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Population spike amplitude

The inset in A is a representative evoked potential recorded from the CA1 pyramidal cell layer. Calibration hards vertical 2 mV, horizontal 10 msec. The population spike amplitude was defined as an average of the amplitude from the first positive peak 1 to the succeeding negative peak 2 and the amplitude from die negative peak 2 to the second positive peak 3. A Time-course of potentiation induced by strong tetanic stimulation in the control slices (O, n=23) and in the slices treated with 30% of ethanol (IS ml/kg) (, n=27 ) and in the slices treated with 30% of ethanol (IS ml/kg) and 20 mg/kg crocin ( A, n-7). (1) and (2) indicated 30% ethanol of IS ml/kg and 10 ml/kg, respectively. Ethanol or crocin was added in the perfusing ACSF from 15 or 20 min, respectively, before tetanic stimulation. The ordinate indicates the population spike amplitude expressed as a percentage of the baseline values immediately before tetanic stimulation. [Pg.317]

B Summary ofthe effects of ethanol and crocin on the induction of LTP. The magnitude ofLTP was evaluated with die population spike amplitude 30 min after tetanic stimulation. The numbers of observations in each group are shown in parentheses. All data are represented as the mean SEM. p<0.01 vs. control, p<0.05 vs. 30% of ethanol (IS ml/kg) alone. Duncan s multiple range test. [Pg.317]

Anesthetized male Wistar rats 7-9 weeks old were used. Extracellular recording of population spike amplitude in the dentate gyrus in hippocampus were performed according to the method employed in our laboratory [10]. CSE was administered orally, ethanol was administered via three different routes, i.e. orally, intravenously or... [Pg.959]

Hippocampal slices (400-500 frm) were quickly prepared from male Wistar rats (8- to 9-weeks-old) and maintained in a chamber at 35 °C, where they were continuously perfused with artificial cerebrospinal fluid as described in our previous paper [11]. A bipolar tungsten electrode was placed in the stratum radiatum to stimulate Schaffer collateral and commissural afferents. The evoked potential was extracellularly recorded from the pyramidal cell layer of the CA1 subfield with a glass capillary microelectrode. A single test stimulation (0.05 msec duration) was applied at intervals of 30 sec. Drugs were delivered by perfusion. To induce potentiation of the evoked potentials, tetanic stimulation was applied at the same intensity through the same stimulating electrode as used for the test stimulation. The magnitude of LTP was evaluated by the population spike amplitude 30 min after tetanic stimulation. [Pg.959]

A Time-course of potentiation of population spike amplitude induced by application of tetanic stimulation (30 pulses at 60 Hz). Saline (, n=9) or ethanol (10%, A, n=5 20%, ... [Pg.961]

A Time-course of potentiation of population spike amplitude. Saline (, 0) or CSE (250 mg/kg, A ) was orally administered 30 min before tetanus, and then saline ( ) or 30% ethanol (O.A ) was orally administered 10 min later (20 min prior to tetanus). B The dose-dependency of the influence of CSE on the LTP-blocking effect of ethanol. The numbers of observations are as follows saline alone (control), n=9 ethanol alone, n=8 ethanol and 125 mg/kg CSE, n=5 ethanol and 250 mg/kg CSE, n=ll. All data are represented mean SEM of n observations. p<0.0l vs. saline group (control). p<0.01 vs. ethanol alone (Duncan s multiple range test). [Pg.962]

The firing rate of hippocampal CA1 pyramidal cells is known to depend on spatial location, that is, contextual environment information related to exploration behavior is encoded by cell activity (Hollup et al., 2001 Thompson and Best, 1990). In the present study, the population spike amplitude (PSA), measured with simultaneous determination of locomotor activity, in the CA1 field evoked by Schaffer collaterals stimulation was slightly decreased during exposure to the open field (Fig. 1). However, no significant difference in changes of synaptic transmission in the CA1 field was observed between the FS groups and non-FS controls (Koseki et al., 2007). [Pg.97]

