| Describe how the nervous system is organized | The nervous system is structurally composed of: The Central Nervous System and Peripheral Nervous system CNS - consists of the brain and spinal cord PNS - composed of the ganglia (group of neurons) and efferent/afferent nerve fibers that relay signals between the CNS and other parts of the body. |
| Define the major functions of the CNS | Subconsiouly regulates our internal environment through neural means Allows the exeprience of emotions controls voluntary movement Controls perception, allowing you to conciously be aware of the body and it's surroundings Engages in cognititve process such as thought and memory |
| Define major functions of the PNS | Afferent division: detetcs, encodes and transmits peripheral signals to the CNS Afferent input: used to plan for voluntary actions and infrom centres of the CNS controlling homeostasis Efferent division: trasnsmits signals from CNS that control the activities of effector organs (e.g. msucles and glands) |
| State the major steps of the process of scientific theory | Observation: observe natural phenomenon and come up with question Hypothesis: propose an explanation of the phenomenon with the limited evidence provided as a starting point for further investigation Experiment: test the hypithesis and collect data Analysis: analyse the data collected Conclusion: draw a conclusion supported by the data, which can adjust the hypothesis or be used to design a new hypothesis Application: the result of the expiment e.g. new drug, treatment etc. |
| Describe the characteristics of Myotonia Congenita | Muscle stiffness and delayed relaxation (generally painless) upon intitial activity Unusual exertion asscoiated with muscle hypertrophy (increased muscle mass) Myotonia Congenita can be hereditary in an autosomal dominant (e.g. Thomsen Disease) OR recessive (e.g. Becker Disease). Myotonia Congenita can be caused by poisoning from certain weedkillers. |
| Describe the symptoms of Myotonia Congenita | Myotonia Congenita is a symptom of cerain neuromuscular disorders with symtoms characterised by: The slow relaxation of muscles after voluntary contraction or electrical stimulation Note: Repeated effort is needed to relax muscles and the condition impoves once muscles have warmed up |
| Explain the molecular bases for dominant and recessive forms of Myotonia Congenita | A313T mutation that causes dominant myotonia congenita shifts open probability of the channels to positive potentials by ~120 mV All mutations causing dominant form of disease shift Po to positive potentials Chemicals that induce myotonia in skeletal muscle (2,4-D; CPP) also shift Po to positive potentials All nonsense mutations and some missense mutations can cause recessive myotonia |
| Briefly describe the role of Cl channels in skeletal muscle action potential | Depolarisation phase (excitation) - Na+ and Ca2+ channels open, letting Na +and Ca2+ ions into the cell Repolarisation phase (recovery from excitation) – K+ and Cl-open, letting K+ ions out and Cl-ions into the cell Skeletal muscle cells have high Cl conductance due to a large number f Cl channels on the plasma membrane ( 80% of total membrane conductance at rest) Increased excitability of the muscle can be caused by an increase in Na+ and/or Ca2+ conductance, or by a decrease in K+ and/or Cl-conductance Myotonia can be induced by blocking Cl-conductance by at least 60-70% |
