3. Receptors Rods – sense low levels of light Cones – sense higher level blue, green & red light Fig

3. Receptors Rods – sense low levels of light Fig Cones – sense higher level blue, green & red light

3. Receptors Rods – sense low levels of light Fig Cones – sense higher level blue, green & red light C. Receptor transduction 1. Rhodopsin

3. Receptors Rods – sense low levels of light Cones – sense higher level blue, green & red light C. Receptor transduction 1. Rhodopsin Retinene (photopigment) + opsin (protein) Fig Light Retinene – cis  trans configuration

C. Receptor transduction 1. Rhodopsin Retinene (photopigment) + opsin (protein) Fig Light Retinene – cis  trans configuration

C. Receptor transduction 1. Rhodopsin Retinene (photopigment) + opsin (protein) Fig Light Retinene – cis  trans configuration 3. trans Retinene Activates g-protein (transducin) cascade Closes Na + channels Hyperpolarizes cell

3. trans Retinene Activates g-protein (transducin) cascade Closes Na + channels Hyperpolarizes cell Fig

3. trans Retinene Activates g-protein (transducin) cascade Closes Na + channels Hyperpolarizes cell D. Dark vs. light Photoreceptors depolarized and inhibitory 1. Dark Inhibit adjacent cells in retina

D. Dark vs. light Photoreceptors depolarized and inhibitory 1. Dark Inhibit adjacent cells in retina Fig Light

Photoreceptors inhibitory and depolarized 1. Dark Inhibit adjacent cells in retina 2. Light Receptors hyperpolarized (inhibited) Fig

Photoreceptors inhibitory and depolarized 1. Dark Inhibit adjacent cells in retina 2. Light Receptors hyperpolarized (inhibited) Light is sensed E. Dark adaptation 1. Light Receptors “bleached”  rhodopsin in receptors 2. Dark 1 st 5 minutes –  rhodopsin in cones ~ 20 minutes – max sensitivity

E. Dark adaptation 1. Light Receptors “bleached”  rhodopsin in receptors 2. Dark 1 st 5 minutes –  rhodopsin in cones ~ 20 minutes – max. sensitivity Due to  rhodopsin in rods Light sensitivity  by 100,000x Chapter 11 – Endocrine Endocrine glands – secrete into blood

Chapter 11 – Endocrine I. General info. A. Classifications Endocrine glands – secrete into blood Fig. 11.1

Chapter 11 – Endocrine I. General info. A. Classifications Endocrine glands – secrete into blood 1. Amines – derived from single amino acids Thyroid hormone Fig Fig. 9.9 Epinephrine

I. General info. A. Classifications 1. Amines – derived from single amino acids Thyroid hormone Epinephrine 2. Polypeptides – chains of amino acids Antidiuretic hormone disulfide bridges Insulin

I. General info. A. Classifications 1. Amines – derived from single amino acids Thyroid hormone Epinephrine 2. Polypeptides – chains of amino acids Antidiuretic hormone Insulin 3. Glycoproteins – carbohydrate + amino acids chains Follicle stimulating hormone (FSH) Luteinizing hormone (LH) 4. Steroids – based on cholesterol (lipid)

3. Glycoproteins – carbohydrate + amino acids chains Follicle stimulating hormone (FSH) Luteinizing hormone (LH) 4. Steroids – based on cholesterol (lipid) Progesterone Testosterone Cortisol Fig. 11.2

3. Glycoproteins – carbohydrate + amino acids chains Follicle stimulating hormone (FSH) Luteinizing hormone (LH) 4. Steroids – based on cholesterol (lipid) Progesterone Testosterone Cortisol B. Pre- vs. Prohormones 1. Prohormones Peptide contained in longer peptide (e.g. opioids)

B. Pre- vs. Prohormones 1. Prohormones Peptide contained in longer peptide (e.g. opioids) Unessential peptide portions cleaved True of all peptide hormones

B. Pre- vs. Prohormones 1. Prohormones Peptide contained in longer peptide (e.g. opioids) Unessential peptide portions cleaved True of all peptide hormones 2. Prehormones Single molecule (e.g. thyroid hormone) Inactive until changed by target cell Fig. 11.3

B. Pre- vs. Prohormones 1. Prohormones Peptide contained in longer peptide ( e.g. opioids ) Unessential peptide portions cleaved True of all peptide hormones 2. Prehormones Single molecule (e.g. thyroid hormone) Inactive until changed by target cell C. Hormone common aspects Blood born Receptors on/in target cells Specific effect on target cell

C. Hormone common aspects Blood born Receptors on/in target cells Specific effect on target cell Can be turned off D. Interactions 1. Synergistic e.g. – epinephrine & norepi. on heart 2. Permissive Additive or complementary

D. Interactions 1. Synergistic e.g. – epinephrine & norepi. on heart 2. Permissive Additive or complementary Hormone increases responsiveness of different hormone e.g. – cortisol allows epi. & norepi. to have catabolic effects 3. Priming effect Hormone presence increases sensitivity/effect of same hormone

