Introduction to Neuroscience II, 1¼h of lectures by Patrick House and Dana Turker for Human Behavioral Biology

Patrick talks about memory and plasticity. Why do some memories last while others are fleeting? How does context (environment) fit into shaping memory? Can neuroscience explain Stephen Wiltshire the autistic who can draw detailed aerial views of whole cities from short helicopter rides.

Dana talks about the autonomic nervous system (ANS) which is part of the peripheral nervous system (that is, the part that deals with systems outside the brain and spinal cord). It manages those functions that happen automatically: the stuff we do not have conscious control over. E.g., heart beating, digestion, goosebumps, orgasm, etc. A highlight of her discussion is an explanation for penile erection and male ejaculation in terms of the two main subsystems of the ANS: the parasympathetic nervous system (PNS) and sympathetic nervous system (SNS). Her slides are fantastic!

Detailed notes on both talks are below.

11. Introduction to Neuroscience II

Detailed notes on Patrick's talk on memory and plasticity.

See Stephen Wiltshire's stunning aerial view of London:

To understand Patrick I had to look up a word in WordNet. Potentiate is a verb meaning to increase the effect of or act synergistically with. Potentiation is the noun form meaning the synergistic (positive feedback) effect of something.

Memory happens, to the best of our knowledge, in the synapse, the space between two neurons. It involves modulation and changes in the synapse. Memory is synaptic plasticity by strengthening and enhancing signal transmission between two neurons. This is known as LTP (long-term potentiation): "neurons that fire together wire together" is a caricature of Hebbian theory (named after Donald Hebb who proposed the idea in 1949).

Information in the brain is transferred by excitation of neurons and glutamate is the chief excitatory neurotransmitter in the vertebrate nervous system. So "repetition drives memory".

Some mechanisms of synaptic potentiation: 1) add more excitatory neurotransmitter, 2) increase sensitivity of the neurotransmitter receptors in the post-synaptic neurons, 3) increase the number of post-synaptic receptors.

But how do the pre- and post-synaptic neurons know when to potentiate? There are retrograde neurotransmitters (e.g., nitrous oxide N₂O) which feedback from the post-synaptic neuron to the pre-synaptic neuron to modulate release of pre-synaptic neurotransmitters. This is the mechanism of LTP. NB: this counters the normal flow of neural information: fascinating!

Autistic savant memories are not rote, but formed by a spatio-geographical "walk" through of their experiences.

The hippocampus is the site of memory and LTP. First evidence: when HM had his hippocampi removed to stop seizures, he lost the ability to form new memories. Brain scanning during learning shows LTP in the hippocampus. If you block LTP pharmocologically, learning and activity in the hippocampus decrease.

There is adult neurogensis and adult plasticity.

How do motor memories work and how does emotion trigger stronger memories?

LTP happens all over the brain

excitation = plasticity = potentiation

Post-traumatic stress is caused by potentiation of emotionally hyperactive memories that are not relevant to the current situation.

Since memory is a physiological process, like every physico-mechanical process it is subject to failure without prior notice (that's my Dad's expression). Patrick simply observes that things can go wrong: even when we try, sometimes we cannot remember something and other memories just fade away.

Some mechanisms for intentional disruption of LTP. When you are hungry (hypoglycemic states), insulin disrupts LTP. Stress hormones can give us short-term enhanced memory (slow-motion rememory of a car crash). Excess stress hormones can weaken memory formation. Alcohol disrupts LTP.

He concludes by explaining how this myoptic view of neurons and synapses misses the complexity of 100 billion neurons each interacting with 10,000 neurons using a chemico-electrical physical system implies some degree of noise in the individual inter-neuron signal transfers. Random and spontaneous generation of action potentials happen. So the brain needs to try to distinguish between signal and noise. Neurons operate in groups giving another layer of complexity to the system.

Inhibition is another mechanism the brain uses to damp out noise. Neurons can inhibit themselves so that their firing contains more signal and less noise. This allows for temporal sharpening of its signal.

Lateral (or spatial) inhibition: a neuron inhibiting its neighbors to enhance its own signal among the noise of those neighbors. For example, in pain sensation, fast sharp pain is carried by one group of neurons while another carries the slow dull pain. The fast, sharp pain can activate the slow dull pain neuron group which then gradually inhibits the fast sharp pain causing it to stop.

