Neuro Exam 2 Study Guide!

4 families of neurotransmitters

- Amine neurotransmitters

- Amino acid neurotransmitters

- Peptide neurotransmitters

- Gas neurotransmitters

Example of amine neurotransmitters:

Amine: Catecholamines

Dopamine and norepinephrine

Example of amino acid neurotransmitters:

GABA, glutamate

Example of Peptide neurotransmitters:

endorphins, oxytocin, vasopressin

Example of Gas neurotransmitters:

nitric oxide (NO)

What are the 3 effects that ligands can have:

- partial antagonists

- competitive antagonists

- noncompetitive ligand

Partial antagonists

produce a medium response regardless of dose

competitive antagonists

are drugs that bind to the same receptor site as the endogenous neurotransmitter.

noncompetitive antagonists

binds instead to a modulatory site on the receptor. A diff site from where the endogenous NT normally binds. These drugs can be noncompetitive agonists or antagonists

What are the 3 different hormone types:

- Protein hormone

- Amine hormone

- Steroid hormone

Protein hormone examples:

Adrenocorticotropic Hormone (ACTH), Follicle-Stimulating Hormone (FSH), Thyroid-Stimulating Hormone (TSH) & Oxytocin (OT)

Amine hormone examples:

Thyroid, Epinephrine, Norepinephrine (NE), Melatonin (MEL)

Steroid hormone examples:

Estrogen (E), Progesterone (P), Testosterone (T,) Glucocorticoids/Mineralocorticoids

Protein hormone activity:

- act rapidly, bind to specific receptors on the surface, (extra cellular receptors), changes receptor shapes, and intracellular part then activates a second messenger

- Insulin → binds receptor → triggers second messengers → increases glucose uptake

Steroid hormone activity:

- acts slowly, pass through cell membrane and bind to cell receptors inside the cell membrane, the steroid receptor complex binds to DNA and acts as transcription factor, act on different receptors isoforms, steroid receptor cofactors help the cell respond to steroids (SRC-1 and CBP

- Estrogen → enters cell → binds receptor → activates genes → promotes growth of reproductive tissues

Releasing hormones FUNCTION:

- secreted by the hypothalamus to control the pituitary release of tropic hormones.

- Tell the anterior pituitary to release its own hormones.

Releasing hormones SITE OF RELEASE:

hypothalamus

Releasing hormones EXAMPLES:

CRH, TRH, GnRH

Tropic hormones FUNCTION:

Act on endocrine glands in the body to make them release their own hormones

Tropic hormones SITE OF RELEASE:

anterior pituitary gland

Tropic hormones EXAMPLES:

ACTH, TSH, LH, FSH

Oxytocin Function:

reproduction, parenting behavior, uterine contraction, milk letdown

Vasopressin Function:

increases blood pressure, inhibits urine formation

ACTH Function:

controls adrenal cortex and steroid hormone release

TSH Function:

increases thyroid hormone release

FSH Function:

stimulates egg-containing follicles or sperm production. Growth and maturation of eggs.

LH Function:

females (ovulation and progesterone production)

males (testosterone)

Prolactin Function:

Stimulates lactation (milk)

Growth hormone Function:

stimulates growth of bones and tissues

what hormones are released by the adrenal gland

- medulla (epinephrine and norepinephrine)

- cortex (glucocorticoids, cortisol, mineralocorticoids, and sex steroids)

what hormones are released by the thyroid gland

T3, T4 (act like steroid hormones)

What are the 3 gonadal steroids:

testostersone

estrogen

progesterone

Where is testosterone produced?

testes

Where are progesterone and estrogen produced?

ovaries

6 stages of neural development

1.) Neurogenesis

2.) Cell Migration

3.) Differentiation

4.) Synaptogenesis

5.) Neuronal cell death or apoptosis

6.) Synapse rearrangement (pruning)

Neurogenesis:

production of nerve cells

Cell migration:

cells move from the ventricular layer to establish distinct population (completed by the time of birth)

Differentiation:

cells become distinctive neurons or glial cells, allows a cell to acquire its specific appearance and function

Synaptogenesis:

- establishment of synaptic connections (growth cones, filopodia and lamellipodia)

- Neurons extend axons and dendrites to make neural connections

Neuronal cell death or apoptosis:

- Caused by death genes

- Death genes are only expressed only during apoptosis.

- Caspases

Caspases:

are a family of proteases that cut up proteins and DNA.

