Molecular Basis of Long-Term Potentiation

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Chapter 3: Binocular and Monocular Recording and Induction

Gathered from the review of the previous literature, visual hLTP appears to be occurring in the visual cortex. However, the original non-invasive paradigm has a limitation, the potentiation was induced to either one or both visual fields. Hence, this meant that visual hLTP could have occurred at any point between the ascending visual pathways and the visual cortex. Further testing was conducted to extend what is currently know in regards to where visual hLTP is occurring in the human brain.
When the left and right eyes register information, the visual content travels along the ascending visual pathways until the information is combined in the visual neocortex (e.g. Baccus & Meister, 2004; Hubel, Wiesel, & Stryker, 1977). In other words, the visual pathways remain separate until the information from each eye is combined in the neocortical region. Therefore, the effect known as inter-ocular transfer can potentially provide more information regarding where visual hLTP is occurring in the human brain (Gilbert et al., 2001; Lu et al., 2005).
If high-frequency visual stimulation is presented to only one eye but hLTP is also seen when the post-induction stimulus is presented to the non-induced eye, it will indicate visual hLTP is occurring in the cortical area. On the other hand, if sensory induced LTP is only evident in the eye that receives the LTP-inducing stimulus, it will suggest that visual hLTP is more likely taking place in the ascending visual pathways. The following experiments incorporated the methodology of inter-ocular transfer with the experimental protocols as carried out in experiment one to examine where visual hLTP is occurring in the brain.

Experiment Two

Like experiment one, experiment two also had both design one and two. In addition, experiment two also allocated participants to receiving the LTP-inducing stimulus to either their left or right eye while the other is covered with an eye patch. Furthermore, during the pre-induction and post-induction blocks, VEP recordings were only taken from the eye that did not receive rapid sensory stimulation. Recording VEP with only one eye viewing the stimuli contrasts to the original non-invasive paradigm (Teyler et al., 2005) and experiment one where both eyes viewed the stimuli during baseline recording. If significant potentiation is still reported it will suggest that hLTP is occurring in the visual cortical area. Failure to induce hLTP will suggest that the effect is likely to have occurred in the ascending visual pathways. This set of experimental protocols should provide some information regarding where visual hLTP is occurring in the brain.

Methods

Participants

A new group of males (16) gave their informed consent prior to participating in the experiment. All the participants reported normal, or corrected to normal vision. The participant’s ages ranged from 18 to 28 years (M = 21.44, SD = 5.07). Half of the participants were right eye dominant and the other half were left eye dominant as determined using the Miles test (Porac & Coren, 1976). All the participants were classified as right-handed by having a laterality quotient of 50 or greater on the Edinburgh Inventory (Oldfield, 1971). The participants’ laterality quotient ranged from 68 to 100, with an average quotient of 91.73 (SD 72). All the participants were reimbursed with $20 petrol vouchers for their participation in the experiment. The University of Auckland Human Participants Ethics Committee approved the experimental procedures.

Stimuli

A flashing circular checkerboard stimulus was presented to participants during the experiment. The stimulus had a diameter subtending 8° of visual angle and was presented on a grey background at full contrast (refer to Figure 2). The presentation of the stimulus was controlled using E-Prime version 2.0.8.22 Psychology Software and presented on a Samsung Sync Master P2270 computer monitor (dimension: 47.5cm x 27cm, resolution: 1920 x 1080 pixels, refresh rate: 60Hz). The screen luminance was measured with a Konica Minolta LS- Luminance Meter before (M =43cd/m2, SD = 2.75) and after (M = 50.16cd/m2, SD = 2.04) the experiment. All the participants maintained a viewing distance of 57cm from the monitor.

Procedure

The participants were evenly allocated into design one and two as described in Chapter 2 (refer to Table 3) with two changes to the procedure. Firstly, during the induction block the LTP-inducing stimulus was only presented to the left or right eye while the other eye was covered with an eye patch. Secondly, during the pre-induction and post-induction blocks VEP was recorded monocularly from the non-induced eye while the other eye was covered with an eye patch.

