Parkinson's Disease results in a(n) (increase or decrease) in D1 mediated effects on striatal medium spiny neurons. This results in excess (inhibition or excitation) of the thalamus and cortex.
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Parkinson's Disease results in a(n) (increase or decrease) in D1 mediated effects on striatal medium spiny neurons. This results in excess (inhibition or excitation) of the thalamus and cortex.
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- A presynaptic neuron in the cerebrum transmits information to hundreds of other neurons. This process is an example of (a) convergence (b) divergence (c) temporal summation (d) spatial summation (e) a graded potentialWhich neurotransmitter is released by the somatic motor neurons, and what type of effect does it have? What neurotransmitter(s) are released by the ANS, and what effect do/does it have? I have already seen a similar answer, and am not satisfied with the Answer. Please provide a very clear and detailed and if possible?The thalamus has been described as a “switchboard.” Explain why, by describing the pathway of somatic sensory information from the receptors to the cerebral cortex. Case Study: Princess Leia has asthma, and had to use her inhaler before taking her physiology exam. Later, in the physiology laboratory, she measured her pulse rate and blood pressure and found them to be higher than usual. The following week, after administering some drugs (epinephrine, atropine) she later developed a severe headache and dry mouth. When she looked in the mirror she noticed that her pupils were dilated.
- Which of the following statements best describes the axonal projection patterns of upper motoneurons located in the primary motor cortex? Upper motoneurons located in the primary motor cortex are cholinergic and their axons project directly to muscle fibres to control voluntary muscle movements. Upper motoneurons located in the primary motor cortex are glutamatergic and their axons project to the thalamus, brain stem and directly to muscle fibres to control voluntary muscle movements. Upper motoneurons located in the primary motor cortex project to the spinal cord where they synapse with cholinergic lower motoneurons that control voluntary muscle movements. Upper motoneurons located in the primary motor cortex project to neurons in the cerebellum, thalamus and brain stem that in turn contact lower motoneurons in the spinal cord to control voluntary muscle movements.There are a broad range of anti-epileptic medications currently on the market, with different therapies prescribed for different types and severities of the condition. Given what you have learned about synaptic transmission, which of the following could be a potential therapeutic approach to prevent the spreading of neuronal excitation? (3 correct answers, select all that apply) O A voltage-gated calcium channel blocker/inhibitor selective to glutamate-releasing neurons. O A voltage-gated calcium channel blocker/inhibitor selective to GABA-releasing neurons. O A glutamate receptor blocker (antagonist). O A GABA receptor antagonist. O A glutamate reuptake inhibitor. O A GABA reuptake inhibitor.Subjecting neurons in the perforant pathway to tetanus stimulation strengthens activity in the dentate gyrus, indicating that long-term potentiation does not occur in the hippocampus. the hippocampus is involved in memory. synapses in the brain do not behave like Hebbian synapses. synapses in the brain can behave like Hebbian synapses.
- The therapeutic effect of Aricept (generic donepezil) is due toA: binding of the drug to voltage-gated sodium channels.C: the drug producing an IPSP on the postsynaptic membrane.D: the drug causing the reuptake of acetylcholine at the synapse.E: the drug maintaining higher concentrations of acetylcholine at synapseExcess neural connections within the brain are reduced through a process of accommodation. true or falseDescribe the 3 functions stated in the lecture notes for the thalamus, especially its role as a relay station/gateway
- Alzheimer’s disease is thought to cause a DECREASE in the amount of acetylcholine (ACH) being released into the synaptic cleft in specific parts of the brain. What would be a possible treatment for this disease? (So basically- what would be a possible way to increase the amount of ACH in the synaptic cleft?)The core neural basis for memory, which is the increase in a cell’s potential to fire, is called:Short-term memory, like remembering a phone number, is stored as a Long Term Potentiation (LTP) of the synapse. Describe what has changed at the synapse when it has undergone LTP.