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Brain and Behavior 345-201 > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

Schizophrenia

A

Psychopathological disorder characterized by emotional withdraw & flat effect (-), w/ hallucinations & delusions (+)

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2
Q

Schizophrenia symptomology

A

Flat effect -
Withdraw -
Hallucinations +
Delusions +
Abnormal behavior +
Cognitive impairment +
-Memory, attention, social perception
-Autism relates w/ social cues

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3
Q

Schizophrenia Prevalence

A

<1% of populations
-60% being M
Onset typically late adolescence /early adulthood
-Large # onset around 40 (usually F, if F, potentially menopause cause)

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4
Q

Schizophrenia & Genetics

A

Concordance Rates:
-50% MZ
-17% DZ

Genome Wide Asssocation Study (GWAS):
-Genes relating w/ DA (COMT, degrading enzyme), ST, & Glutamate
-Overlaps w/ genes implicated in bipolar & autism spectrum disorder (ASD)
-DISC 1 Gene disruption/disabled

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5
Q

SCZ & Environment

A

INC rates in urban areas
-INC stress, population, & hazards (lead, ect)

Working class
-Work environment hazards

Migrants
-INC stress, poverty, & nutritional issues

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6
Q

SCZ & Epigenetics

A

Offspring of older fathers & younger mothers
-Some studies disagree w/ father
-Young mom = INC disposition
-INC ASD risk w/ older mom & dad

Pregnancy difficulties
-Hemorrhaging & T2 diabetes in mom
-Viral infection
*INC viral enzyme in baby brain & CSF (cerebrospinal fluid)
*Jan-Apr baby (cold climates as well)

Low birth weight & small head circumference

Birth difficulties
-lack of O2/emergency C-section

CHICKEN & EGG, WHERE START? CORRELATION!

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7
Q

SCZ Brain structure & function - Ventricles

A

Enlarged ventricles
-Loss of surrounding neurons
-DISC 1 (wiring & organize neurons) (tested in mice, hard to tell SCZ present)

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8
Q

SCZ Brain structure & function - HPC

A

Hippocampus
-Small
-DEC glutamatergic neurons
-Abnormal hpc cytoarchitecture
*neurons out of line

MAY explain cognitive deficits, as contributes to behavior, thought, & speech

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9
Q

SCZ brain structure & function - Frontal Cortex & Cortical Tissue

A

Frontal Cortex
-Overactive
-@ rest during cognitive tasks
-May contribute to - symptoms
*Mood disturbances & social withdraw

Cortical tissue
-Over pruned during adolescence
-Too much lost gray matter from puberty+

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10
Q

SCZ Biochem & treatment

A

Marijuana use
-Worse symptoms
-MAY trigger onset in genetically predisposed ppl
*COMT

Ppl w/ SCZ have INC endogenous cannabinoids
-Attenuates stress response

THC activates receptors & anandimides

Ppl w/ SCZ have INC CB1 receptors
-Independent of marijuana use
-In CNS

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11
Q

SCZ DA hypothesis

A

Too much dopamine/DA receptors & synthesis
-May boost response to irrelevant stimuli
-INC cocaine use causes SCZ like symptoms

COMT may cause DA breakdown
-too many receptors
*Causes inability to may attentions (Causing abnormal behavior)
-Changes brain & neuron layout

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12
Q

SCZ DA Hypothesis 2

A

DA (D2) receptor antagonist revolutionized psychiatry
-Good treating + symptoms
-DA & ST
-Block DA receptor
*Side effects: Tardive dyskinesia (muscle control), pseudo-PD
*DA plays role in muscle movement & control

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13
Q

SCZ Typical VS Atypical antipsychotics

A

Typical:
Primarily block DA
-No work in 1/4 w/ SCZ

Atypical:
Greater ST receptor block/antagonism
Better treats - symptoms
Produces tardive dyskinesia
INC chance of weight gain

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14
Q

SCZ Glutamate Hypothesis

A

Glutamate (GLT) is everywhere
-DEC GLT receptors
-DEC glutamate n/t in those w/ SCZ w/ age (IDK???)
-PCP & Ketamine mimic psychotic symptoms
*NMDA receptor agonists
-Glutamate receptor (NMDA) agonist = DANGER!
*Too much = BAD!

