Week 3 Flashcards
describe the structure of a chemical synapse. What is on either side of the synapse, how big is a synapse, what maintains the distance
The presynaptic cell ends with terminal boutons then there is a space between this and the postsynaptic cell. The space between is called the synaptic cleft and is very narrow (10 nm) so that neurotransmitter molecules are released very close to receptors. The physical association of the pre and postsynaptic cells is maintained by Cell Adhesion Molecules (CAMs) which are proteins that project from the cell membranes and bond in the cleft.
Describe the release of a neurotransmitter. What triggers release, how are they released
Release is triggered by action potentials that stimulate the entry of Ca2+ into the axon terminal through voltage gated Ca2+ channels. The neurotransmitters are contained in membrane bound synaptic vesicles which exocytize (exocytosis idk what word I want there) at the membrane, releasing the contents as the membranes fuse
What are the steps in the process of a synaptic vesicle fusing with the plasma membrane
- Docking happens before an action potential arrives:
SNARE proteins include one in the vesicle membrane (synaptobrevin-2) and two anchored in the plasma membrane (syntaxin and SNAP-25). They form a SNARE complex and bridge the two structures - Action potential arrives and Ca2+ enters the cytoplasm. A sensor protein called synaptotagmin (located on the synaptic vessicle) interacts with the SNARE complex and leads to fusion
What is another name for a neurotransmitter as it binds a receptor?
Ligand. A ligand is a small molecule that binds to and forms a complex with a larger protein molecule.
What type of receptor is associated with neurotransmitters?
Chemically regulated or ligand regulated (gated ion channels) which open in response to the binding of a ligand, in this case the neurotransmitter
Compare voltage and chemically regulated ion channels
Voltage: found primarily in the axons. open in response to depolarization
Chemical: found in the postsynaptic membrane. open in response to the binding of a postsynaptic receptor protein to its neurotransmitter ligand
Explain the types of potentials produced by chemically regulated ion channels
Opening of chemically regulated channels produces a graded potential. There are two types of graded potentials, either a depolarization or a hyperpolarization
Excitatory Postsynaptic potential (ESPS): depolarization event moves membrane potential toward the threshold required for an action potential (e.g. influx of Na+ or Ca2+)
Inhibitory Postsynaptic potential (ISPS): hyperpolarization event moves membrane potential farther away from the threshold for an action potential (e.g. influx of Cl-)
How are synaptic potentials (graded potentials) conducted to the axon? What does this indicate about signal strength?
EPSPs and IPSPs are produced at the dendrites and must propagate to the initial segment of the axon to influence acton potential production. They are conducted by cable properties only! This means that they decrease in amplitude as they move along dendrites to the cell body and axon.
describe the features of the axon initial segment
it is unmyelinated and has a high concentration of Na+ and K+ channels. This is the region where the action potential is first produced and serves as the site of synaptic integration (summation of IPSPs and EPSPs)
*Types of cholinergic receptors
Nicotinic ACh receptors: ALWAYS EXCITATORY. located on skeletal muscles, autonomic ganglia, and specific brain regions. stimulates muscle contraction. named because nicotine is an agonist as well for this receptor
Muscarinic ACh receptors: Can be excitatory or inhibitory because they are G protein coupled. Located on smooth muscle cells, cardiac muscle cells, brain, and particular glands. Required for cardiovascular system and digestive system. Named because muscarine (drug from shrooms) is an agonist
What are drugs called that activate receptor proteins? Examples? Drugs that inactivate and examples?
Agonists. Muscarine is an agonist of the muscarinic receptors. Nicotine is an agonist of the nicotinic receptors
Antagonists. Atropine is an antagonist of muscarinic receptors. Curare and a-bungarotoxin (krait snake venom) are antagonists of nicotinic receptors
What are ligand gated channels? (not the same thing as ligand regulated!) Give an example
Ligand gated channels are when the receptor protein is also an ion channel that opens and closes in response to the ligand binding. The one protein has two functions as a receptor and a channel.
Nicotinic ACh receptors are ligand gated channels. It binds 2 ACh and opens to permit simultaneous diffusion of Na+ and K+ into and out of the cell. The flow of Na+ is the dominant effect because of its steeper gradient. This produces a depolarization and an Excitatory Postsynaptic potential.
Compare action potentials and Excitatory Postsynaptic potentials
Action potentials: occur in the axons where voltage gated channels are located. Have a threshold requirement to produce the potential. Potential does not summate, has a refractory period, and is all-or-none.
EPSPs: occur in postsynaptic membrane of dendrites and cell body. They have no threshold and are graded in magnitude (more impulses = greater depolarization) and have no refractory period so are capable of summation (depolarizations of several different EPSPs can be added together)
What other type of chemically regulated channel exists besides ligand gated? Give an example of this type of receptor
G protein coupled channels. These consist of different, separate membrane proteins. Neurotransmitters indirectly opens ion channels via a G protein signal
The Muscarine ACh receptors are an example. The receptor is a single subunit which binds one ACh molecule and activates a G-protein complex. The alpha separates from beta-gamma and they migrate through the membrane and interact differently depending on the specific case and may open or close channels.
