HNS48 Limbic System And Central Autonomic Function Flashcards
Emotion
Primary (reflexive): fear, anger, surprise, disgust, happiness, sadness
Secondary (cognitive): envy, shame, guilt
Emotion and reward
Emotional experience and ability to reflect upon our emotions:
—> Enrich sense of satisfaction, Guide actions
Rewards (Good / Bad):
—> Modulate emotions + Motivated behaviour
Emotions: mediated by Limbic system
***Limbic system
Interconnected brain areas:
Integrate information about sensory stimuli, memories, cognitive plans
—> Produce emotional learning + emotional experince
Diencephalon components:
- ***Anterior group of thalamic nuclei
- ***Hypothalamus
- Mamillary body (of Hypothalamus)
Cerebrum components:
- ***Cingulate gyrus
- ***Hippocampal formation (Hippocampus + Dentate gyrus + Subicular complex)
- Parahippocampal gyrus
- Entorhinal cortex
Other components:
- Fornix + Fimbria
- ***Amygdala (negative emotion)
Cannon-Bard theory of Emotion and Sham rage
Forebrain outflow pathway (Cerebral cortex) transected
—> Rage response (e.g. hissing, increased BP, HR) despite innocuous stimuli / no stimuli (Sham rage)
—> Animals retained emotional responses but responses lack aspects of emotional behaviour that was normally observed during rage
—> Sham rage also subside rapidly upon stimulus removal / undirected
—> animals may even bit themselves
Progressive transaction of Anterior / Posterior hypothalamus
—> NO coordinated rage response
—> Show that emotions are ***regulated in Hypothalamus
Limbic system anatomy
Limbic lobe (Initial emotion circuit):
- **Ring (環狀) of “primitive” cortex around brainstem:
1. Cingulate cortex
2. Parahippocampal gyrus (Entorhinal cortex)
3. Hippocampal formation (Dentate gyrus)
4. Mamillary body (of Hypothalamus)
5. Anterior nucleus of Thalamus
Functions of Emotions
- Internal feelings
- Behaviour patterns
- ***Autonomic control
***Papez circuit
Cingulate gyrus (Emotional experiences) —> Parahippocampal gyrus —> Entorhinal cortex —> Hippocampus (Dentate gyrus) —> Fimbria —> Fornix —> Mamillary body (Emotional expression) —> Mammillothalamic tract —> Anterior nucleus of Thalamus —> Cingulate gyrus (posterior) —> Parahippocampal gyrus —> Hippocampus
N.B.: NO Amygdala / Hypothalamus
***Paul MacLean: Amygdala + Hypothalamus
Extend neural circuits to include additional interconnected brain areas:
- **Amygdala
- Key coordinator
- Linking Cortex to Hypothalamus + other subcortical brain structures
Proposed additional neural circuit for emotion (Maclean加埋Amygdala + Hypothalamus): Emotion stimulus —> Association cortex —> Hippocampal formation (Hippocampus + Dentate gyrus + Subicular complex) OR Cingulate gyrus (Papez circuit) —> ***Amygdala —> ***Hypothalamus —> ***Prefrontal cortex —> Association cortex
Amygdala and Kluver-Bucy syndrome
Removal of temporal lobes including Amygdala (and Hippocampus) bilaterally
—> dramatic change in emotional behaviour
- Tame, fearless, “blunted” emotions
- Increased oral activity, placing inedible objects in mouth
- Increased sexual behaviour, mounting inappropriate objects
Subsequent studies:
- Stimulation of Amygdala can produce **fear and anxiety
- Imaging studies: show more activity in Amygdala when viewing expressions of fear
- Amygdala activated differentially by emotional facial expressions —> identify emotions (眉頭眼額)
- Amygdala respond to emotionally arousing stimuli (e.g. seeing a spider)
—> Conclusion: Amygdala is a **key structure in ***mediating emotional effects
- **Temporal lobe ablation (木頭人):
1. Loss of fear
2. Less aggression
3. Hyperorality
4. Forget rapidly
Examples:
- Kluver-Bucy syndrome: Amygdala damage (reduces fear)
- Autistics have problems identifying emotions of other people (abnormal Amygdala)
***Neural pathways for emotional stimulus
- Central component: Cerebral cortex (evaluative components of emotion)
- Peripheral component: Hypothalamus (autonomic)
Pathway:
Emotional stimulus
—> ***Thalamus —>
- Direct pathway
—> **Amygdala (—> Emotional responses)
—> **Hypothalamus + Brainstem nuclei
—> Autonomic NS
OR
2. Indirect pathway —> ***Cortex —> ***Amygdala (—> Emotional responses) —> ***Hypothalamus + Brainstem nuclei —> Autonomic NS
Peripheral (Autonomic) control
Emotionally significant stimuli
—> Hypothalamus
—> act on Autonomic NS by modulating visceral reflex circuitry (organised at level of brainstem)
—> HR, BP, respiration changes
Hypothalamus:
- Autonomic control
- Internal homeostasis
- Motivation
(Many nuclei in Hypothalamus and each for specific function:
e. g.
