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Neurotransmitters Amines Quaternary amines Acetylcholine (ACh) Monoamines Catelcholamines Epinephrine (EPI) Norepinephrine (NE) Dopamine (DA) Indoleamines.

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Presentation on theme: "Neurotransmitters Amines Quaternary amines Acetylcholine (ACh) Monoamines Catelcholamines Epinephrine (EPI) Norepinephrine (NE) Dopamine (DA) Indoleamines."— Presentation transcript:

1 Neurotransmitters Amines Quaternary amines Acetylcholine (ACh) Monoamines Catelcholamines Epinephrine (EPI) Norepinephrine (NE) Dopamine (DA) Indoleamines Serotonin (5-HT) Melatonin Amino acids Gamma-aminobutyric acid (GABA) Glutamate (GLU) Glycine Histamine (HIST) Neuropeptides Opioid peptides Enkephalins (ENK) Endorphins (END) Peptide Hormones Oxytocin (Oxy) Substance P Cholecystokinin (CCK) Vasopressin (ADH) Neuropeptide Y (NPY) Hypothalamic Releasing Hormones GnRH TRH CRH

2 Cholinergic (Ach) System

3 Alzheimer's: Biology chromosomes 1, 14, 19, and 21 general brain atrophy neuronal degeneration decreased cerebral metabolism general decay of acetylcholine system – especially in the basal forebrain neurofibrillary tangles beta-amyloid plaques

4 General Brain Atrophy

5 Neuronal Degeneration Normal Alzheimer’s

6 Decreased Cerebral Metabolism Alzheimer'sNormal

7 Neurofibrillary Tangles Microtubules: Provide structural support Are pathways for: Nutrients Waste products Neurotransmitters Made of Tubulin In Alzheimer’s Disease: Excess Tau protein binds builds up Tau binds with Tubulin and tangles the microtubules preventing them from properly functioning

8 Beta-Amyloid Plaque Formation Key enzymes: Alpha-secretase Beta-secretase Gamma-secretase Beta-Amyloid Precursor Protein (  APP) is cut or cleaved by these enzymes three different protein fragments form Protein fragments: p3 alpha and gamma harmless 40 amino acid string beta and gamma harmless 42 amino acid string beta and gamma TOXIC

9 Beta-Amyloid Plaques Tau Filaments Beta-Amyloid Plaques Pathology: Interferes with Ca 2+ regulation Increases free radicals Stimulates microglia aggregation Increases inflammation

10 Noradrenergic (NE) System

11 Ascending Reticular Activating System (ARAS) Arousal Center

12 Serotoninergic (5-HT) System

13 Major Depressive Episode Characteristics Onset is in early to mid 20’s but not age specific Onset age has been dropping 16% of population experience MDD in their lifetime 2:1 women to men ratio 41% occurs just before or just after menstruation

14 Depression and Neurochemistry

15 Depression and Stress Hormones cortisol steroid hormone

16 Depression: Treatment Medical Chemical Electroconvulsive Shock Therapy Psychotherapy Cognitive Behavioral Therapy Interpersonal Therapy

17 Cognitive Behavioral Therapy make patient examine thought process and recognize errors arbitrary interference overgeneralization try to correct cognitive errors concentrate on less depressive thoughts - be more realistic target negative cognitive schemes use journals to identify faulty thinking do hypothesis testing put fun back into the patients life increase exercise takes about 10-20 sessions

18 Depressions Vicious Cycle Must control brain chemistry e.g., Prozac Must reshape the negative thought processes e.g., CBT

19 Dopaminergic (DA) System

20 Schizophrenia Onset can be slow or sudden Typically exists chronically Affects ~1% of population Diagnosis must have at least two symptoms for more that 1 month

21 Schizophrenia Symptoms Positive Symptoms (abnormal states) hallucinations (auditory, visual) delusions (grandeur, persecution) Negative Symptoms (insufficient functioning) avolition (inability to initiate/persist in activities) alogia (absence of speech) anhedonia (inability to experience pleasure) affective flattening (flat emotional response) Disorganized Symptoms inappropriate affect (laughing/crying at the wrong times) disorganized speech (illogical, rambling, tangential) disorganized behavior (catatonia, agitation/immobility)

22 Schizophreni Genetic Risk by Relatedness The Evidence: Family History Twin Studies monozygotic (50%) same handed (92%) dizygotic (15%) both are carriers Adopted Children more like bioparents Single Gene? Probably not

23 Dopamine Hypothesis of Schizophrenia Abnormal levels of Dopamine lead to the schizophrenic symptoms 1. Amphetamine Psychosis Chronic users develop schizophrenic symptoms paranoia, delusions of persecution, auditory hallucinations Amphetamine exacerbates schizophrenic symptoms Amphetamines promote the release of catelcholamines particularly dopamine 2. Antipsychotic Drugs chlorapromazine is a dopamine antagonist and antipsychotic block specifically D2 and D4 receptors in the limbic system effectiveness is related to magnitude of blockade 3. Parkinson’s Disease some patients receiving L-dopa become psychotic some schizophrenic patients on antipsychotics develop Parkinson’s symptoms

24 Chemical Messengers Autocrine self signal Paracrine neighbor signal Endocrine distant signal Pheromone airborne signal same species Allomone airborne signal different species

25 Endocrine System

26 Homeostasis Mechanism Receptors input signals skin responds to cold temperature sends signal to brain Control Center integrating center brain interprets temp signal makes you shiver Effectors output mechanism muscles shiver creating heat

27 Negative Feedback Results in an immediate reversal of the imbalanced system Immediately negates the disruption Most systems in the body work via negative feedback systems temperature glucose balance water balance blood pressure

28 Positive Feedback Immediate further disruption of the imbalance so as to later return to homeostasis childbirth ovulation

29 Positive Feedback: Childbirth

30 Posterior Pituitary Hormones synthesized in the hypothalamus Released by the posterior pituitary Oxytocin milk ejection orgasm Vasopressin or ADH water balance blood pressure

31 Anterior Pituitary Releasing hormones synthesized in the hypothalamus CRF/CRH GnRH GHRH TRH PRH Triggers hormone release in anterior pituitary ACTH LH/FSH GH TSH PRL


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