How does ACh effect the heart
ACh interacts with Muscarinic receptors which activate G-protein to dissociate. Beta-gamma binds K+ channels in heart muscle cells, cause to open = K+ leaves cell = hyperpolarized = IPSP. Vagus nerve (a parasympathetic nerve) does this when synapsing with pacemaker cells, slowing heart beat!
How does ACh effect the smooth muscle of the stomach
ACh binds muscarinic receptors and causes G-protein to activate and dissociate. Alpha subunits bind K+ channels and causes them to close. outward diffusion of K+ is reduced = depolarized = EPSP = contractions of the stomach
What removes acetylcholine from the synapse and how?
ACh and receptor dissociate quickly but will reform quickly if free ACh is present. In order to stop activity, the free ACh is inactivated by Acetylcholinesterase which is present on the postsynaptic membrane. AchE hydrolyzes the acetylcholine into acetate and choline which can then reenter the presynaptic cell and resynghesize ACh
How does Acetylcholine affect the skeletal muscle cells
The synapses (neuromuscular junctions) are at the postsynaptic membrane of the muscle fiber, known as the muscle end plate. So EPSPs are called end-plate potentials here. Only nicotinic receptors are located in muscle cells so all potentials are excitatory. Voltage gated channels open in response to the depolarization produced by ACh and the action potentials are reproduced along voltage gated channels down the sarcolemma (muscle membrane). This is analogous to axon action potential conduction. The result is muscle contraction
What is a drug that competes with ACh for attachment to the nicotinic receptors and what is the effect of the drug?
Curare is an antagonist for nicotinic ACh receptors and so reduces the size of the end-plate potentials in the muscles. Produces flaccid paralysis and death because diaphragm stops working. Used as a muscle relaxant in surgery and in electroconvulsive shock therapy to prevent muscle damage. Can also be used to counteract the effects of tetanus which contracts the muscles.
Explain the effect of ACh on the two classes of autonomic motor neurons
Sympathetic: ????
Parasympathetic: most of these neurons innervate the effector organs via ACh as their neurotransmitter. In some cases there is an inhibitory effect through binding of ACh to muscarinic receptors (such as the vagus nerve slowing heart beat). Other cases ACh can be excitatory like via nicotinic receptors.
What is the normal stimuli for the production of action potentials?
Excitatory postsynaptic potentials conducted from the dendrites and cell body.
The dendrites and cell body serve as the receptive area where receptor proteins for neurotransmitters and ligand gated channels are located. Graded, local EPSPs and IPSPs spread into the initial segment of the axon located by the axon hillock. If the EPSP depolarization is at or above threshold at the initial segment, an action potential will occur. A stronger EPSP will determine the frequency at which action potentials are produced. The action potential travels down the axon without loss of amplitude and ends at the terminal boutons of the axon where neurotransmitter is released.
Define monoamines and give some examples and what they are derived from
Monoamines are regulatory molecules derived from amino acids.
Dopamine, norepinephrine (noradrenaline), epinephrine (adrenalin) are derived from tyrosine and are a subfamily of monoamines called catecholamines.
Serotonin is derived from tryptophan
Histamine is derived from histidine
*What monoamine related medication is associated with drowsiness and why?
Histamine promotes wakefulness and alertness, so antihistamines for allergies can promote drowsiness
Where is norepinephrine and epinephrine secreted from? What family of monoamines are these neurotransmitters part of?
Secreted from the adrenal medulla
Part of the catecholamines
How is the action of monoamines at the synapse stopped?
- Reuptake of the neurotransmitter from the synaptic cleft into the presynaptic terminal.
- Degredation of the monoamine by an enzyme in the terminal bouton called Monoamine Oxidase (MAO)
These two mechanisms are good targets if you want to inhibit monoamine breakdown and prolong a signal!
How do monoamines open ion channels in the postsynaptic membrane? Give an example pathway
Indirectly through second messengers, specifically cAMP for the catecholamines.
Example:
Norepinephrine binds its receptor and stimulates dissociation of the G-protein alpha subunit. It diffuses through the membrane and binds adenylate cyclase. This enzyme converts ATP to cAMP and pyrophosphate within the postsynaptic cell. cAMP then activates protein kinase which phosphorylates other proteins and opens ion channels.
What neurotransmitter is found in Raphe nuclei along the midline of the brain stem? What is it made from and what functions does it have?
Serotonin or 5-hydroxytryptamine (5-HT). It is derived from the amino acid L-tryptophan, which can be increased/decreased through diet (milk and turkey are high in tryptophan). Physiological functions of Serotonin include regulation of mood and behavior, appetite, and cerebral circulation.
What drugs interact with 5-hydroxytryptamine signaling?
Serotonin receptors are activated by LSD, mescaline, and psilocybin (hallucinogens).
Antidepressants such as Prozac, Paxil, Zoloft, and Luvox act as serotonin-specific reuptake inhibitors (or selective serotonin reuptake inhibitors) and reduce the production of serotonin transporter (SERT) proteins thereby reducing the ability of these proteins to clear serotonin from the synaptic cleft. This increases the ability of serotonin to stimulate its receptors.
