Modulatory and Arousal Systems Flashcards
Modulatory system:
What does it control?
What are its neural responses?
Which type of synaptic transmission does it have?
What is their primary receptor type?
Where do the modulatory inputs from the brainstem go?
- Controls state of the system
- Non-specific, linked to the Sleep-wake cycle, Behavioural state
- Slow, Imprecise
- Metabotropic
- Diffuses out all over the cerebrum
Sleep-Wake Cycle:
When awake, where does the sensory information travel?
What does this look like on an ECG and EEG?
When asleep, what does the brainstem do to the modulatory inputs?
What does this look like on an ECG and EEG?
How does the EEG change from stage 1 to stage 3 of sleep?
Which stages do you drift between during sleep? What occurs in the body during this?
What is REMs (deep) sleep?
Why don’t we remember the early dreams?
- Thalamic cells relay sensory information to SS cortex
- Desynchronised, Low amplitude, High-frequency EEG
- Withdraws modulatory inputs = Thalamic cells become insensitive to sensory input
- Synchronised, High amplitude, Low-frequency EEG
- ↑Synchronisation, Amplitude, ↓Frequency of EEG
- Stages 2 and 3; Desynchronised EEG, Activity in Limbic and Sympathetic systems, Paralysis
- Rapid Eye Movements = Dreaming
- Multiple sleep-wake cycles throughout the night, with the time spent in REMs sleep increasing
Main Modulatory Pathways: LOOK AT PICTURES
CHOLINERGIC:
What is the pathway?
What is it involved in?
What does loss of its function cause?
How is this dysfunction treated?
NORADRENALINERGIC:
What is the pathway?
What is it involved in?
What does loss of its function cause?
How is this dysfunction treated?
DOPAMINERGIC:
What is the pathway?
What is it involved in?
What does loss of its function cause?
What does over-function of it cause?
How is this dysfunction treated?
HISTAMINERGIC:
What is the pathway?
What is it involved in?
Based on its control, what can Antihistamines cause?
OREXIN:
What is the pathway?
What is it involved in?
What does dysfunction of it cause?
SEROTONIN:
What is the pathway?
What is it involved in?
What does dysfunction of it cause?
How is this dysfunction treated?
CHOLINERGIC:
- • Pontomesencephalic Tegmentum projecting into Thalamus
• Basal Forebrain projecting into the Neocortex & Hippocampal complex
- MEMORY, COGNITION, Wakefulness, Attention, Learning
- Dysfunction (↓) = Cognitive decline, Memory Loss = Alzheimer’s
- AchE Inhibitors
NORADRENALINERGIC:
- Locus Coeruleus projecting all over the CNS
- MOOD, Attention, Learning, Memory
- Dysfunction (↓) = Anxiety and Depression
- NA reuptake inhibitors, MAOIs
DOPAMINERGIC:
- • Substantia Nigra projecting into Basal ganglia
•Ventral Tegmental Area projecting into Frontal cortex & Limbic lobe
- VOLUNTARY MOVEMENT, Attention to rewarding stimuli
- Dysfunction (↓) = Parkinson’s
- Dysfunction (↑) = Schizophrenia, Addiction
- DA antagonists
HISTAMINERGIC:
- Hypothalamus projecting into Thalamus & Cortex
- Wakefulness, Attention
- Drowsiness
OREXIN:
- Hypothalamus projecting all over the CNS
- WAKEFULNESS, Food seeking, Activity
- Dysfunction = Narcolepsy; disruption of sleep-wake cycle, walking dreamlike episodes, cataplexy
SEROTONIN:
- Raphe Nuclei projecting all over the CNS
- MOOD, Quiet waking, Patience/Impulse control, Appropriate responses
- Dysfunction = Anxiety and Depression
- Serotonin reuptake inhibitors, MAOIs
Modulatory pathways and Arousal:
SLEEP → WAKE:
What occurs in the modulatory pathways during this?
What does this effect relay cells? How does it show on an EEG?
What is the ARAS essential for? So, what can lesions of the brainstem cause?
QUIET WAKING → FULL ATTENTION:
What occurs in the modulatory pathways during this?
What mimics these effects to cause full attention?
- ↑Hypothalamus (Orexin, Histamine) = ↑Brainstem Ascending Reticular Activating System/ARAS (Ach, NA, Serotonin) AND Basal Forebrain (ACh)
- o Prevents relay cells bursting and restores Thalamus as relay
o ↑Response strength & selectivity, Low amplitude, High-frequency EEG - Waking up; lesions cause Coma
- More amplified version of inputs = ↑↑Response strength & selectivity, Cognitive function, Motivation, Plasticity, Learning & Memory
- Performance-enhancing drugs
FALLING ASLEEP:
What occurs in the modulatory pathways during this?
What does this effect relay cells? How does it show on an EEG?
What promotes sleep? How? In terms of this, how does Caffeine produce its effects?
- ↑VLPN = ↓Hypothalamus (Orexin, Histamine), Brainstem (ACh, NA, Serotonin), Basal Forebrain (ACh)
- o Relay cells start bursting and cortex is disconnected
o High amplitude, Low-frequency EEG - Circadian rhythm via Suprachiasmatic nucleus, Tiredness (Build-up of Adenosine), Illness (↑Immune by-products causing tiredness)
o Caffeine reduces stimulatory effects of Adenosine on VLPN
