Physio Final

Explain characteristics of a regulatory mechanism

Explain characteristics of a regulatory mechanism

- system variable (temperature in the room), set point, detector(thermostat), and correctional mechanism  

Describe the fluid compartments of the body

2/3 of body’s water is contained in the intracellular fluid (the fluid portion of the cytoplasm of the cells)  

The rest is extracellular fluid (which includes the intravascular fluid (blood plasma), the cerebrospinal fluid and the interstitial fluid (the fluid that stands between our cells 

explain the control of osmometric and volumetric thirst. 

Osmometric thirst – occurs when the solute concentration of the interstitial fluid increases Osmometric refers to the fact that the detectors are responding to (metering) changes in the concentration of interstitial fluid that surrounds them  

Volumetric thirst – occurs when the volume of the blood plasma, the intravascular volume, decreases. 

Discuss the neural control of thirst.

The osmoreceptors that initiate drinking are in the OVLT and SFO. Signal for volumetric thirst is provided by angiotensin II. The median preoptic nucleus acts as an integrating system for most or all the stimuli for osmometric and volumetric thirst.  

A nucleus in the lamina terminalis, the median preoptic nucleus, receives and integrates osmometric and volumetric information. The anterior cingulate cortex also receives information from the OVLT via dorsal midline nucleus of the thalamus 

Describe the characteristics of the two nutrient reservoirs

Short term reservoirs

- stores carbohydrates, located in the cells of the liver and the muscles, filled with complex insoluble carbohydrates called glycogen.

-Cells in the liver convert glucose into glycogen and store glycogen. They are stimulated to do so by the presence of insulin. Fall of glucose is detected by pancreas and in the brain. The effect of glucagon is opposite of insulin. This reservoir is mainly reserved for the CNS.

Long term reservoir

- stores fats/adipose tissue. More precisely triglyceride.

- what keeps us alive when fasting

- as we begin to use contents of short term carb reservoir fat cells start converting triglycerides into fuels that the cells can use and releasing into the bloodstream.

Absorptive Phase of metabolism

- the phase of metabolism during which nutrients are absorbed into the digestive system; glucose and amino acids constitute the principle source of energy for cells during the phase, and excess nutrients are stored in adipose tissue in the form of triglycerides. 

Fasting phase of metabolism

the phase of metabolism, during which nutrients are absorbed from the digestive system; glucose, amino acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase.  

Discuss social and environmental factors that begin a meal

- presense of other people sitting around the table, smelling food, certain times of the day. We know that we eat at certain times so we anticipate those times even if we are not hungry.  

Long term hunger signals

-peptide hormone – ghrelin  

- leptin and insulin  

- adipose tissue  

Short term hunger signals

- short-term satiety signals control the size of the meal. Feedback from the nose and mouth about food eaten. Gastric factors  

- The short-term regulation of hunger deals with appetite and satiety. It involves neural signals from the GI tract, blood levels of nutrients, and GI-tract hormones.  

Head factors responsible for stopping a meal

– several factors related to receptors located in the head 

- the eyes, nose, tongue, and throat 

- taste and odor of food can serve as stimuli that permit animals to learn about caloric contents of different foods.  

Gastric factors responsible for stopping a meal

– receptors that can detect presence of nutrients 

- this shows that we can tell that our food is in our stomach and if it is removed we would also know.  

Intestinal factors for stopping a meal

– nutrient detectors  

- axons arising from the duodenum are sensitive to the presence of glucose, amino acids, and fatty acids.

Describe research on the role of the brain stem in hunger

The brainstem is another key brain area involved in regulation of food intake and energy balance. Satiety signals from the gastrointestinal (GI) tract primarily relay to the solitary tract nucleus (NTS) through the sensory vagus nerve, a major neuronal link between the gut and the brain. 

Describe research on the role of the hypothalamus in hunger

Two peptides of hypothalamus – melanin-concentrating hormone (MCH) and orexin (appetite inducing chemicals) stimulate hunger and decrease metabolic rate. 

Genetic manipulation that increased the production of NPY in the hypothalamus increased food intake  

Ghrelin provides a potent hunger signal in brain  

Terminals of hypothalamic NPY neurons release another orexinogenic peptide in addition to neuropeptide Y (agouti-related protein) increase in food intake 

Endocannabinoids stimulate eating

Describe research on the role of the hypothalamus in satiety

Leptin suppresses eating by binding with leptin receptors in arcuate nucleus. Leptin inhibits NPY/AGRP neurons which suppresses feeding 

Leptin activates CART (cocaine-and amphetamine-regulated trasncript) / α-MSH (α-melanocyte-stimulating hormone) which then inhibit MCH (melanin-concentrating hormone) and orexin neurons in lateral hypothalamus and prevent their stimulatory effect of appetite.  

Discuss the physiological factors that may contribute to obesity. 

Many factors can contribute to excess weight gain including eating patterns, physical activity levels, and sleep routines. Social determinants of health, genetics, and taking certain medications also play a role. 

Perceptual learning

– ability to learn and recognize stimuli that have been perceived before.  