Serotonin has a wide range of effects (over a dozen known receptor types) so there are many drugs which have many results
What is the term for neurons which respond to dopamine and how can we detect them?
Dopaminergic neurons can be identified in the living brain by a Positron Emission Tomography (PET). This has revealed a high concentration in the midbrain.
*What are the two systems of dopaminergic neurons?
Nigrostriatal Dopamine System: involved in motor control
Mesolimbic Dopamine System: involved in emotional reward
Describe the location of the Nigrostriatal dopamine system
Cell bodies are located in part of the midbrain called the substantia nigra. Neurons in the substantia nigra send fibers to a group of nuclei known collectively as the corpus striatum (because of their striped appearance), hence the term Nigro-Striatal.
These systems are part of the basal nuclei - large masses of neuron cell bodies deep in the cerebrum involved in initiation of skeletal movements
*What disease is associated with the nigrostriatal dopamine system
Parkinsons Disease is caused by a degeneration of the dopaminergic neurons in the substantia nigra. It is associated with muscle tremors, rigidity, difficulty initiating movements and speech, and severe motor problems.
Treatments often include L-dopa and monoamine oxidase inhibitors in an attempt to increase dopaminergic transmission in the nigrostriatal system.
What condition is associated with the Mesolimbic dopamine system?*
Addiction. The mesolimbic system is primarily involved in behavior and reward. Addictive drugs such as cocaine, morphine, nicotine, and amphetamines are known to activate dopaminergic pathways (D2 receptor). The pathway is primarily neurons that arise in the midbrain and terminate in the nucleus accumbens (considered the CENTER for addiction!)
What are some drugs developed to treat schizophrenia and their effects?
Early drugs were antagonists of the D2 dopamine receptor and so caused side effects similar to Parkinsons disease. (this also explains why people with Parkinson’s disease might develop schizophrenia symptoms if treated with too much L-dopa)
Newer drugs called Atypical Antipsychotic Drugs target many receptors including norepinephrine, serotonin, and histamine. Their efficacy suggests other monoamine neurotransmitters also contribute to schizophrenia.
Describe norepinephrine’s effect in the PNS and CNS
PNS: sympathetic neurons use norepinephrine at synapses with smooth muscle, cardiac muscle, and glands
CNS: neurons involved in behavioral arousal use norepinephrine. This helps explain the mental arousal elicited by amphetamines, which stimulate norepinephrine pathways. Drugs that increase norepinephrine stimulation of CNS (tricyclic antidepressants) are used to treat clinical depression, but also cause PNS pathways that raise blood pressure so be careful with them!
What are the excitatory neurotransmitters in the CNS
Glutamate (glutamic acid) and Apartic acid. Glutamate is the major excitatory neurotransmitter in the brain, producing EPSPs in at least 80% of the cerebral cortex synapses. The maintenance of the gradient to produce the EPSPs is the major energy requirement of the brain
How do glutamate receptors work?
Each glutamate receptor encloses an ion channel similar to ACh nicotinic receptors. One subtype of glutamate receptor is the NMDA receptors which allow for the entry of Ca2+ (and movement of other ions) when activated. These are involved in *memory storage
What are the inhibitory neurotransmitters of the CNS and what common mechanism do they share?
Gamma-Aminobutyric Acid (GABA) and Glycine. Both receptors are ligand-gated ion channels that open when the neurotransmitter binds to allow Cl- to diffuse into the cell and hyper polarize the postsynaptic membrane (IPSP). This is true as long as the Cl- gradient is higher outside the cell and the membrane potential is less negative than the Cl- potential (I don’t think that is super important…). However, when an EPSP partially depolarizes the membrane, this promotes Cl- moving inside the cell and so hyper polarizes it, making the excitatory impulse less effective
What is the unique role of Glycine in the spinal cord? What drug inhibits this effect?
Glycine is particularly important in the spinal control of skeletal movements. Flexion of an arm, for example, involves the stimulation of the flexor muscles by motor neurons in the spinal cord, BUT the motor neurons that innervate the antagonists extensor muscles are inhibited by IPSPs produced by glycine. Basically, glycine inhibits the muscle that would prevent another muscle from contracting (inhibits tricep as you flex bicep).
Strychnine is a poison that cause spastic paralysis by specifically blocking the glycine receptor proteins. Death caused by asphyxiation because diaphragm cannot relax
What is the role of Gamma-Aminobutyric Acid in the CNS? What is the result of deficiency of GABA release?
GABA is the most prevalent neurotransmitter in the brain. It is inhibitory and hyper polarizes the postsynaptic membrane by opening Cl- channels. For example, large neurons called the Purkinje cells mediate the motor functions of the cerebellum by producing IPSPs in their postsynsaptic neurons.
A deficiency of GABA-releasing neurons is responsible for uncontrolled movements in people with Huntington’s Disease (caused by defect in huntingtin gene)
Drug that affects GABA neurotransmitter
Propofol is drug that potentates GABA receptor activity and can lead to cardiac arrhythmia, hypotension, and suppression of respiratory activity. Potentiation of the receptor activity = higher Cl- inside cell = IPSP = less responsive to stimulus
What are two polypeptide neurotransmitters? (neuropeptides)
Cholecystokinin: secreted as a hormone from the small intestine but also released from neurons and used as a neurotransmitter in the brain. Promotes feelings of satiety after eating
Substance P: polypeptide found in many organs, functions in the brain to mediate sensations of pain. Some people have more or less substance P and so have different pain thresholds.