Synapse rearrangement (pruning):

- loss or development of synapses, fine-tuning

- Influenced on synaptic survival:

- Neural activity

- Neurotropic factors

How do cells migrate from the inner surface of the ventricular zone to the outer layers

cells start in the ventricular zone, then the radial glial cells guide the cells up to the cortex. Either become neurons of glial cells. CAMS are proteins that help guide the cells that are found on the surface of the cell

Radial Glial cells:

guide cells that stretch from ventricular zone to the cortical plate

Cell Adhesion Molecules: (CAMs)

- Promote adhesion of part of the nervous system to guide cells

- CAMs are proteins found on the surface of the cell that guide cell migration and axon paths. CAMs act as a glue to help the migrating neurons adhere to the radial glial cells (glue)

Process of Apoptosis:

- Ca2+ influx causes mitochondria to release a protein, Diablo.

- Diablo binds to inhibitors of apoptosis proteins (IAPs).

- Caspases dismantle the cell.

- Bcl-2 blocks apoptosis by preventing release of Diablo.

Influences on apoptosis:

- Size of synaptic target

- Availability of neurotrophic factors

- Nerve growth factor (NGF)

- Brain-derived neurotrophic factor (BDNF)

Cell autonomous:

independent of other cells and driven by genes (Purkinje cells)

Neural environment:

cells are affected by the influence of other cells (proteins) affects what neurons become

Down Syndrome:

- inheritance of an extra chromosome 21.

- Normally you have a pair of chromosomes, but in Down's you have 3 or a trisomy at Chromosome 21.

- Higher age of mother leads to likelihood of baby with Down's. (age 35 >)

- Low IQ

- abnormal formation of dendritic spines—they are longer and thinner and often tangled together.

- Severity of cognitive impairment varies. (large range of impact)

Fragile X Syndrome

- breakage of fragile site on arm of X chromosome, and extra trinucleotide repeats.

- Nucleotides are strings of chemicals that make up DNA, and the sequence of nucleotides code for specific proteins.

- 200 or more CGG repeats in fragile site on X chromosome, in unaffected individuals 4-55 repeats

- Excess of small dendritic spines that haven't been pruned back properly after birth, with can lead to abnormal connections in the brain.

- Modified facial appearance, cognition can be mild to severely impaired.

ADHD 3 core symptoms:

distractability, hyperactivity, impulsiveness

ADHD brains differ in :

- Volume of brain smaller

- Cortex thins later in development than in control children

- Reduced signaling in DA reward centers

Autism

May perseverate:

Showing repeating behaviors

ex: hand clapping

Autism

Structural differences in the brain:

- Reduced corpus collosum & cerebellum

- greater amygdala activation

Autism

Difficulty with:

empathizing, mimicking movements or facial expressions.

- May be due to low activation of a frontal cortex area containing mirror neurons.

High-functioning autism:

- do not lose language capabilities

- have difficulty interpreting emotional facial expressions in others

- go off to lead normal lives (careers, STEM: high attention to detail)

What is high-functioning autism called?

Asperger's syndrome

Dementia:

drastic failure of cognitive ability

Alzheimers:

a form of senile dementia, brains show reduced metabolism and cortical atrophy, changes in emotional stability as well as mental function

Alzheimer's produces cellular changes:

- Senile plaques formed by β-amyloid buildup

- Neurofibrillary tangles, including the tau protein

- Basal forebrain nuclei disappear

β-amyloid buildup occurs when amyloid precursor protein (APP) is cleaved by two enzymes:

β -secretase and presenilin

β-amyloid breakdown is done by

apolipoprotein (ApoE).

Pathway that leads to dementia:

1.) Amyloid precursor protein is cleaved by beta secretase (extracellular portion) and presenilin (intracellular).

2) b-amyloid clumps together forming plaques which accumulate on the neuron.

3.) Also accumulates inside cells causing the formation of tangles.

4.) Neurotoxicity of plaques leads to cessation of Ach production leading to dementia.

5.) ApoE works both inside and outside the cell to break down b-amyloid. Again, this doesn't happen if you have a couple of copies of ApoE4

Neural target feature:

precise

Hormonal target feature:

throughout the body

neural speed feature:

fast

hormonal speed feature:

slow

Neural distance feature:

synapse

hormonal distance feature:

up to 1 meter

neural message feature:

digital

hormonal message feature:

analog

neural release feature:

voluntary

hormonal release feature:

involuntary