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15
Q

Pros & Cons of SCZ Meds

A

PROS:
No straight jackets & sedatives
Patients involved in activities
Patients can leave hospitals (complicated)

CONS:
Changed roles of psychiatrists (not just prescribing meds)
INC non-compliance outside hospital (no want take meds)
-Leads to homelessness, jail, or prison (New asylums)
*Lack of proper treatment, keeping them jailed
*More likely to try to commit suicide

THERE IS NO MAGIC FIX!

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16
Q

Feeding Behavior

A

Homeostasis- Internal equilibrium
-We eat because we NEED to!

Regulatory systems (hormones & neurons) defend our set points
-Temp- 98.6F
-Fluid lvls (Vasopressin - BP)
-Body weight & Glucose lvls in blood
*Those on show gained weight after leaving show from not keeping diet

We can make new set points!

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17
Q

Why we eat

A

Nutrients needed for energy
Satisfaction of eating
-Dorsal striatum (food thought, planning, & eating movement)
-NAc (Nucleus accumbens) & Orbital Frontal Glucoreceptors (OFC)
*Control eating motivation & reward

Complex cultural & psychological
-Overwhelm regulatory systems
-May lead to eating disorders

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18
Q

DIGESTION & PANCREATIC HORMONES

A

Digestion- fats, proteins, carbs metabolized into usable chemicals in stomach
-ST: Glucose (GLC) stored as glycogen in liver/muscle cells & neurons
*GLC needs maintained at certain lvl

-LT: Excess fat stored in adipose tissue
*Use fat when GLC lvls low

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19
Q

Pancreatic Hormones

A

GLC regulation (sugar & energy regulation)
1) Insulin moves GLC
-GLC signal pancreas, beta cells release insulin
-Insulin stores GLC in liver & muscle cells as glycogen
-INC ST storage

2) Glucagon: Glycogen to GLC
-Useable for energy
-Still ST

20
Q

INSULIN & DIABETES

A

Type 1
-“Childhood”
-Disorder insulin production = No insulin, no GLC storage, RIP (kills) cells & neurons from too much GLC
-Give insulin

21
Q

INSULIN & DIABETES 2

A

Type 2
-Adult onset
-Cell receptors don’t recognize insulin/produce energy
-Treat w/ metaphormin, INC receptor sensitivity
-Lifestyle changes needed, obesity risk factor
-Lvls of GLC INC for longer

22
Q

BIOLOGICAL INITIATION OF FEEDING 1/3

A

1) Low GLC & fat lvls
Glucoreceptors (in liver) talk w/ feeding initiation center of HPC
-Glucoreceptors → GLC lvls travel vegus nerve, INC feeding
-INC GLC = INC insulin released to store/utilize

23
Q

BIOLOGICAL INITIATION OF FEEDING 2 & 3 /3

A

2) Insulin
If low, DEC GLC = INC appetite
Small INC of insulin = DEC appetite
*If too much GLC = hypoglycemia

3) Those w/ T2 diabetes untreated have INC GLC lvls but always hungry from low insulin

24
Q

BRAIN & HORMONES INTERACT IN FEEDING

A

Ventromedial Hypothalamus (VMH)- Stops eating
-Lesions here = over eating & obesity (FAT RAT)
-Is our satiety area

Lateral Hypothalamus- Makes hungry
-Lesions here = stop eating & weight loss

When these areas are lesioned, eventually a new set point is made

25
Q

BRAIN & HORMONES INTERACT IN FEEDING pt 2

A

Arcuate Nucleus (AN)- Bunch of cell bodies & neurons
-Receive signals about GLC lvls from insulin & other signals
-Fat cell, leptin (hormone), released from adipose tissue
*Generally inhibits feeding hormone
*Those obese have leptin insensitivity, INC feeding

26
Q

BRAIN & HORMONES INTERACT IN FEEDING pt 3

A

Gut hormones: ST energy
-Stomach → Ghrelin → hungry
-Intestines → PYY336 → stop eating
*PYY336 low in obese ppl

27
Q

Neurons in the AN

A

POMC Neurons- Inhibit appetite / = satiety
NPY- Stimulates appetite / = hunger
-Can inhibit POMC
-Ghrelin activates, causing feeding

28
Q

B&HIIF pt 4

A

Insulin & PYY336 inhibit feeding. They dot not activate POMC, they inhibit NPY, DEC appetite

Leptin stimulates POMC while inhibiting NPY, DEC feeding

Feeding is a balance of 2nd order neurons
-Lateral Hypothalamic = Orexigenic = INC appetite
-PVN (Para ventricular nucleus) = anorexigenic = DEC appetite