Define divergence and convergence
Divergence: one neuron makes synapses with a number of other neurons
Convergence: A number of axons synapse on a single neuron
2 ways that synaptic signals are summated
- Spatial summation: occurs due to convergence of terminal boutons from different presynaptic axons on the dendrites/cell body of postsynaptic neuron. Short version: 2 different synapses fire at the same time and so summate and produce a larger signal
- Temporal summation: rapid bursts of activity of a single presynaptic axon cause corresponding bursts of neurotransmitter release resulting in successive waves of EPSPs/IPSPs that summate
Both are important for determining the strength of the depolarization stimulus at the initial segment of the axon and thereby the frequency of action potential production.
Two types of synaptic inhibition
- Postsynaptic inhibition: occurs via neurotransmitters that hyper polarize the membrane (like GABA or glycine) and thus inhibit depolarization from occurring.
- Presynaptic inhibition: the amount of an excitatory neurotransmitter released at the end of an axon is decreased by the effects of a second neuron whose axon makes a synapse with the axon of the first neuron. Neurotransmitter exerting this inhibition may be GABA or it could be an excitatory one like ACh or glutamate which produce depolarization of the terminal boutons, inactivating Ca2+ channels and inhibiting neurotransmitter release
How do opiates work?
Opiates reduce pain (promote analgesia) by presynaptic inhibition. They reduce Ca2+ flow into axon terminals containing Substance P and inhibit the release of the neurotransmitter involved in pain transmission
Describe the development of the CNS from an embryonic stage
Early embryo contains a surface tissue layer called the ectoderm. Then, a groove appears in the ectoderm along the dorsal midline of the embryo’s body. The groove depends and by day 20 fuses to form the neural tube (later to be the CNS). The part of the ectoderm where fusion ossuary becomes the neural crest (later to be the PNS). By the middle of the 4th week after conception, three shillings are evident on the anterior end of the neural tube:
forebrain or prosencephalon
midbrain or mesencephalon
hindbrain or rhombencephalon
During week 5 these areas become modified to the five regions, named the same as in the adult brain (other card for that info)
*What are the five regions of the brain? (formed at week 5 of development continuing to adulthood)
from the forebrain: Telencephalon (cerebrum) and diencephalon (thalamus and hypothalamus)
from the midbrain: mesencephalon
from the hindbrain: metencephalon (Pons, cerebellum) and myelencephalon (medulla oblongata)
what does the telencephalon grow to become?
The telencephalon grows disproportionately in humans to form the two enormous cerebral hemispheres (cerebrum) that cover the diencephalon, midbrain, and part of the hindbrain.
The CNS begins development as a hollow neural tube, what does this hollow space become?
The CNSS remains hollow as the brain is formed. The cavities of the brain are known as ventricles and become filled with cerebrospinal fluid. The cavity of the spinal cord is called the central canal and is also filled with cerebrospinal fluid.
How is cerebrospinal fluid formed? How does it exit the CNS?
By structures called choroid plexuses found in all 4 ventricles. Tight junctions between epithelial cells of choroid plexuses contribute to blood-brain barrier, thus the epithelium forms the CSF by secretion rather than filtration where transport of secreted ions into the CSF is followed by the movement of water. CSF flows from first to fourth ventricle then to the central canal of spinal cord and the subarachnoid space (surrounds spinal cord).
It then exits through openings in the Pia mater covering the brain to the subarachnoid space (between the Pia mater and arachnoid mater) then is secreted by arachnoid villi and granulations into the blood filled sinuses of the outermost dura mater, then it’s finally reabsorbed by blood
Where are white and grey matter found? define what makes them white or grey
Gray matter: contains neuron cell bodies and dendrites, found in the cerebral cortex (surface layer) of the brain and in deeper aggregations called nuclei
White matter: contains axon tracts (myelin sheaths are white) that underlie the cortex in a region called cerebral medulla that surround nuclei.
*Where does neurogenesis occur in adults?
Subventricular zone: thin layer of cells adjacent to the ependymal cells that line the lateral ventricles. In non-human mammals, these new neurons migrate to olfactory bulbs and are involved in smell. In humans, new interneurons migrate to the striatum and help with regulation of motor control and cognitive functions
Subgranular zone of hippocampus: results in interneurons that function within the hippocampus to aid learning and memory
what are the three major constituents of the Cerebrum
the right and left hemispheres and the corpus collosum
*Names for the folds and grooves of the cerebral cortex
Generally called convolutions, the elevated folds are a gyrus (gyri) and the depressed groove is a sulcus (sucli)
*Describe the frontal lobe functions
- voluntary motor control of skeletal muscles
- personality
- higher intellectual processes (concentration, planning, decision making)
- verbal communication
*Parietal lobe functions and two important structures within the parietal
- somatesthetic interpretation (muscular sensations)
- understanding speech and formulating words to express throughs and emotions
- interpretation of textures and shapes
Precentral gyrus: the motor cortex consisting of interneurons called upper motor neurons that regulate muscles
Postcentral gyrus: somatosensory cortex area responsible for perception of sensations arising from cutaneous, muscle, tendon, or joint receptors
What features take up the largest regions of the sensory and motor cortexes?