Vision gives a more complex example. Nobel laureates David Hubel and Torsten Wiesel found a spatiotopic (orientation and alignment) relationship between neurons in the primary visual cortex (V1) in the occipital lobe and neurons in the retina of the eye. At the next layer up (V2), they discovered that certain visual patterns stimulated neurons in V2 even though stimulation of individual retinal neurons did nothing. Different features are extracted out by the different levels of neuronal analysis in the visual cortex.

Neural networks: when you combine 100 billion neurons each with about 10,000 synaptic connections to other neurons we can imagine how the neural representation of context or environment must be stored somehow in the network itself. So concepts & categories and indeed memories themselves are a kind of emergent property of brains. Individual genetic and cellular and historical differences can affect these neural networks yielding the differences that make each of us unique.

Details from Dana's talk about the autonomic nervous system (ANS) which is part of the peripheral nervous system (which includes the ANS plus the somatic nervous system which delivers sensory inputs to the CNS (central nervous system: brain and spinal cord) and the voluntary nervous system which transmits motor signals between the CNS and muscles, this system is myelinated and therefore fast; it move muscles). The ANS is unmyelinated and therefore slow. The ANS is involuntary and moves organs.

The ANS is subdivided into the parasympathetic nervous system and the sympathetic nervous system. The parasympathetic and sympathetic tend to work in opposition to one another. So usually when one is on, the other is off (but one thing by now in this course you will have noticed is that it tends to be more complicated than that!). The sympathetic deals with arousal, alertness, stress, emergencies, fight or flight whereas the parasympathetic deals with growth and repair and calm, vegetative functions (e.g., digestion).

For example, the fight or flight response of the sympathetic nervous system gets the body ready for action: it releases adrenaline, raises blood pressure, releases glucose for muscle energy, slows digestion, releases cortisol to suppress the immune system. Then our pupils dilate, mouth gets dry, neck & shoulders tense, heart pumps faster, we sweat, breathe faster, etc.

The sympathetic nervous system releases the excitatory hormone norepinephrine (NE) in the target organs. It releases epinephrine (also called adrenaline) in the adrenal gland. Norepinephrine is oxidized (loss of electron(s)) to epinephrine, so they are separated by one biochemical step. The parasympathetic nervous system releases acetylcholine (ACh) in target organs.

Comparison of parasympathetic and sympathetic effects:
Parasympathetic Sympathetic
- constricts pupils - dilates pupils
- stimulates tear glands - no effect on tear glands
- strongly stimulate salivation - weakly stimulate salivation
- inhibits heart - accelerates heart
- dilates arterioles - constricts arterioles
- constricts bronchi - dilates bronchi
- stimulates stomach, pancreas - inhibits stomach, pancreas
- stimulates intestines - inhibits intestines
- contracts bladder - relaxes bladder
- stimulates erection - stimulates ejaculation

Sympathetic is not always excitatory (it inhibits the GI tract) and the parasympathetic is not always inhibitory (it stimulates the GI tract), it depends on the organ. So we need two different receptors for each system (an excitatory one and an inhibatory one), that is, the sympathetic (parasympathetic) system can have excitatory NE (Ach) receptors in some organs and inhibatory ones in other organs.

Homeostasis is a dynamic balance between the parasympathetic and sympathetic systems.

Stress can impair the parasympathetic system sometimes leading to erectile dysfunction (60% of cases) and immune functions can also weaken.

Regulation of the autonomic nervous system is controlled by the hypothalamus (which also controls the pituitary gland and the endocrine system). The cells of the hypothalamus are just one synapse away from the neurons that project to the target organs. E.g., barorecptors in blood vessels detect low blood pressure and send signals to hypothalamus which then sends a signal via the spinal cord to adjust blood pressure by projection into the heart which then beats faster.

The limbic system (emotions, behavior, memory) surrounds the hypothalamus. E.g., seeing things or people you like can cause a sympathetic (fight or flight) response.

Our cortex is also wired in, so that purely cognitive thoughts can trigger the ANS. A test can trigger the sympathetic system.

Hypothalamus is found even in reptiles. The limbic system is in all mammals. The cortex is in primates.

ANS function is highly plastic (malleable): receptivity can change over time. E.g, sustained stress (lots of NE needed) can stimulate the production of more NE to sustain the stress response. Habituation or sensitization are both possible changes that the ANS can experience. Biofeedback (think pleasant thoughts) can decrease blood pressure.
Shared publiclyView activity