Origins of Biopsychology

I. Introduction

II. Course Overview

III. History of Behavioral Neuroscience

IV. Course Goals

Biopsychology

• Seeks to describe the physiological mechanisms of the body that mediate our movement and mental activity.

• “Mental activity” includes a vast array of things including feeling, thinking, consciousness, communication, learning, and memory.

• A.k.a. psychobiology or behavioral neuroscience

Topics to be Covered

• History• The Neuron• Brain Structures• Drugs• Sensation (vision,

etc…)• Sleep

• Eating and Drinking • Learning and Memory• Language and

Communication• Psychological

Disorders• Emotions (if extra

time at the end)

Two Sides to the Mind-Body Question

• Dualism: The belief that the mind and body (or the mind and the brain) are separate entities.– Often assumes the existence of a non-material soul or

spirit– Most popular view throughout history– May be “wired” to view ourselves this way

• Monism: The belief that the mind and body (or the mind and the brain) are one.– Mind and brain are almost synonymous– The mind is a product of the brain– Most common view among biopsychologists

III. History of Behavioral Neuroscience

A. Aristotle (384-322 BC)– dualist

B. Hippocrates (460-370 BC)– monist

C.Descartes (17th Century)– modified dualist

D.Galvani (17th Century)– frog muscles contract with electricity

III. History of Behavioral Neuroscience (Continued)

E. Muller (19th Century): – doctrine of specific nerve energies– advocate of experimentation

F. Flourens (19th Century)– experimental ablation

G. Broca (19th Century)– aphasia

H. Fritsch and Hitzig (19th Century)– stimulation of dog cortex produces body movement

I. Darwin and Wallace (19th Century)– theory of evolution and common descent

Lateralization of Function versus Localization of Function

• Localization of Function: The tendency for a function to be located in a particular area of the brain (i.e., a great deal of advanced visual processing occurs in the occipital lobe).

• Lateralization of Function: The tendency for a function to be primarily located on one side of the brain (i.e., Broca’s area is typically in the left frontal lobe).

Cells of the Nervous System

I. Introduction

II. Neurons

III. Ways of Classifying Neurons

IV. Nervous System Support Cells

V. Communication Within a Neuron

VI. Communication Between Neurons

VII. Major Neurotransmitters

How Long Would it Take to Count to 100 Billion?

• 60 seconds per minute × 60 minutes per hour × 24 hours/day × 365.25 days/year = 31,557,600 seconds per year

• 100,000,000,000 ÷ 31,557,600 =

3168.8 years!

Structures of the Nervous System

I. Divisions of the Nervous System

II. Orienting within the Brain

III. The Developing Brain

IV. The Adult Brain

V. Brain Plasticity

Anatomy Directions(See figure 3.2, Page 65)

Anterior/Rostral Posterior/Caudaltowards the head or front towards the rear or behind

Ventral (Inferior) Dorsal (Superior)towards the belly (below) towards the back (above)

Medial Lateralclose to the neuraxis away from the neuraxis

Ipsilateral Contralateralon the same side on the opposite side

Convolutions of the Cortex

• Bump or ridge = gyrus (plural is gyri)

• Groove = sulcus (plural is sulci)

• Big groove = fissure

Receptors at the Synapse

• Receptor: Protein molecule embedded in a membrane that has a binding site for one or more neurotransmitters– The binding site is like a key slot– Neurotransmitter is like the key

Ionotropic Receptor

• Receptor contains an ion channel (or door) that opens or closes when neurotransmitter (NT) attaches to its binding site

• Example: door to your house (ionotropic receptor) has a key slot (binding site on the receptor) that opens when you put in and turn the key (neurotransmitter)

Metabotropic Receptor

• Receptor doesn’t contain an ion channel

• When Neurotransmitter attaches to binding site, a G-protein changes

• Altered G-protein can affect near by ion channels or activate “second messengers”

• Second messengers: 1) affect near by ion channels and/or 2) activate DNA to perform other cellular functions

Metabotropic Receptor Example

• Putting a key (neurotransmitter) into a key slot (binding site on the receptor) causes a near by elevator to turn on and open it’s doors (G-protein or second messenger opens near by ion channel) and sends a message that the elevator is operating to a control center elsewhere in the building (G-protein affects other cellular processes)

Psychopharmacology

I. Introduction

II. Principles of Psychopharmacology

III. Sites of Action

Psychopharmacology

• The study of how drugs effect the nervous system and behavior.

