PSYC1002 NOTES NEUROSCIENCE W1 Divisions of the nervous system Nervous system: - CNS o Brain and spinal cord - Peripheral Nervous System o Sensory nerves o Motor nerves o Autonomic nervous system o Enteric nervous system Peripheral Nervous System: - Sensory input to CNS from sensory organs (eye, ear, vestibular apparatus, nose, tongue, skin) - Motor output from CNS to muscles - Autonomic nervous system o Controls many non-voluntary bodily functions (e.g. digestion, HR, BP, sweating, pupil size and genitals (THE 4 F S) o 2 branches: Sympathetic vs Parasympathetic Have opposite effects: Sympathetic prepares for action; whereas parasympathetic involved in rest and recuperation Both are controlled by the brain o Uses same neurotransmitters as brain (Ach and NA)à some drugs used to treat psychological/neurological conditions in brain can affect function of ANS - Enteric Nervous System o Half a billion neurons located in the gut (in walls of intestinal tract, from oesophagus to anus) o Interacts with brain via Sympathetic and Parasympathetic NS, but can also function independently. Sometimes referred to as the 2 nd brain o Controls digestive activity (peristalsis and secretion of enzymes) and senses physical and chemical conditions of gut o Uses same neurotransmitters as in brain, including dopamine and serotonin (95% of all serotonin in body comes from gut) - CNS o Contains about 100 billion neurons o Brain and spinal cord are protected by: bone, meninges and blood brain barrier
W1_L2 Divisions of the brain
W1_L3 Anatomy and Physiology of neurons Hyperpolarisation after action potential prevents it from moving back on itself Depolarisation can only occur at gaps between myelin sheath - Anaesthetics penetrate neuronal membrane and block opening of ion channels
- Alcohol can also penetrate neuron membrane and impair generation of action potentials W2_L1 How we study the brain Mapping the functional organisation of the brain: - Studying the effects of brain lesions (experimental in animals; accidental in humans) - TMS - Single-cell recording/ electrical stimulation/ microinjection of drugs - Imagingà ECG, PET, fmri, MEG Transcranial Magnetic Stimulation: - Uses brief magnetic pulse next to the skull to induce a small electrical current in the underlying brain, which depolarises neurons and can invoke action potentials Single-cell recording / Electrical stimulation: - Microinjection into a specific region of the brain Functional imaging of the brain: - Measuring which brain areas become active - Electroencephalography (EEG) o Electrode plates against skull can record electrical fields generated by combined electrical activity of many neurons o EEG has very good temporal resolution can show activity changes on a very fine time scales (approx. 20 ms) o However, it has poor spatial resolution not good for seeing exactly where activity occurred
- Positron Emission Tomography (PET) o Measures activity in brain by measuring changes in blood flow o Person given radioactively-labelled oxygen (or glucose) o Any area that is active will be highlighted because it draws more blood and receives more 02 o Areas that are working harder use more oxygen o Quite good spatial resolution, but is worse at temporal resolution - Function Magnetic Resonance Imaging (fmri) o Measures changes in 02 in blood (differences in the magnetic properties of O2 rich and O2 depleted blood o Has good spatial resolution, especially when combined with a MRI o Response lags behind actual brain activity and temporal resolution no so high - Magnetic Resonance Imaging (MRI) o Bombarding brain with high frequency radio waves, whilst inside a strong magnetic field, to measure orientation of protons o This identifies different types of brain tissue, to allow visualisation of brain structures - Magnetoencephalography (MEG) o Measures magnetic fields emitted from brain (created by electrical activity in neurons) o 3D construction of where the electrical activity was arising from, to create functional map of the brain response o has excellent temporal resolution and good spatial resolution and completely non-invasive o but equipment is hugely expensive and extremely sensitive to any source of electromagnetic interference Correlations between brain activity and psychological function doesn t prove causal link (methods that directly intervene in neural function, such as TMS can do this) W2_L2 Sleep, Feeding and Reward What keeps us awake - Noradrenaline neurons in Locus Coreuleus inc serotonin and acetylcholine neurons in the Pons - Disconnecting the forebrain from the brainstem causes profound and almost continuous sleep - Neurons are active while awake and dormant while sleeping - Electrical stimulation of such neurons can wake a sleeping animal - Effects of stimulant drugs (amphetamines, ecstasy) Destruction of the anterior hypothalamus can cause insomniaà neurons contain GABA and inhibit: Ach, 5HT and NA arousal systems in the brainstem o Stimulation of the anterior hypothalamus can induce sleep Sleep cycles: - When awake electrical activity is high
- Sleep is characterised by slow rhythmic patterns of electrical activity in the brain (slow wave sleep) o Role of reciprocal connections between thalamus and cortex in orchestrating synchronised neuronal activity - REM sleep o Brain waves become desynchronised just like when awake o Eyes dart back and forth o If woken during REM sleep we typically say we were dreaming o Caused by neurons in pons that contain acetylcholine (Ach) and stimulate neurons in the thalamus, which project to the visual cortex o Ach neurons in pons stimulate neurons in medulla, which inhibit motor neurons in the spinal cordà paralysed à stops us hurting ourselves while sleeping o Destruction of the neurons in medulla causes animal to become very active during REM sleep (no longer paralysed) Regulation of feeding: - Hunger and satiety determined by contents of stomach and substances circulated in blood (hormones, sugars, fats) - But the brain is responsible for the subjective experience of hunger/satiety and behavioural response (find food/stop eating)à hypothalamus is extremely important in this matter - Lateral hypothalamus (LH) o Destruction of the LH causes rats to reduce eating dramatically o LH regulates feeding by Controlling release of insulin à therefore high blood glucose Regulating attentionà without LH they ignore food Influencing taste à rats without LH dislike food - Ventromedial Hypothalamus (VMH) o Destruction of the VMH causes rats to become overeaters making them gain weight o Rats with damaged VMH do not lack satiety àeach meal is of normal size, however they eat less often o VMH destruction can cause rats to overeat for 2 reasons Increases gut motility (stomach empties sooner = cue to eat) Rats release excessive amounts of insulin à gain weight because food is quickly turned into fat. Also, high insulin means they have low blood glucose, thereby increasing appetite The Paraventricular Nucleus of the Hypothalamus: The paraventricular nucleus (PVN) is important in satiety. - Rats with damage to PVN eat bigger meals. - Satiety due to cholecystokinin (CCK) in PVN o CCK is a hormone released from gut when food passes from stomach into the small intestine o Therefore, at end of meal, CCK levels in blood rise and eating stops.