Body regions with the highest densities of receptors are the largest in the sensory cortex and regions with the greatest number of motor innervations are the largest areas of motor cortex. The hands and face are served by larger areas than the rest of the body
*functions of the temporal lobe
- interpretation of auditory sensations
2. storage (memory) of auditory and visual experiences
*functions of occipital lobe
- integration of movements in focusing the eye
- correlation of visual images with previous visual experiences and other sensory stimuli
- conscious perception of vision
*functions of insula
- encoding of memory
- integration of sensory information (principally pain) with visceral responses
- believed to be important in the assessing of bodily states that accompany emotions
When do mirror neurons activate?
Mirror neurons in the premotor areas of the frontal lobes become active when a person performs a goal directed action or sees another individual perform the same action. Mirror neurons in the somatosensory cortex of parietal lobe respond when a person is touched in a body location or sees another person touched in the same location.
They also have connections to the insulation and cingulate gyrus which can provide an emotional component to vicarious experience
What disorder may be related to mirror neuron function
Autism spectrum disorder involves impairments in social interactions, language ability, sensitivity to stimuli, and the ability to understand the feelings of others. So it is thought that autism may at least partly involve impairment of mirror neuron function
How do we clinically diagnose epilepsy (and other abnormal brain states, including brain death)
Through an Electroencephalogram (EEG) which measures the potential produced by axon firing through electrodes placed on the scalp
types of normal electroencephalogram waves, what part of the brain they come from, and when they are seen
Alpha (parietal and occipital): when person is awake and relaxed with eyes closed
Beta (frontal, esp precentral gyrus): produced by visual stimuli and mental activity
Theta (temporal and occipital): common in newborn infants and sleeping adults. Increase in awake adults during tasks that require attention and memory, during sleep deprivation, and during severe emotional distress
Delta (cerebral cortex): common during sleep and awake infant. In an awake adult indicates brain damage
What triggers puberty in humans?
Increased secretion of Luteinizing Hormone. LH is high for first 6 months of life but then declines to very low levels until puberty. The increased pulsatile LH secretion (both frequency and amplitude increase) is caused by changes in the hypothalamus that allow an increased secretion of GnRH which stimulates LH secretion.
Human increased secretion of GnRH is independent of gonadal hormones. Prior to puberty, GnRH secretion is inhibited by GABA. Kisspeptins (neurotransmitters) also stimulate GnRH release from hypothalamus
What triggers puberty in animals (like rats and sheep)
Triggered by increased secretion of Luteinizing hormone. Prior to puberty, LH secretion is low due to high sensitivity of the hypothalamus to the negative feedback effects of gonaldal hormones. A decrease in the sensitivity of the hypothalamus to these effects then increases GnRH secretion and LH secretion
Not the same case for primates (humans)!
What is produced as a result of the increased LH secretion at puberty?
The gonads secrete increased sex steroid hormones (testosterone and estradiol-17B, the major estrogen). These then cause secondary sex characteristics to develop
Estradiol:
Epiphyseal growth plates of bones, causing growth spurt (first sign in females)
Breast development
Menarche = first menstrual flow
Testosterone: Growth of penis and testes Spemarche = first release of sperm Epiphyseal growth plates of bones, causing growth spurt (later age than girls) Gain muscle mass
How is the pubertal growth spurt triggered? males vs females
By stimulatory effects of the rising secretion of gonadal steroid hormones on the secretion of growth hormone from the pituitary, and by effects of gonadal hormones on osteoclasts/osteblast activity. Estrogen and androgens both stimulate increased bone mass at puberty, but the extent varies. Testosterone directly stimulates addition of new bone under periosteum, resulting in thickening of bones. This accounts for larger, thicker bones in males compared to females and higher bone density as men age, making women more prone to osteoporosis
How is pubertal growth of hair triggered in boys vs girls
In both it is stimulated by increased secretion of androgens from the adrenal cortex (in the kidneys). Maturation of the pituitary-adrenal axis is separate from the pubertal changes in the pituitary-gonad axis
What is required to start the onset of menstruation?
A minimum amount of body fat for the secretion of leptin from white adipose tissue. Leptin secretion promotes onset of puberty by stimulating GnRH production by hypothalamic neurons and LH secretion from the anterior pituitary.
The age at which puberty begins is related to the amount of body fat and level of physical activity because this impacts Leptin secretion. Average age of menarche is later in very active girls and earlier in obese girls
Factors that can cause amenorrhea
Amenorrhea is the cessation of menstruation. Women who are very lean and physically active may have irregular cycles and amenorrhea, this is also related to percent body fat. There is also evidence that physical exercise may independently evoke a stress-induced inhibition of GnRH and gonadotropin secretion. Amenorrhea can also occur in response to psychological and emotional stress
What is the role of the pineal gland in humans?
