Memory I

2. MemoryI • Episodic or expelicit or declerative • Limbic and temporal lobe are essential • Semantic or Implicit or nondeclerativeor reflexive , Tehran is captial of iran

3. Memmory cont.I • PRS:Perceptual representation system for distingushing of word and object • 1-visual word system 2-Auditory word system 3-structural descriptive system

4. Memmory cont.I • Procedural: habits and skills (Cortco striatum system),B.G.Cerebellum • Working :storage memory in many seconds periods or on-line ,they are necsessary for cognition,comprehension , solving .

9. conditioning • Extinction: i-Internal inhibition:Cs without Us,no response ii-External inhibition:Cs with Us , no response • Biofeed back: conditioning of visceral system(HR,RR,BP)

10. Types of conditioning • Simple classical conditioning 1-delay conditioning 2-trace conditioning 3-backward conditioning

11. Operant Conditioning • 1-Avoiding Reflex 2-Food Aversion Reflex • Hippocampus, Para hip, temporal (perirhinal ) • Retrograde or antrograde amnesia

13. Figure 13.1  Procedures for classical conditioning and operant conditioning In operant conditioning the learner’s behavior controls the presentation of reinforcement or punishment.

14. Memory and timeII • Short time. seconds and minutes,7-10 digit Mechanism • Continual activity of reverberating circuits • Facilitation and modulation of synaptic junctions • Accumulation of presynaptic Ca ions

15. Memory and time cont. • Intermediate long term memory • Physical and chemical changes • 5HT cAMP PK K current decrease long term A.P. Ca current increase exocytosis

16. Intermediate memory cont.

17. Long term memory • Recent(days) • Remote(years) • Synaptic vesicle increase • Releasing site increase • Synaptic terminal increase • Change in form,size and number of post synaptic branches

18. Long-term Potentiation (LTP) and Depression (LTD) • LTP: a burst of stimulation from axons, e.g., 100 excitations per second for 1-4 seconds onto dendrites results in potentiated synapses for minutes, days or weeks • specificity: only active synapses become strengthened • cooperativity: nearly simultaneous stimulation by two or more axons results in LTP • associativity: pairing a weak input with a strong input enhances later response to the weak input • LTD: prolonged decrease in response to a synaptic input where two or more axons have been active together at 1-4 times per second

19. Biochemical Mechanisms of LTP in Hippocampus • AMPA and NMDA receptors are involved in LTP • glutamate receptors that open channels in postsynaptic neurons to let in one or more kinds of ions (ionotropic) • AMPA receptors: glutamate opens sodium channels • similar to what we have studied

20. Biochemical Mechanisms of LTP in Hippocampus cont. • NMDA receptors: normally blocked by magnesium but responds to glutamate when depolarized by AMPA receptors • calcium enters and activates protein CaMKII, which is necessary for LTP, and sets several processes in motion: • structure of AMPA receptors change, becoming more responsive to glutamate • some NMDA receptors change to AMPA receptors and increase their responsiveness to glutamate • dendrites may build more AMPA receptors and make more branches • Once established, LTP no longer depends on NMDA synapses

21. Figure 13.21 The AMPA and NMDA receptors during LTP. If one or (better) more AMPA receptors have been repeatedly stimulated, enough sodium enters to largely depolarize the dendrite’s membrane. Doing so displaces the magnesium ions and therefore enables glutamate to stimulate the NMDA receptor. Both sodium and calcium enter through the NMDA receptor’s channel.

22. Specific memory area • Hippocampus lesion 1-antrograde amnesia:for information learned before the onset of illness 2-retrograde amnesia:for information that presented itself after onset of illness

23. Aging and memory • Neuronal death will be started after maturation , • Cognition will be worsen since 30 . • AD risk factor:age,brain glucose metabolism disorder,alchohol abuse,sleep disturbance,environmental factor, depression • Antirisk factor,education,estrogen,Vit E,

25. "We remember what we understand; we understand only what we pay attention to; we pay attention to what we want." - Edward Bolles

26. How We Forget and the Importance of Review • Fading. According to the fading theory, the trace or mark a memory etches into your brain is like a path you make in the woods when you continually walk along the same route. If you don't take that same path, it eventually becomes overgrown until it disappears. In the same way, facts that you learn are forgotten when you don't review them.

27. How We Forget and the Importance of Review • Retrieval. According to this theory, a forgotten fact hasn't faded, it has been misplaced in the "file cabinet" of your mind. Whether the information has disappeared completely, or has been lost, the result it the same-it has been forgotten.The key to avoiding retrieval problems is to label and file information correctly. You can also assist your memory by studying in "meaningful chunks."

28. How We Forget and the Importance of Review • Interference. This theory is based on the principle of limited space. As you keep adding new information, a conflict develops between the old and new information over the space available. The key to avoiding this problem is to look for connections and relationships between ideas so that they can be "filed together" or combined. Ask yourself, "What do I already know about this?" or any of the "cognitive questions."

29. How We Forget and the Importance of Review • Interactive interference. When you are learning a great deal of information at one time, you tend to remember best what is read or presented first and last. The rest gets lost in the shuffle. To avoid this problem, study one subject at a time, in meaningful chunks.