Immunohistochemistry and fos expression

Answer 46

You can apply these chemicals (antibodies) to the brain slices. These antibodies strain and detect fos. They will bind to fos and you have a secondary antibody that binds to the primary antibody but this secondary antibody has a flurophore (this is a molecule that glows green)

sum- you can detect fos using a biochemical technique called immunohistochemistry and you can find these neurons which glow green. These are neurons which can turn on so more activation = more fos, more number of neurons with fos

Question 47

What do aggression SA and seeking activate?

Answer 47

• This is correlational evidence regarding the role of the reward system in aggression
• We also need causal role evidence

light green bar= mouse lever pressing for reward and an intruder coming in and showing aggressive sign. During that time you see more fos compared to the control.

agression seeking- lever pressing for a lever that used to mean intruder comes in and could show you agression. This also activates the nuclues accumbens- more fos, more neurons coming in

This is correlational evidence (activity goes up when animals administer aggression) when they seek out aggression.

Question 48

How to use optogenetics

Answer 48

1. piece together genetic construct
2. insert construct into virus
3. inject virus into animal brain; opsin is expressed in targeted neurons
4. insert fibre-optic cable
5. laser light of specific wavelength opens ion channel in neurons
6. shine light and measure changes in behaviour

• Blue light turns on the excitatory channelrhodopsin (ChR2)➝Stimulate
• Green light turns on the inhibitory archrhodopsin (ArchT)➝Inhibit

Question 49

What are optogenetics and stimulation linked to brain region?

Answer 49

Optogenetics- light-induced neuronal activity manipulations using neurons

Optogenetic stimulation of the VTA increases aggression

Question 50

Optogenetic stimulation of the VTA increases aggression: Yu et al., 2014

Answer 50

• In this experiment you have a mouse that normally lever presses for aggression.
• The exhibit behaviours like biting, rattling the tail, mounting onto the intruder.
• The VTA projects to the nucleus accumbens
• They transfected the virus so that neurons have channeled up and become light sensitive.
• They shined blue light and turned on this reward pathway.
• You see these mice exhibiting more aggressive behaviour towards the intruder compared to the non-stimulated conditions
• So by turning on the reward system in aggression experience mice, you can increase aggression. So there is a causal link between the activation of the reward system as well as aggression.

Question 51

Summary:
STRESS
1. can be neurotoxic to _____
2. how is PTSD treated?
3. brain regions linked to PTSD

ANXIETY DISORDERS
4. list disorders
5. brain region activated during panic attack?
6. treatment?

AGGRESSION
7. controlled by?
8. implicated?
9. what can it be and where can it be examined?

Answer 51

1. Can be neurotoxic to hippocampus
2. PTSD treated with exposure therapy, SSRIs
3. Altered PFC and amygdala activity, decreased hippocampal volume associated with PTSD
4. Panic disorder, agoraphobia, GAD, social anxiety have a biological component
5. Increased amygdala activity during panic attack
6. BDZ, SSRIs, D-cycloserine for treatment
7. Controlled by Amygdala and hypothalamus (via PAG)
8. Low serotonin implicated (increasing it may reduce aggression)
9. Is rewarding for some and can be examined in laboratory animals