• Drugs have…– effects: changes in behavior and/or

physiology– sites of action: place in the body where the

drug interacts with the cells, causing some kind of change

Pharmacokinetics

• Pharmacokinetics: The study of how drugs are…– absorbed– distributed within the body– metabolized (used) and – excreted (gotten rid of)

Factors Influencing Drug Effects

• Route of administration– Ingested vs. smoked vs. injected (Figure 4.1)

• Solubility– Water soluble molecules can’t cross the BBB– Lipid (or fat) soluble molecules can cross BBB– Heroin more soluble in fat than morphine– Given equal initial doses, more heroin gets to

the brain than morphine

Agonist

• Drug that facilitates or enhances the effect of a neurotransmitter – Nicotine is an ACh agonist– Cocaine and amphetamines are dopamine

agonists

Antagonist

• Drug that counter-acts the effect of a neurotransmitter– 1st schizophrenia meds dopamine antagonists– Botulinum toxin (botulism) is an ACh

antagonist

Tolerance

• Refers to how with repeated use of a drug, it takes more of it to achieve the same effect.– Receptors on postsynaptic membrane may

disappear in response to repeated cocaine use (cellular tolerance)

– With repeated consumption, more enzymes are present in liver and blood to break down alcohol, thus less gets to cells (metabolic tolerance)

Tolerance Effects

• 100 milligrams of morphine typically causes profound sedation and even death in first time users

• Users with morphine tolerance have been known to consume 4000 milligrams (40 times more) without adverse effects

• Amphetamine users can consume up to 100 times initial dose with tolerance

Withdrawal

• Symptoms opposite to those of a drug that occur when someone stops taking a drug that they have been using repeatedly.

• For example, if drug makes you happy and euphoric, withdrawal symptoms may make you depressed and down

Sensitization

• Refers to how with repeated use of a drug, it takes less of it to achieve the same effect.

• Less common than tolerance

• Thought to occur in response to occasional or infrequent use

Would it help or hinder the effect of a neurotransmitter if you…

1. Added more of the material needed to make the neurotransmitter?

2. Interfered with the process of creating NT?

3. Prevented the NT from being stored in the vesicles?

4. Tricked the vesicles into releasing NT (without an action potential)?

5. Prevented calcium from triggering the release of NT from the vesicles?

Would it help or hinder the effect of a neurotransmitter if you…

6. Artificially activated a binding site of a receptor?

7. Blocked the binding site of a receptor?

8. Artificially activated an autoreceptor?

9. Blocked an autoreceptor so that it couldn’t detect neurotransmitter?

10.Prevented reuptake from happening?

11.Prevented the destruction of ACh?

Vision

I. Introduction

II. Nature of Light

III. Anatomy of the Visual System

IV. Coding of Visual Information in the Retina

V. Analysis of Visual Information

Sleep and Biological Rhythms

I. Introduction

II. Measuring Sleep

III. Stages of Wakefulness and Sleep

IV. Why Do We Sleep?

V. Physiological Mechanisms of Sleep

VI. Biological Clocks

VII. Sleep Disorders

Neurotransmitters Involved in Arousal

Norepinephrine Locus coeruleous (pons)

Acetylcholine Basal forebrain and reticular formation (in pons and medulla)

Serotonin Raphe nuclei (pons and medulla)

Histamine Tuberomammillary nucleus (hypothalamus)

Hypocretin Hypothalamus

Neural Control of Slow-Wave Sleep

• Ventrolateral preoptic area (basal forebrain, in front of the hypothalamus)

• Destruction produces insomnia, coma, & death

• Injection of adenosine into the basal forebrain produces sleep

Neural Control of REM Sleep

• Peribrachial Area (in dorsolateral pons)

• Medial Pontine Reticular Formation (MPRF)– Remember reticular formation also involved in

alertness

• Damage to either area eliminates REM sleep

Reproductive Behavior

I. Sexual Development

II. Hormonal Control of Sexual Behavior

III. Neural Control of Sexual Behavior

Gametes

• Almost all cells of the human body contain 23 pairs of chromosomes (46 Total) in their nuclei

