2. synaptic plasticity is the ability of the connection, or synapse, between two neurons to change in strength in response to either use or disuse of transmission over synaptic pathways. Imp. Mechanism of learning and memory. Dynamic entity, Depends on Calcium Plasticity is of Time scale of miliseconds to years.

3. Short-term Synaptic Plasticity Lasts for few minutes or less. readily observed during repeated activation of any chemical synapse Facilitation,Potentiation,Augmentation,Depres sion

4. Synaptic facilitation is a rapid increase in synaptic strength that occurs when two or more action potentials invade the presynaptic terminal within a few milliseconds of each other. is the result of prolonged elevation of presynaptic calcium levels following synaptic Activity.

5. Facilitation at the squid giant synapse. A pair of presynaptic action potentials el1cits two EPSPs. Because of facilitation. the second EPSP is larger than the first.

6. Opposing facilitation is synaptic depression, which causes neurotransmitter release to decline during sustained synaptic activity. Amount of depression is proportional to the total amount of transmitter released from the pre- synaptic terminal. more depression is observed after the size of the reserve pool is reduced by impairing synapsin, a protein that maintains vesicles in the Reserve pool

7. Synaptic depression at the frog neuromuscular synapse increases in proportion to the amount of transmitter released from the presynaptic terminal.

8. other forms of synaptic plasticity, such as synaptic potentiation and augmentation,also are elicited by repeated synaptic activity and serve to increase the amount of transmitter released from pre-synaptic terminals. Both augmentation and potentiation enhance the ability of incoming Ca2+ to trigger fusion of synaptic vesicles with the plasma membrane, but they work over different time scales. repeated activity first causes facilitation and then augmentation to enhance synaptic transmission.

9. Facilitation and augmentatton of the EPP occurs at the beginntng of the stimulus train and are followed by a pronounced depression of the EPP. Potentiation begins late in the stimulus tratn and persists for many seconds after the end of the stimulus, leading to post- tetanic potentiation.

10. Long Term Plasticity and Behavioral Modification plausible Mechanism for more permanent changes in brain function. The Gill withdrawal function of Aplysia exhibit two forms of Plasticity: Habituation(a process that causes the animal to become less responsive to repeated occurrences of a stimulus) and Sensitization.

11. High/Correlated activity HighCalcium LTP Low/uncorrelated activity Moderate Calcium Calcium LTD LTD Magic High NMDA-R activation Moderate NMDA-R activation

12. Long Term Potentiation produce a long-lasting increase in synaptic strength. Studied extensively in mammalian Hippocampus. In rodents, hippocampal neurons fire action potentials only when an animal is in certain locations. Such "place cells" appear to encode spatial memories.

14. Terje Lomo and Timothy Bliss discovered that a few seconds of high -frequency electrical stimulation can enhance synaptic transmission in the hippocampus of intact rabbits for days or even weeks. If the Schaffer collaterals are stimulated only two or three times per minute, the size of the evoked EPSP in the CA1 neurons remains constant.However, a brief, high-frequency train of stimuli to the same axons causes LTP, which is evident as a long- lasting increase in EPSP amplitude

15. Molecular Mechanism of LTP

16. During low-frequency synaptic transmission, glutamate released by the Schaffer collaterals binds to both NMDA-type and AMPA type glutamate receptors. While both types of receptors bind glutamate, if the postsynaptic neuron is at its normal resting membrane potential, the pore of the NMDA receptor channel will be blocked by Mg2+ ions and no current will flow. Under such conditions, the EPSP will be mediated entirely by the AMPA receptors. high-frequency stimulation will cause summation of EPSPs, leading to a prolonged depolarization that expels Mg2+ from the NMDA channel pore. NMDA Receptor is thus a molecular Coincidence detector: The channel of this receptor opens (to induce LTP) only when two events occur simultaneously. Maintenance of LTP continues as addition of New AMPA receptors occurs.

18. Spatial maps of the glutamate sensitivity of a hippocampal neuron dendrite before(left) and 120 minutes after Induction of LTP. LTP causes an increase in the glutamate response of a dendritic spine due to increase in number of AMPA receptors of a dendritic spine.

19. Early and Late phase of LTP

20. Features of LTP Strong Coincidence of Pre-Synaptic and Post- Synaptic activity to induce LTP.(post synaptic depolarization should occur with in 100ms of transmitter release by schaffer collateral which is model for learning given by Hebb.) Attractive mechanism for selective information storage because it is input specific: LTP Produced by one synapse does not affect other inactive synapse that contact the same neuron. LTP is Associative as weak stimulus releases glutamate but can’t depolarize post synaptic cell to relieve the Mg2+ Block which is done by strongly stimulated synapse.

22. Long term Depression Required because new information is to be stored and hence to prevent efficacy of LTD undergoing synapse. LTD happens when Schaffer collaterals are stimulated at a low frequency for long period. Like LTP, It also affects NMDA-type glutamate receptors. But small and slow rises in Ca+2 leads to depression where as large and fast increase in Ca+2 triggers potentiation.