NST (Nucleus of Solitary Tract) = integrate signal from gut & brain
-Comes in from GI tract

29
Q

Appetite Modulators

A

Orexin- Has receptors in hypothalamus

⇅ - STIMULATE feeding in animals

Anandamide- Body’s THC
-CB1 (in brain) & CB2 receptors

30
Q

Parkinson’s Disease (PD) Def & symptoms

A

Tremors of hands & face at rest
-Rigid walking
-“mask like” appearance - no face muscle control
-Apraxia - Difficulty engaging in effortful movement

31
Q

PD Prevelance

A

1-2% of US ages 65&+
-Rare but not never in Y-A

M x2.5 more than F to get
-Possibly from working in hazardous environments

32
Q

NEUROBIOLOGY OF PD

A

Genes
Defect in genes that encode for
-Alpha-synuclein
*Found in synaptic buttons
*Releases n/t (Not enough DP)
-Parkin
*Degrades unneeded proteins

33
Q

PD NEUROBIOLOGY THEORY

A

Defects in either gene leading to accumulation of alpha-synuclein
-Forms Lewy bodies, screwing up neurons
*Mitochondria cannot power neuron, killing it

34
Q

BRAIN AREA COMPROMISED

A

Midbrain!
Degeneration of DA containing cells in substantia niagra

Dopaminergic neurons project to striatum
-DA to striatum controls voluntary movement

35
Q

PD TREATMENT

A

-Agonist at DA receptors (No work well)
-MAOIs (INC DA activity)
-LDOPA
*Precursor for DA
*Can cross BBB (DA cannot)
*Side effects: Tolerance, hallucinations, INC libido
*Only treats symptoms, not cell death
-DBS- Pacemaker stimulates striatum (axon terminal from substantia niagra) to release DA

36
Q

Exercise and PD

A

Postmortem examinations reveal DA loss in the substantia nigra pars compacta (SNc), and the consequent loss of DA in the striatum in the brains of PD patients.
-Exercise restores BDNF levels and has has neuroprotective effects against the neurotoxicity induced by 6-OHDA.
-No BDNF = No TH
-TH decrease in both SED group and SED + K252a group
-When K252a added, all groups that received 6-OHDA showed decreases of
TH levels.
-intermittent treadmill exercise employed an increase of BDNF levels
-Treadmill running at 5 days/week during 18 weeks DEC dopaminergic cell loss, INC dopamine and its transporter expression, and consequently improves balance and motor coordination
-The intermittent exercise protocol could be more beneficial than continuous exercise, in addition to being closer to the exercise protocols undertaken in PD patients.

37
Q

Exercise & PD pt 2

A

-TH in the CPu, and showed reduced motor symptoms
-treadmill exercise = changes in BDNF lvls = activate TrkB-dependent mechanisms (related to survival of nigrostriatal dopaminergic neurons)
-blockade BDNF–TrkB signaling = worsened neuroprotective effects of exercise after K252a injection
-Physical activity INC serum BDNF, which cross the blood–brain barrier, and may decrease the PD risk

38
Q

First-rank symptoms of SCZ

A

Auditory hallucinations
Highly personalized delusions
Changes in affect (emotion)

39
Q

Supersensitivity Psychosis

A

Exaggerated “rebound” psychosis when antipsychotic meds are reduced, probably as a consequence of the up-regulation of receptors during drug treatment

40
Q

Basal Metabolism

A

Use of energy for
-Heat production
-Maintenance of membrane potentials
-All the other basic life-sustaining functions of the body.

41
Q

Cephalic Phase of feeding

A

Triggered by sights, smells, and tastes that we have learned to associate with food

42
Q

Digestive Phase of feeding

A

Food entering the digestive tract prompts an additional release of insulin

43
Q

Absorptive Stage

A

As digested food is absorbed into the bloodstream, gluco-detectors detect the increase in circulating glucose and signal the pancreas to release still more insulin

44
Q

Orexigenic Neurons VS Anorexigenic Neurons

A

Orexigenic neurons promote feeding behavior.
Anorexigenic neurons inhibit feeding behavior.

45
Q

Cholecystokinin (CCK)

A

Peptide hormone released by gut after ingestion of food high in protein and/or fat.

Brain and Behavior 345-201 (3 decks)

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