Stimulus-response learning

– ability to learn to perform a particular behavior when a particular stimulus is present 

Motor learning

– a component of stimulus-response learning. Establishment of changes within the motor systems (cannot occur without sensory guidance) learning to make a new response.  

Relational learning

– learning relationships among individual stimuli.  

Discuss research on how learning affects neural structures

changes in the strength and number of the connections between existing neurons, a process called synaptic plasticity 

the induction of long-term potentiation

intense electrical stimulation of axons leading from the entorhinal cortex to the dentate gyrus caused a long-term increase in the magnitude of excitatory postsynaptic potentials in the postsynaptic neurons 

Role of NMDA receptors

controls calcium ion channel. The channel is usually blocked by magnesium ion which prevents calcium ions from entering the cells even when receptor is stimulated by glutamate. But if postsynaptic mambrane is depolarized, the magnesium ion is ejected from the ion channel and channel is free to admit calcium ions. Thus calcium ions enter the cells through the channels controlled by NMDA receptors only when glutamate is present. This means that the channel controlled by the NMDA is a neurotransmitter and voltage gated channel.  

Discuss the mechanisms responsible for the increase in synaptic strength that occurs during long-term potentiation. 

Strengthening of an individual synapse is accomplished by insertion of additional AMPA receptors into the postsynaptic membrane of the dendritic spine. With more AMPA receptors present, the release of glutamate by terminal button causes larger excitatory postsynaptic potential (the synapse becomes stronger).  

Discuss the physiology of the classically conditioned emotional response to aversive stimuli.Describe the role of the basal ganglia and premotor cortex in instrumental conditioning and motor learning. 

Basal ganglia receives sensory information and information about plans for movement from the neocortex. Instrumental conditioning activates the basal ganglia and damage to the basal ganglia or infusion of a drug that blcoks NMDA receptors there disrupts instrumental conditioning. Basal ganglia are passive observers but as behaviors are repeated again and again they begin to learn what to do.  

Premotor cortex main role is the execution of the actions or behaviors.  

Discuss how the reinforcement system may detect reinforcing stimuli

- neural circuits detect a reinforcing stimulus and cause the activation of dopaminergic neurons in ventral tegmental area. Activation depends on the state of the individual. The reinforcement system appears to be activated by unexpected reinforcing stimuli. Prefrontal cortex possibly turns on reinforcement mechanism.  

Discuss how the reinforcement system may strengthen synaptic connections

- dopamine serves a role. Application of dopamine and glutamate in hippocampal field CA1 produced L-LTP but this effect was prevented by the application of ZIP which indicates PKM-zeta is essential for dopamine-dependent establishment of L-LTP.  

- dopamine induces plasticity by facilitating associative long-term potentiation (in the nucleus accumbens, amygdala, and prefrontal cortex. Establishment of long-term memories involve production of PKM-zeta.  

Review the connections of the hippocampal formation with the rest of the brain

- receives input from subcortical regions via the fornix, fornix carries dopaminergic axons from the ventral tegmental area, noradrenergic axons from the locus coeruleus, serotonergic axons from the raphe nuclei and acetylctriglholinergic axons from the medial septum. The fornix also connects the hippocampal formation with mammillary bodies located in posterior hypothalamus.  

describe evidence that damage to the hippocampal formationand related structures causes anterograde amnesia. 

- case in 1986 – this guy they studied had cardiac arrest\, his heart was successfully restarted but he had brain damage from the temporary halt in blood flow. And he had permanent anterograde amnesia. They found that his hippocampal formation was gone, neurons completely degenerated. 

Anterograde amnesia can be caused by alcoholism which primarily damages mammillary bodies.  

Describe the role of the hippocampus in relational learning including spatial learning

The role of the hippocampus in relational memory is in binding together multiple inputs to create and allow for the storage of representations of the associations among the constituent elements of scenes and events [7]. This function ultimately results in the storage of long-term memory in widespread cortical regions. 

Several lines of evidence, including the discovery of place cells, have contributed to the notion that the hippocampus serves primarily to navigate the environment, as a repository of spatial memories, like a drawer full of charts; and that in some species it has exapted on this original one an episodic memory function 

Describe the use of subjects with brain damage in the study of language

Most people that were studied were those who have suffered strokes or cerebrovascular accidents. There were also studies using functional imaging devices. They used these devices to gather information about language processes from normal subjects.  

Lateralization

– one hemisphere (the left) has greater influence on things like language than the other.

Describe Broca’s aphasia

damage to this area in the inferior left frontal lobe disrupts the ability to speak. Characterized by slow, laborious, and nonfluent speech. People with this aphasia have a hard time finding the right words.  

Agrammatism

– patient’s difficulty in using grammatical constructions (such as –ed or auxiliaries such as have).  

Anomia

– word-finding difficulty, frequent ‘uh’ or unsure facial expressions trying to find the word

Difficulty with Articulation

– patients mispronounce words often altering the sequence of sounds. (such as likstip instead of lipstick) 

Symptoms of Wernicke’s apashia

poor speech comprehension and production of meaningless speech. Fluent and unlabored unlike Broca’s aphasia. Appears to be grammatically correct but uses few content words and the words that are strung together do not make sense.