Pineal gland is located deep within the brain and secretes melatonin which is influenced by light-dark cycles. Some vertebrates (not mammals/humans) have pineal photoreceptors directly sensitive to light. The inhibitory effect of light on melatonin secretion in mammals is indirect. Pineal secretion is stimulated by postganglionic sympathetic neurons that originate in the superior cervical ganglion. Activity of these neurons is inhibited by nerve tracts that are activated by light striking the retina.
There is evidence that melatonin can influence the pituitary-gonad axis in seasonally breeding mammals, but the role of melatonin in regulation of human reproduction has not been clearly established
Describe the stages of the human sexual response
- Excitation/arousal: characterized by myotonia (increased muscle tone), and vasocongestin (engorgement of sexual organ with blood). Results in erection of nipples (caused by smooth muscle contractions), clitoris swells, labia minora swells, erection of penis, secretion of vaginal fluid and vaginal lubrication, enlargement of uterus, and breast enlargement
- Plateau: clitoris is partially hidden behind labia minora and nipples partially hidden by areolae swellings. Engorgement of outer third of vagina produces “orgasmic platform”
- Orgasm: uterus and orgasmic platform of the vagina contract several times, analogous to the contractions that accompany ejaculation in a male. only lasts a few seconds
- Resolution: body returns to preexcitation conditions. Men enter refractory period where they may produce erection but cannot ejaculate. Women lack a refractory period.
Neurotransmitters that promote sleep and wakefulness
Histamine promotes wakefulness
Adenosine and GABA promote sleep
Two categories of sleep and what waves are associated
Rapid Eye Movement sleep: dreams occur, eyes move, EEG consists of theta waves
non-REM or resting sleep: four stages based on EEG waves, 3 and 4 are called slow wave sleep because of the delta waves
Describe the stages of a typical night of sleep
First fall asleep and enter non-REM sleep of four different stages, then ascend back through these stages to REM sleep. Do this descent and ascent again about 5 90-minute cycles a night. During the first half of the night, a great deal of time is spent in slow-wave sleep. During the second half, mostly REM sleep. People naturally wake up from REM sleep.
Describe the brain’s metabolism through the stages of sleep
Neurons decrease firing rate as transition from waking to non-REM sleep, metabolism and blood flow also decrease. During REM sleep, there is a higher total brain metabolism and a higher blood flow than in the waking state. The limbic system is also active during REM sleep (amygdala involved in emotions - fear/anxiety common in dreams, makes sense to be active)
What effect does sleep have on memory and learning
Non-REM sleep aids the neural plasticity required for learning. The consolidation oof short-term memory into long term memory is promoted by sleep as well. Slow-wave sleep benefits consolidation of spatial and declarative memories (can be verbalized). REM sleep benefits consolidation of nondeclarative memories. But, both stages of sleep may participate in consolidation of either type of memory
Longer durations of sleep are required for maximum benefit of memory consolidation. It is also important to have a delay between learning and sleep of about 3 hours
What effect does sleep have on memory and learning
Non-REM sleep aids the neural plasticity required for learning. The consolidation oof short-term memory into long term memory is promoted by sleep as well. Slow-wave sleep benefits consolidation of spatial and declarative memories (can be verbalized). REM sleep benefits consolidation of nondeclarative memories. But, both stages of sleep may participate in consolidation of either type of memory
What are basal nuclei? Name the important components of this system
Basal Nuclei or Basal Ganglia: masses of gray matter (neuron cell bodies) located deep within the white matter of the cerebrum
Corpus Striatum: most prominent of the basal nuclei consisting of the Caudate Nucleus and Lentiform Nucleus (lateral portion = Putamen, medial portion = Globus Pallidus)
Subthalamic nucleus of the diencephalon
Substantia Nigra of the midbrain
Describe the motor circuit
The areas of the cerebral cortex that control voluntary movements (pre central motor cortex) send axons to the basal nuclei, primarily the putamen. These axons release glutamate which excites the putamen neurons. Those neurons release GABA to other basal nuclei and inhibit them. The globus pallidus and substantia nigra send GABA inhibitory signals to the thalamus. The thalamus sends excitatory axons to the motor areas of the cerebral cortex.
Motor circuit allows intended movements to occur while inhibiting unintended movements.
Explain cerebral lateralization (function in one hemisphere vs the other)
Each cerebral cortex controls movements of the contralateral (opposite) side of the body and somatesthetic sensation from each side of the body projects to the contralateral post central gyrus as a result of decussation (crossing over) of fibers. However, each hemisphere receives information from both sides of the body because the two hemispheres communicate with each other via the corpus callosum.
What is a split brain procedure?
When the corpus callosum is surgically cut to isolate each hemisphere and alleviate epilepsy symptoms. There is surprisingly no evidence of disability
What is aphasia? Describe two important types of aphasia
Aphasias: speech and language disorders caused by damage to the brain through head injury or stroke. Language areas of the brain are primarily located in the LEFT hemisphere
Broca’s aphasia (non-fluent): people are reluctant to speak and when they try, speech is slow and poorly articulated. Comprehension is unimpaired. Motor neurons for right arm and right side of face are nearby and weakness of these muscles is a common symptom. Note that this is not due to simply a motor control problem, musculature control is unaffected.