• Gametes (sperm and ova) have 23 individual chromosomes in their nuclei (23 Total)

Organizational Effects

• Hormone effect that directly changes tissue differentiation and/or development

• Causes changes in structures of the organism

• Organizational effects occur early in development

• Not reversible

Activational Effects

• Effect of a hormone on the fully developed (or mature) organism

• Act on pre existing structures, causing some type of change

• Activational effects often depend on prior organizational effects

• Examples: changes to boys and girls with puberty, ovulation in women

Primordial Gonads(bipotential or bisexual)

Genetic Females (XX)No SRY gene

Genetic Males (XY)SRY gene makes testis determining factor

Gonads become ovaries Gonads become testes

No testicular hormones Testicular hormones (anti-Müllerian hormone &

androgens)

Müllerian System

Develops (feminization)

Wolffian System Withers

(demasculinization)

Müllerian System Withers

(defeminization)

Wolffian System Develops

(masculinization)

Activational Effects of Sex Hormones at Puberty (See Figure 9.5 in Text)

HYPOTHALAMUSsecretes: GnRH (Gonadotropin Releasing Hormone)

ANTERIOR PITUITARYsecretes: gonadotropic hormones (FSH & LH)

GONADSSecrete: sex steroids

OVARIES Secrete: estradiol (some testosterone)

TESTES Secrete: testosterone (some estradiol)

hips widen, breast develop, and other changes

facial hair, voice drops, and other changes

Ingestive Behavior

I. Physiological Regulatory Mechanisms

II. Drinking and Thirst

III. Eating and Metabolism

IV. Signals that Start a Meal

V. Signals that Stop a Meal

VI. Brain Areas Involved in Eating

Learning & Memory

I. Nature of Learning

II. Learning and Synaptic Plasticity

III. Perceptual Learning

IV. Stimulus-Response Learning

V. Relational Learning

Definitions of Learning

• Psych 100:– A relatively long lasting change in behavior or

potential behavior that is due to experience.

• This Class:– The process by which experience changes

our nervous system and ultimately our behavior.

The Hebb Rule

• A synapse will be strengthened (more easily activated and/or produce larger depolarizations) if…

1. a synapse is repeatedly active when…

2. the post-synaptic neuron is firing.

Long-Term Potentiation (LTP)

• Defined: A long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high-frequency activation of that input.

• Though found to occur in numerous brain areas, LTP was initially demonstrated in the hippocampal formation

• Useful information: The entorhinal cortex is the gateway to the hippocampus

A

B C

A

B C

A

B C

A

B D

A B

C

Object-Memory Task(inferior temporal lobe

more active)

Spatial-Memory Task(parietal lobe more

active)

Target

Opiates

• Examples: morphine, heroin, codeine, methadone

• Effect (site of action)– Analgesia (periaquaductal gray matter)– Hypothermia (preoptic area)– Sedation (reticular formation)– Reinforcement (mesolimbic system and

nucleus accumbens)

Addictive Behaviors and Classical Conditioning

Drug (UCS) Compensatory response (UCR)

Drug paraphernalia Compensatory & environment (CS) response (CR)

Many fatal drug overdoses occur when the person uses in a non-familiar environment. Why?

Alcohol & the NMDA Receptor

• Alcohol is an indirect antagonist of the NMDA receptor

• Alcohol impairs LTP

• Other NMDA antagonist drugs…– produce sedative effects– produce anxiety reducing effects– stimulate the release of DA in the nucleus

accumbens

Alcohol & the GABAA Receptor

• Indirect agonist for the GABAA receptor• With alcohol, more inhibitory potentials are

created and thus more neurons are hyperpolarized

• Drug Ro-15-4513 blocks this binding site for alcohol on the GABAA receptor

• Impairment of GABAA receptors in the cerebellum disrupts balance and coordination

Integrating Schizophrenia Theories

• PFC is underactive (hypofrontality), perhaps because of abnormal brain development, negative symptoms produced

• PFC fails to excite DA neurons in the midbrain• Underactive DA neurons in the midbrain create

further underactity in the PFC; more negative symptoms are produced

• PFC fails to inhibit the release of dopamine in the nucleus accumbens, making this area overactive; positive symptoms are produced