Electroencephalographic Recording

EEG was recorded continuously with 1000Hz sampling rate and 0.1 – 100Hz analogue band-pass filter, using 128- channel Ag/AgCl electrode nets (Electrical Geodesics Inc., Eugene, OR, USA). All electrode impedances were below 40kΩ, this is an acceptable level for this system (Ferree, Luu, Russell, & Tucker, 2001). The recordings were taken in an electrically-shielded room. EEG was acquired using a common vertex (Cz) reference and later re-referenced to the average reference off-line.

Data Analysis

Electroencephalographic recordings were segmented into epochs comprising of a 100ms pre-stimulus baseline and a 500ms period post-stimulus onset. From all waveforms, DC offsets were calculated from the pre-stimulus baseline and were removed. The correction of eye-movement artifacts were made on all segments using the method suggested by Jervis, Nichols, Allen, Hudson, and Johnson (1985). Epoch is discarded if either eye have “moved” or “blinked. Trigger and stimulus synchronization accounted for the 8ms delay the hardware filters imposed upon the EEG signals. For each individual participant, the average over the N1b time window was obtained from two clusters of seven electrodes centred on approximately P7 and P8 under the 10-20 system (Luu & Ferree, 2000), as seen in Figure 4.
In the preliminary analysis, dominant eye (left and right), hemisphere (left and right), induced eye (left and right), viewing eye (left and right), and block (Pre1/Pre2/Post1/Post2/Post3 and Pre1/Pre2/Pre3/Post1/Post2) were involved as factors in the analysis. Dominant eye, hemisphere, induced eye, and viewing eye never reached significance as main effects or interaction. Therefore, the data was reanalyzed with only block (Pre1/Pre2/Post1/Post2/Post3 and Pre1/Pre2/Pre3/Post1/Post2) as a within subject factor. If sphericity cannot be assumed on F-statistics, Greenhouse-Geisser corrections were utilized.
Planned contrasts were employed to test critical predictions. For design one (refer to Table 1), the first contrast compared the pre-induction blocks for stability and was predicted to be non-significant. Contrast two and three investigated the linear and quadratic trends over post-induction blocks to determine if there is any decrease over blocks due to repeated testing which could potentially result in long-term depression (Teyler et al., 2005). The last contrast compared pre-induction to post-induction blocks and this is the critical test for LTP.
For design two (refer to Table 2), contrast one and two investigated the linear and quadratic trends over the pre-induction blocks and these were expected to be non-significant. Contrast three compared the post-induction blocks for stability and was predicted to be non-significant. The last contrast compared the pre-induction to post-induction blocks and this is the critical test for hLTP. In all the experiments, none of the pre and post stability contrasts reached significance and so only the critical post-pre contrast testing for hLTP will be presented.
To investigate the odds of any change to the N1b component being due to effects of altered attention or general cortical excitation, the amplitude of the P1 and P2 component were also analyzed in a similar way to the amplitude of the N1b component.

Chapter 1: General Introduction
1.1 Long-Term Potentiation
1.2 Molecular Basis of Long-Term Potentiation
1.3 Phases of Long-Term Potentiation
1.4 Properties of Long-Term Potentiation
1.5 Long-Term Depression
1.6 Prior Study of Long-Term Potentiation
1.7 Adrenal Glands
1.8 Corticosterone and Memory Performance
1.9 Corticosterone and Long-Term Potentiation
1.10 New Non-Invasive Induction and Measurement of Long-Term Potentiation
1.11 NMDA Receptor Dependence of Long-Term Potentiation
1.12 Input-Specificity of Long-Term Potentiation
1.13 Locus of Visual Human Long-Term Potentiation
1.14 Inter-Ocular Transfer
1.15 Cortisol and Memory
1.16 Cortisol and Long-Term Potentiation
1.17 Aims of the Current Thesis
Chapter 2: Experiment One
2.1 Methods
2.2 Results
2.3 Discussion
Chapter 3: Binocular and Monocular Recording and Induction
3.1 Experiment Two
3.2 Experiment Three.
3.3 Experiment Four
3.4 Experiment Five
3.5 Further Analysis
3.6 Discussion
Chapter 4: Cortisol and Human Long-Term Potentiation
4.1 Experiment Six
4.2 Experiment Seven
4.3 Experiment Eight
4.4 Comparison
4.5 Discussion.
Chapter 5: General Discussion
5.1 Summary of Findings
5.2 Clinical Implications of Human Long-Term Potentiation
5.3 Concluding Remarks
References
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Visual human long-term potentiation

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