2. Permissive Hormone increases responsiveness of different hormone e.g. – cortisol allows epi. & norepi. to have catabolic effects 3. Priming effect Hormone presence increases sensitivity/effect of same hormone e.g. – GnRH causes AP to be more sensitive to GnRH 4. Antagonistic Opposite effects

3. Priming effect Hormone presence increases sensitivity/effect of same hormone e.g. – GnRH causes AP to be more sensitive to GnRH 4. Antagonistic Opposite effects e.g. – Insulin (  glucose stores) & glucagon (  glucose stores) E. Hormone levels 1. Half-life Time for metabolic clearance of half of hormone

E. Hormone levels 1. Half-life Time for metabolic clearance of half of hormone 2. Physiological levels Normal levels 3. Pharmacological levels Abnormally high levels Different physiological effects 4. Downregulation/desensitization Prolonged exposure  sensitivity of target tissue

4. Downregulation/desensitization Prolonged exposure  sensitivity of target tissue II. Hormone mechanisms A. Steroid hormones 1. Transport On carrier protein in blood

II. Hormone mechanisms A. Steroid hormones 1. Transport On carrier protein in blood Passive diffusion through membrane Fig. 11.4

A. Steroid hormones 1. Transport On carrier protein in blood Passive diffusion through membrane Fig Binds receptor in cytoplasm 2. Receptor Ligand binding domain – binds steroid DNA binding domain – binds DNA 3. Receptor-ligand complex

Fig Receptor Ligand binding domain – binds steroid DNA binding domain – binds DNA 3. Receptor-ligand complex Translocates to nucleus Fig Two complexes bind two receptor half sites on DNA (dimerization)

3. Receptor-ligand complex Translocates to nucleus Two complexes bind two receptor half sites on DNA (dimerization) Fig Fig Form homodimer Activate transcription

3. Receptor-ligand complex Translocates to nucleus Two complexes bind two receptor half sites on DNA (dimerization) Fig Form homodimer Activate transcription 4. On DNA Hormone response element recognized by complex

Fig Form homodimer Activate transcription 4. On DNA Hormone response element recognized by complex 2 must bind (dimerization) for activity B. Thyroid hormone T 3 and T 4 Based on # of iodines

B. Thyroid hormone T 3 and T 4 Based on # of iodines Fig T 4 converted to T 3 (active form) in cell 1. Transport Most carried on proteins in blood

B. Thyroid hormone T 3 and T 4 Based on # of iodines T 4 converted to T 3 (active form) in cell 1. Transport Most carried on proteins in blood Passive diffusion into cell

T 4 converted to T 3 (active form) in cell 1. Transport Most carried on proteins in blood Passive diffusion into cell Fig Receptor-ligand complex Formed in nucleus Complex forms heterodimer

Fig Receptor-ligand complex Formed in nucleus Complex forms heterodimer Other site bound by receptor-RXR (vit. A) complex Fig Transcription produces specific enzymes

2. Receptor-ligand complex Formed in nucleus Complex forms heterodimer Other site bound by receptor-RXR (vit. A) complex Transcription produces specific enzymes C. 2 nd messenger – adenylate cyclase

Other site bound by receptor-RXR (vit. A) complex Transcription produces specific enzymes C. 2 nd messenger – adenylate cyclase Membrane receptor binding Fig Intracellular g-protein  subunit dissociation

C. 2 nd messenger – adenylate cyclase Membrane receptor binding Fig Intracellular g-protein  subunit dissociation Subunit activates adenylate cyclase Forms cAMP from ATP

Fig Intracellular g-protein  subunit dissociation Subunit activates adenylate cyclase Forms cAMP from ATP cAMP activates protein kinase

Fig Subunit activates adenylate cyclase Forms cAMP from ATP cAMP activates protein kinase Protein kinase phosphorylates (adds a phosphate) specific enzymes

Fig Forms cAMP from ATP cAMP activates protein kinase Protein kinase phosphorylates (adds a phosphate) specific enzymes Enzymes activated or inhibited

Forms cAMP from ATP cAMP activates protein kinase Protein kinase phosphorylates (adds a phosphate) specific enzymes Enzymes activated or inhibited D. Phospholipase C-Ca ++ second messenger Membrane receptor binding G-protein dissociates intracellularly

D. Phospholipase C-Ca ++ second messenger Membrane receptor binding G-protein dissociates intracellularly Fig Activates phospholipase C (PLC) Releases inositol trisphosphate (IP 3 ) from lipid IP 3 releases Ca ++ from endoplasmic reticulum

Membrane receptor binding G-protein dissociates intracellularly Fig Activates phospholipase C (PLC) Releases inositol trisphosphate (IP 3 ) from lipid IP 3 releases Ca ++ from endoplasmic reticulum Ca ++ activates calmodulin Calmodulin has a variety of effects