Symptoms of pure word deafness

– The ability to hear, to speak, and (usually) to read and write without being able to comprehend the meaning of speech; caused by damage to Wernicke’s area or disruption of auditory input to this region

Symptoms of transcortical sensory aphasia

– A speech disorder in which a person has difficulty comprehending speech and producing meaningful spontaneous speech but can repeat speech; caused by damage to the region of the brain posterior to Wernicke’s area.  

Relation between Wernicke’s, pure word deafness, and transcortical sensory aphasia

– Transcortical sensory aphasia can be seen as Wernicke’s aphasia without a repetition deficit. The symptoms of Wernicke’s aphasia consist of those of pure word deafness plus those of transcortical sensory aphasia.  

Discuss the brain mechanisms that underlie our ability to understand the meaning of words and to express our own thoughts and perceptions in words.

Words such as action words are memories that are stored in parts of the brain such as regions of the association cortex rather than primary speech areas. Different memory categories can be stored in different regions, and certain actions words activate all the parts because they are tied together via things like hippocampal formation. The brain mechanisms act as a dictionary in our brain.  

Describe neurological causes of stuttering is reflected in decreased activation of their temporal cortex. 

Stuttering seems to be from problems in the neural mechanisms that are involved in planning and intiation of speech. People who stutter tend to show excessive activation of the Broca’s area and the insula, the supplementary motor area and the vermis of the cerebellum and an absense of activation in auditory regions of the temporal lobe. Suggest that a problem would be caused by faulty auditory feedback from sounds of the stutterer’s own speech, shown by the lack of activity in the temporal lobe.  

Neurological causes for seizures

- scarring (produced from injury), stroke, developmental abnormality, or the irritating effect of a growing tumor.  

- drugs and infections that cause a high fever  

- genetic factors 

Neurological causes of strokes

- strokes have to do with neuron death and this can happen with the presence of excessive amounts of glutamate.  

Causes of Parkinson’s disease

degeneration of nigrostriatal system (the dopamine-secreting neurons of the substantia nigra that send axons to the basal ganglia). Mutation on chromosome 6 produces a gene called parkin, causes a loss of funtion. Mutation on gene on chromosome 4 that leads to α-synuclein.  

Symptoms of Parkinson’s

muscular rigidity, slowness of movement, a resting tremor, and postural instability.  

Treatment for Parkinson’s

L-DOPA (precurser of dopamine) the increased level of L-DOPA causes the patient’s remaining dopamine cells to produce and secrete more dopamine and for a time alleviate the symptoms. It is not a permanent solution. Possible use of deprenyl usually in conjuntion with L-DOPA. Administration of deprenyl slows the progression of Parkinson’s  

Causes of Huntingtin’s disease

degeneration of caudate nucleus and putamen. First signs of neural degeneration occur in putamen with the inhibtory neurons called GABAergic medium spiny neurons. Hereditary disorder. Repeated sequence of mutant gene huntingtin, on chromosome 4.

Symptoms of Huntingtin’s disease

uncontrollable movements, progressive disease (includes cognitive and emotional changes) eventually causes death (usually within 10-15 years after symptoms begin) 

Treatments for Huntingtin’s disease

no official treatment, possible help if preparing a special antibody that acts intracellularly called Happ1. Or possibly injecting small interfering RNAs into the striatum.  

Causes of Alzheimer’s disease

unknown origin. Produces severe degeneration of the hippocampus, entohinal cortex, neocortex, nucleus basalis, locus coeruleus, and raphe nucleus. Amyloid plaques are found in people with AD. These are extracellular deposits that consist of a dense core of a protein known as β-amyloid, surrounded by degenerating axons and dendrites, along with activated microglia and reactive astrocytes, cells that are involved in destruction of damaged cells.  

-hereditary 

-mutation in gene for apolipoprotein E 

- mutation of two presenilin genes found on chromosome 1 and 14 

-Abnormal filaments are seen in the soma and proximal dendrites of pyramidal cells in the cerebral cortex, which disrupt transport of substances within cells and cell dies, leaving behind a tangle of protein filaments such as the neurofibrillary tangles. Formation of the amyloid plaques are from production of defection form of β-amyloid. (this has to do with the β-amyloid precursor protein (APP)  

Symptoms of Alzheimer’s

Cognitive: mental decline, difficulty thinking and understanding, confusion in the evening hours, delusion, disorientation, forgetfulness, making things up, mental confusion, difficulty concentrating, inability to create new memories, inability to do simple math, or inability to recognize common things 

Behavioral: aggression, agitation, difficulty with self care, irritability, meaningless repetition of own words, personality changes, lack of restraint, or wandering and getting lost 

Mood: anger, apathy, general discontent, loneliness, or mood swings 

Psychological: depression, hallucination, or paranoia 

Whole body: loss of appetite or restlessness 

Also common: inability to combine muscle movements or jumbled speech 

Possible treatments of Alzheimer’s

acetyhlcholinesterase inhibitors (donepezil, rivastigmine, and galantamine). And an NMDA receptor antagonist (memantine). Possible injection of antibodies against β-amyloid (but this approach had caused inflammatory reactions and caused a patient to die of pulmonary embolism