Wernicke’s aphasia (fluent): people speak rapidly and fluidly but without meaning, speech is a “word salad” that may be real words chaotically mixed together or made-up words. Comprehension is destroyed.
Where is Broca’s area? What is it’s function?
Left inferior frontal gyrus
This is the motor speech area in charge of controlling the muscles to produce speech and the ability to formulate words/sentences.
Where is Wernicke’s Area? What is it’s function?
Superior temporal gyrus of the left hemisphere
The concept of words originates in Wernickes area. In order to understand words that are read, information from the visual cortex must project to Wernicke’s area. To understand spoken words, the auditory cortex must send info to Wernicke’s.
What parts of the brain are important in the basis of emotional states?
Hypothalamus (diencephalon) and limbic system (forebrain nuclei around the brain stem)
The limbic system includes the cingulate gyrus, amygdaloid body, hippocampus, and septal nuclei. The amygdaloid body is a particularly important center of emotional learning, particularly fear conditioning.
What feelings and behaviors are involved in the hypothalamus and limbic system?
Aggression: amygdaloid body and hypothalamus produce rage/aggression
Fear: amygdaloid body and hypothalamus. If damaged or removed, subject shows no fear in response to terrifying stimuli and doesn’t recognize facial expressions of fear/anger
Feeding: hypothalamus contains a feeding and satiety center
Sex: hypothalamus and limbic system are involved in regulating sexual drive/behavior. However, cerebral cortex is also critically important for sex drive in lower animals and cerebrum is more important in humans
Goal-directed behavior: electrodes stimulating sites between frontal cortex and hypothalamus cause reward feelings. In slightly different position, punishment.
What features are characteristic of Alzheimer’s disease
Alzheimers is associated with a loss of brain weight/volume and decreased cortical thickness correlated with cognitive decline. Specific neuronal populations (hippocampus and cerebral cortex) have loss of function. There is an accumulation of extracellular protein (called amyloid beta) that forms deposits called amyloid senile plaques. There is also an accumulation of intracellular proteins called tau that form neurofibrillary tangles
how does emotion influence memory
It can strengthen or hinder memory formation. The amygdaloid body is involved in the improvement of memory with an emotional content. However, stress can impair memory consolidation by the hippocampus and the cognitive functions and working memory performed by the prefrontal cortex. Stress can promote storage of emotionally strong memories, but hinder the retrieval of those memories and working memory
What brain result is often seen with Post traumatic stress disorder
Atrophy of the hippocampus. There is increased secretion of “stress hormones” (primarily cortisol from adrenal cortex) and the hippocampus and amygdaloid body are rich in receptors for these hormones.
What is the function of the prefrontal cortex? Describe two important areas
Prefrontal cortex is involved in higher cognitive functions like memory, planning, judgement, motivation, interpersonal skill, and social behavior.
Orbitofrontal area: ability to consciously experience pleasure and reward. Receives all sensory inputs and connects with many limbic system regions. These are notably important for the emotional reward of goal-directed behavior. Injury causes severe impulsive behavior, verging on sociopathic (Phineas Gage)
Lateral prefrontal area: motivation and sexual desire. Injury lowers those feelings and causes cognitive function deficits.
Cause, symptoms, and treatment of myasthenia gravis
autoimmune disease caused by antibodies that block the nicotinic ACh receptors, particularly in the motor end plates of skeletal muscle cells. This produces muscle weakness, especially in the eyes, eyelids, and face. Neostigmine, which blocks the AChE in the synaptic cleft, can help treat symptoms.
What are 2 toxins produced in fish and what do they do?
Saxitoxin: a poison produced by dinoflagellates (Red Tide algae) in the ocean that becomes concentrated in filter-feeding clams and mussels. binds to voltage-gated Na+ channels in axons, blocking action potentials, producing paralytic shellfish poisoning. can be fatal if paralysis of the diaphragm causes suffocation.
Tetrodotoxin: a poison produced by pufferfish, bind to voltage-gated Na+ channels in axons, blocking action potentials, producing paralytic shellfish poisoning. can be fatal if paralysis of the diaphragm causes suffocation.
What are cholinesterase inhibitors?
Cholinesterase inhibitors are drugs that block the action of acetylcholinesterase (AChE), thereby increasing the amount of ACh in the synaptic cleft and enhancing cholinergic synaptic transmission. Neostigmine, physostigmine, pyridostigmine, and others are used to treat myasthenia gravis, and are important in the treatment of Alzheimer’s disease. However, nerve gas and organophosphate pesticides can kill their intended victims by inhibiting AChE and overstimulating cholinergic synapses causing rigid paralysis and suffocation if diaphragm is paralyzed.
How do MAO inhibitors work and what do they treat? What potential complication can arise from the diet?
