Associativity

Augmentation

coincidence detector

In the hippocampus, the enhancement of a weakly activated group of synapses when a nearby group is strongly activated. 

worsening of symptoms due to ongoing treatment

a process by which a neuron or a neural circuit can encode information by detecting the occurrence of temporally close but spatially distributed input signals.

Timing-dependent activity, probably the result of calcium signaling in the postsynaptic cell, that is required for the establishment of some forms of synaptic plasticity. 

What is plasticity?

Describe Briefly the short term responses. 

Synaptic connectivity between neurons is dynamic and constantly changing. 

Short-term plasticity affect the amount of neurotransmitter released. 

Facilitation, augmentation, and potentiation enhance neurotransmitter release and are caused by persistent actions of calcium ions within the presynaptic terminal. 

Another form of short term plasticity, synaptic depression, decreases the amount of neurotransmitter released and appears to be due to an activity-dependent depletion of synaptic vesicles. 

Long term forms of synaptic plasticity alter synaptic transmission over time scales of 30 minutes or longer. 

Initial changes in synaptic transmission arise from posttranslational modifications of existing proteins, most notably changes in the trafficking of glutamate receptors, while later phases of synaptic modification result from changes in gene expression. 

Result in enduring changes such as synaptic growth. 

Causes neurotransmitter release to decline during sustained synaptic activity. Lowering external calcium concentration slowed the rate of synaptic depression. 

Depression is proportional to neurotransmitters released.

Caused by progressive depletion of a pool of synaptic vesicles that are available for release. 

Rapid increase in synaptic strength that occurs when two or more action potentials invade the presynaptic terminal within a few milliseconds of each other. 

Result of prolonged elevation of presynaptic calcium levels following synaptic activity. 

Slow mechanism to return calcium levels to normal so signals that are close together result in a build up. 

Don't know what this residual calcium targets, potentially synaptotagmin. 

Enhances the ability of incoming calcium ions to trigger fusion of synaptic vesicles with the plasma membrane. 

Augmentation rises and falls over a few seconds. 

Poorly understood mechanism, proposed that augementation results from calcium enhancing the actions of the presynaptic protein munc-13. 

What is responsible for the short-term changes in synaptic strength in post-tetanic potentiation?

Same as potentiation

Enhances the ability of incoming calcium ions to trigger fusion of synaptic vesicles with the plasma membrane. 

Acts over a time sccale of tens of seconds to minutes. 

May arise when calcium activates presynaptic protein kinases that go on to phosphorylate substrates that regulate transmitter release. 

During repetitive synaptic activity, these forms of short-term plasticity can interact to cause synaptic transmission to change in complex ways. 

The process that causes the animal to become less responsive to repeated occurrences of a stumuli. 

Repeated light touches to the siphon of the mollusk resulted in the decrease in response of gill withdrawal. 

Sensitization is the process by which an animal generalizes a noxious response to a non-harmful one. 

In the mollusk they sensitized gill withdrawal by pairing a strong electrical stimulus to the animal's tail with another light touch of the siphon. 

Transmission at the flutamatergic synapse between the sensory and motor neurons is depressed. This synaptic depression is thought to be responsible for the decreasing ability of siphon stimuli to evoke gill contraction. 

Depression is due to the reduction in number of vesicles. 

Sensory neurons arew stimulated and then excite modulatory interneurons that release serotonin onto the presynaptic terminals of the sensory neurons of the syphon. Serotonin enhances neurotransmitter release and thus increases the stimulation of the post synaptic motor cell. 

Serotonin binds to a G-coupled protein receptor and stimulates the production of cAMP. cAMP activates protein kinase A that goes on to phosphorylate other proteins probably including K+ channels. This would inhibit the k+ channels increasing the pre-synaptic stimulus. Serotonin also stimulates the increased movement of calcium into the cell. 

It is thought to occur in a similar manner to the short term, except there is a prolonged effect that leads to the transcriptional activator CREB to stimulate production of the proteins involved in the response. 

Ubiquitin hydrxylase is synthesized and this degrades the regulatory subunit of PKA causing persistent activity. 

AD is a type of dementia(most common) 60-80% of cases in elderly. Afflicts 5-10% of pop. Dementia is a syndrome characterized by failure of recent memory and other intellectual functions. 

Brain weigh decreases, but we don't think that the actual number of neurons decreases. There is on the other hand a decrease in synaptic connections. 

Difficult time learning new skills. 

(only possible to trully diagnose in post-mortum)

Mild forgetfulness.

More serious symptoms of disease. interferes with daily life and cannot recognize people or familiar places. 

Anxiety, aggression or wandering away from home

Confined to nursing home and death. 

Chromosome 21 mutations. Mutation of the gene encoding amyloid precursor protein. Mutations identified in almost 20 families of early onset autosomal form of AD.

Presenilin 1 and 3 mutations. Result in increased amount of a toxic form of A beta peptide called Abeta42 

Sometimes the breakdown product of proteins can be toxic. Abeta42. 

Causes formation of beta amyloid plaques. 

Presenilin 1 and 2 proteins interfere with the alpha secretase enzyme that breaks down amyloid. 

Who began work on the long term potentiation?

What did they find/show?

Terje Lumo and timothy bliss. 

Found that a few seconds of high-frequency electrical stimulation can enhance syaptic transmission in the rabbit hippocampus for days or even weeks. 

In the CA1 cells what happens when there is a stimulus from schaaffer collaterals only 2-3 times per minute. 

What happens when you send a high frequency train of signals?

You see a constant EPSP in the CA1 neurons. 

You see an LTP form. This is due to the long lasting increase in EPSP amplitude. 

1. LTP requires a strong activity in both pre- and post-synaptic neurons. 

2. LTP is input specific. It only occurs in the synapse that is activated. 

3. associativity: Weak stimulation of a pathway will not trigger LTP but if you have strong activation neighboring a weakly activated pathway then you do see LTP in both. 

It is carried out through the alteration of gene expression. This is initiated by protein kinase A. Which activates CREB. CREB then stimulates the expression of other proteins, including transcription factors, protein kinases, and AMPA receptors. 

Not known what these proteins due but it is possible that they help construct new synaptic contracts. 

Storage and retrieval of material that is avalable to consciousness and can in princliple be expressed by language. 

Examples of declarative memory are the ability to rememver a phone number, a song, or a past event. 

Immediate memory: Routine ability to hold ongoing experiences in mind for fractions of a second. 

Working memory: the ability to hold and manipulate information in mind for seconds to minutes while it is used to achieve a particular short goal. 

Long-term memory: entails retaining information in a more permanent form of storage for days weeks, or even a lifetime. Memories from one type can enter a different type. 

change in the processing of a stimulus due a previous encounter with the same or a related stimulus with or without conscious awareness of the original encounter

Chess experts were able to remember the location of chess pieces in a real game much better than the average people but the average person did slightly better when the pieces were placed at random. 

We remember best when the thing has meaning. 

What did they find in London taxi drivers?

They found that taxi drivers had larger posterior hippocampi and that the longer they were taxi drivers the larger their posterior hippocampus. 

This region is responsible for spatial information.