- Posterior hypothalamus —> ↑ BP, pupil dilation, shivering
- Posterior preoptic / Anterior hypothalamic area —> body temperature, panting, sweating
- Dorsomedial nucleus —> GI stimulation
- Perfornical nucleus —> rage, hunger, ↑ BP)
Flow of information controlling Autonomic nervous system
Major descending inputs to Brainstem autonomic nuclei
- Amygdala
- Hypothalamus
Visceral sensation (sensory information esp. from visceral organs, taste receptors)
—> ***Solitary nucleus
—> Brainstem (+ Hypothalamus)
—> Brainstem nuclei
—> Preganglionic efferents
—> Sympathetic (T1-L2) + Parasympathetic (CN3, 7, 9, 10 + S2-4)
Feeding behaviour
- **Lateral hypothalamus (Hunger / Feeding centre)
- Set point + Internal drive for food intake
- Lesions in lateral hypothalamus —> ↓ in food intake (Hypophagia)
***Septal region, Hypothalamus, Ventral tegmental area
- Septal region:
Structure of Limbic system closely connected to Hypothalamus, Hippocampal formation, Amygdala
—> **Pleasure centre
—> part of Mesolimbic pathway (Dopaminergic)
—> project to **Nucleus accumbens (Rewarding, Addiction)
Electrical self-stimulation experiment:
- Stimulation of septal region
—> Pleasant sensation
—> rats continuously press bar to experience euphoric feeling
- Ventral tegmental area:
Brain stimulation activates neurons in Ventral tegmental area (Midbrain, next to Substantia nigra)
—> ***Dopamine neurons (forming most of Mesolimbic and Mesocortical pathway involved in reward)
—> Dopamine release
—> rats choose self-stimulation over food / sex - Hypothalamus:
Brain stimulation to parts of Hypothalamus (and related structures)
—> ***Reinforcer
—> work independently of drive state (e.g. hunger)
Ventral tegmental neurons and experiment
Wolfram Schultz:
Rewards can be learned to be expected (Reward predicted)
- even though the association between stimulus and reward is unknown initially
When reward is predicted —> VTA neurons fire
Conclusion:
- VTA neurons provide a learning signal that reflect reward expectation
- Cell’s firing rate is modulated when reward received differ from expectation
—> this learning signal can be used by other brain areas to
- Guide behaviour
- Modulate emotional responses to reward-predicting stimuli
***Drug abuse and addiction
Cocaine, Amphetamines:
- ↑ dopamine release in brain esp. in shell of Nucleus accumbens
- block dopamine reuptake transporter
Nicotine:
- ↑ dopamine release by acting on presynaptic cholinergic receptors
Nucleus accumbens shell:
receives Dopaminergic input from VTA (midbrain dopamine neurons)
—> project to Hypothalamus + Limbic structure
—> mediate emotional responses
Self-stimulation experiment
Cocaine and nicotine:
- ↑ rate of self-stimulation by rats for a given stimulation frequency compared to baseline
Conclusion:
Cocaine and nicotine enhance pleasure produced by self-stimulation
***Brain reward circuitry and self-stimulation
- **Medial forebrain bundle:
- Descending myelinated fibres innervating VTA
- most effectively site for stimulation
- activates VTA directly
Different drugs can intervene at different levels of brain-reward circuitry:
Amphetamine, Cocaine, Nicotine, Opiates, Ketamine —> act on Nucleus accumbens
Monoamine and Emotion
ALL in brainstem
- Dopamine (VTA, Substantia nigra):
- **Reward (motivation)
- **Pleasure, euphoria
- ***Motor function (fine tuning)
- Compulsion
- Perseveration - Serotonin (Raphe nucleus):
- ***Mood
- Memory processing
- Sleep
- Cognition - Norepinephrine (Locus coeruleus)
Others: ACh (Basal forebrain)
Major depression
Based on Diagnostic and statistical manual of mental disorder (DSM-5)
- Anxiety, ↓ mood
- Anhedonia (lack of pleasurable feeling)
- Insomnia / hypersomnia
- Fatigue
- Appetite changes
- ↓ Motivation
- Worthlessness
- Suicidal thought
60% of patients inadequate response to pharmacological / deep brain stimulation / talk therapies
Monoamine hypothesis of depression
Depression caused by low levels / deficit in functions of NT
Anxiety
Lower-grade form of fear, generalised and often non-referential (being afraid of nothing in particular but still feeling the nervousness)
- Panic disorder
- GAD
- PTSD
- Social phobia / social anxiety disorder
- Simple phobias
- OCD
Psychosurgery - Deep brain stimulation
Surgical treatment involving implantation of brain pacemaker
—> send electrical impulses to specific part of brain
—> modulate neural transmission by:
1. ↑ / ↓ firing of neurons
2. ↑ / ↓ neurogenesis
***Mesolimbic pathway and Mesocortical pathway
Mesolimbic pathway:
VTA —> ***Nucleus Accumbens —> Hypothalamus + Limbic structure —> mediate emotional responses
Mesocortical pathway:
VTA —> ***Prefrontal cortex