Monoamine oxidase (MAO) inhibitors are drugs that block the degradation of monoamine neurotransmitters, thereby increasing the action of dopamine, serotonin, norepinephrine, and melatonin at synapses. MAO inhibitors treat of depression, panic disorder, anxiety, and others. Also used to treat Parkinson’s disease by enhancing the synaptic effects of dopamine. MAO inhibitors have potentially dangerous interactions with over-the-counter tryptophan and St. John’s wort, as well as with foods such as cheeses, certain beans, pickled and fermented foods, and others that contain the molecule tyramine (a monoamine also degraded by MAO). Interactions could provoke a hypertensive crisis, because the increased norepinephrine (due to less degradation) released by sympathetic axons stimulates vasoconstriction and increased cardiac pumping, dangerously raising blood pressure.
How does cocaine work?
Cocaine elevates energy and mood through the activation of the mesolimbic reward pathway of the brain. Cocaine exerts these effects because it crosses the blood–brain barrier and blocks the reuptake of dopamine. It also blocks the reuptake transporters for norepinephrine and serotonin—it is a triple reuptake inhibitor. In addition to this broad action, cocaine is dangerous because it also blocks membrane Na+ channels. Through all of these actions, cocaine constricts coronary arteries, raises cardiac rate and blood pressure, and promotes heart disease, stroke, seizures, ulcers of the digestive tract, and kidney damage.
What are benzodiazepines and what can they treat?
Benzodiazepines, including Valium and Xanax, were developed to treat anxiety and promote sleep. These drugs bind to a subgroup of GABA receptors, thereby increasing their permeability to Cl− when these receptors also bind to GABA. The increased flow of Cl− into the postsynaptic neuron enhances the inhibitory effect of GABA at their synapses in the brain and spinal cord. Benzodiazepines, acting through inhibitory effects on spinal motor neurons that innervate skeletal muscles, are also widely used to treat the muscle spasms of epilepsy and other causes of seizures.
What does an excess of glutamate in the CNS cause?
An excess of glutamate in the synaptic cleft promotes excitotoxicity. In excitotoxicity, excessive amounts of glutamate cause excessive entry of Ca2+ into neurons, which leads to the activation of digestive protease enzymes and the release of reactive oxygen species from mitochondria. These trigger a cascade of events that result in the apoptotic cell death of the neurons.
Excitotoxicity is responsible for neuron death in ischemic strokes (due to obstructed arteries, which account for 80% of all strokes; the remainder are hemorrhagic strokes due to ruptured blood vessels). This occurs because ischemia impairs glutamate uptake from the synapse. Excitotoxicity is also believed to contribute significantly to neuron death in such neurodegenerative disease as Alzheimer’s, Parkinson’s, multiple sclerosis, amyotrophic lateral sclerosis (ALS), and others.
What is the Babinski Reflex and when does it occur?
The Babinski reflex (or the Babinski sign) occurs normally in infants and children under two years old. This reflex involves an upward movement of the big toe and a fanning of the other toes when the sole of the foot is stimulated, due to a reflex contraction of the extensor muscles of the toes. Once the central nervous system has developed more fully, the reflex is inhibited. In adults, the same stimulation usually evokes a downward flexion, or curling, of the toes. A Babinski reflex in an adult can indicate CNS damage due to such conditions as spinal cord injury, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), brain tumors, and others.
What causes Huntington’s disease? What are they symptoms
Huntington’s: caused by a mutation in the HTT gene on chromosome 4 that triggers extensive repeats in the CAG sequence of DNA (codes for the production of glutamine). As the gene is passed through generations, the number of repeats increases, leading to an earlier age of symptom onset. Excess glutamine aggregates in the caudate and putamen, causing death of the neurons, expansion of the lateral ventricles, and a loss of cortical neurons. Since the neurons of the caudate and putamen are primarily GABAnergic, significant loss of inhibitory function occurs, leading to a variety of involuntary movements, or dyskinesia. Chorea, rapid involuntary movements of the limbs, and athetosis, writhing movements of the hands, are common. Acetylcholine levels in the brain are also decreased. In addition to movement problems, there is a gradual decline in mental function and a progressive onset of serious psychiatric conditions.
What causes Parkinson’s disease? what are the symptoms and treatment?
Parkinson’s disease is a disorder of the basal nuclei and its circuits. Its symptoms include dyskinesia, muscle tremor, slow movements, speech impairments, and muscle rigidity. These symptoms are produced by the degeneration of dopaminergic neurons that extend to the caudate nucleus from the substantia nigra. Believed to be caused by an interaction of genetic and environmental factors. An autosomal dominant form of Parkinson’s disease exists, which causes a mutation in the α-synuclein protein which then stick together to form tiny fibrils of Lewy bodies that promote neurodegeneration.
Parkinson’s disease is treated with L-dopa (Levodopa), which enters brain and converts to dopamine, as well as other dopamine agonists and MAO inhibitors. Some Parkinson’s disease patients benefit from deep brain stimulation, where an electrode is implanted into the subthalamic nucleus or globus pallidus.
Describe language recovery after a TIA
A spontaneous full recovery of language ability often occurs within a few days of a transient ischemic attack (TIA), but there is usually only partial recovery over the longer term after a stroke. Recovery is faster in children, possibly because of transfer of language ability from the left to the right hemisphere, but is reduced after adolescence. Recovery is aided by speech therapy and other techniques. Some recovery usually occurs after damage to the motor speech area (Broca), but damage to Wernicke’s area produces more severe and permanent aphasias.