Fig. 1. Behavioral response and hippocampal synaptic transmission during exposure to open field stress in freely moving rats. Behavior analysis and electrophysiological experiments were performed simultaneously during the postadolescent period (10-12 weeks old). (A) Locomotor activity estimated by total crossings for 30 min and (B) time-course of crossings during exposure to open field stress. (C) Time-course of population spike amplitude (PSA) in the hippocampal CA1 field evoked by Schaffer collaterals stimulation. Values are expressed as a percentage of the baseline level before open field stress. Non-FS, pups exposed to the footshock (FS) box without FS 2W-FS and 3W-FS, pups exposed to FS during the second and third postnatal weeks, respectively. Each value represents the mean S.E.M. p < 0.05 versus non-FS controls (modified from Koseki etal., 2007). Fig. 1. Behavioral response and hippocampal synaptic transmission during exposure to open field stress in freely moving rats. Behavior analysis and electrophysiological experiments were performed simultaneously during the postadolescent period (10-12 weeks old). (A) Locomotor activity estimated by total crossings for 30 min and (B) time-course of crossings during exposure to open field stress. (C) Time-course of population spike amplitude (PSA) in the hippocampal CA1 field evoked by Schaffer collaterals stimulation. Values are expressed as a percentage of the baseline level before open field stress. Non-FS, pups exposed to the footshock (FS) box without FS 2W-FS and 3W-FS, pups exposed to FS during the second and third postnatal weeks, respectively. Each value represents the mean S.E.M. p < 0.05 versus non-FS controls (modified from Koseki etal., 2007).
Contrary to the majority of published reports, some labs reported that nicotine neither enhanced nor depressed HFS-induced LTP in normal animals [85,109], For example, Itoh et al. [109] found that in slices from Ap-infused (300 pmol/day Apl 40> 11-12 days) rats, 50 pM of nicotine, perfused for 10 min, decreased population spike amplitude in area CAl of control rats. Similarly, studies by Freir et al. [85] found that coinjection of 3 mg/kg nicotine with 1 or 10 nmol Api 40,1 h prior to HFS, significantly depressed LTP, measured 1 h post-tetanus, more than Apl-40 alone. [Pg.1476]

The preparation time should be short, a prolonged ischemic penod is associated with a fall in intracellular ATP and reduction in the recovery of population spike (6-8) Although most investigators think diat the brain slice preparation should be accomplished in <5 min, another group found that there was no significant change in the amplitude of the population spike even with 30 mm postmortem delay at room temperature (9). [Pg.5]

Fig. 6. The relationship between hippocampal excitability and ambient temperature. Guinea pig slices were prepared in the usual way and incubated in standard media and perforant path stimulation held constant at a level where a 5 mV population spike was recorded from the cell body layer. In (A) are shown records recorded at five different temperatures, and (B) shows the time course of the experiment. Note at time 0 the temperature was 28°C and no activity could be elicited from the hippocampus. As the temperature was raised activity was increased until it reached a maximum of near 40 C. The temperature was then slowly lowered and the entire cycle repeated once more. At temperatures above 40°C the response declined precipitiously. In (C) the amplitude of the cumulative population spike is plotted as a function of temperature. From Skrede, Teyler and Westgaard (unpublished, quoted from Teyler, 1980.)... Fig. 6. The relationship between hippocampal excitability and ambient temperature. Guinea pig slices were prepared in the usual way and incubated in standard media and perforant path stimulation held constant at a level where a 5 mV population spike was recorded from the cell body layer. In (A) are shown records recorded at five different temperatures, and (B) shows the time course of the experiment. Note at time 0 the temperature was 28°C and no activity could be elicited from the hippocampus. As the temperature was raised activity was increased until it reached a maximum of near 40 C. The temperature was then slowly lowered and the entire cycle repeated once more. At temperatures above 40°C the response declined precipitiously. In (C) the amplitude of the cumulative population spike is plotted as a function of temperature. From Skrede, Teyler and Westgaard (unpublished, quoted from Teyler, 1980.)...
Fig. 12. The relation between field epsp amplitude and perforant path stimulus intensity in young ( ) and old (O) rats is shown for the in vivo (A) and in vitro (D) preparations. For comparison, stimulus intensity is expressed as the product of current and duration since these two parameters were varied differently in the two preparations. For the in vivo experiment, response wave forms were averaged across animals within the young (B) and old (C) groups. Superimposed traces at the various stimulus levels recorded simultaneously from the granule layer (E) and the molecular layer (F) are shown from a single slice preparation. The dashed lines in B, C, and E indicate the time of measurement of the field epsp (2 msec after stimulus onset). The sharp negative deflections in B, C, and E are population spikes (asterisks), whereas the early negative deflection in F represents the presynaptic fiber response (arrow). (From Barnes and McNaughton, 1980.)... Fig. 12. The relation between field epsp amplitude and perforant path stimulus intensity in young ( ) and old (O) rats is shown for the in vivo (A) and in vitro (D) preparations. For comparison, stimulus intensity is expressed as the product of current and duration since these two parameters were varied differently in the two preparations. For the in vivo experiment, response wave forms were averaged across animals within the young (B) and old (C) groups. Superimposed traces at the various stimulus levels recorded simultaneously from the granule layer (E) and the molecular layer (F) are shown from a single slice preparation. The dashed lines in B, C, and E indicate the time of measurement of the field epsp (2 msec after stimulus onset). The sharp negative deflections in B, C, and E are population spikes (asterisks), whereas the early negative deflection in F represents the presynaptic fiber response (arrow). (From Barnes and McNaughton, 1980.)...
Fig. 13. (A) The effect of increasing the stimulus intensity on the intracellularly recorded granule cell response, and on the extracellular response recorded simultaneously in the molecular layer. Note from this record that the latency of the action potential in the intracellular record corresponds well with the latency of the population spike in the extracellular record. Note also that the fiber potential (arrow) is not contaminated by directly activated action potentials in the granule cells. The dashed lines indicate the points from which the epsp amplitude measures were taken. (B) Relationship between intracellular epsp amplitude and the extracellularly recorded fiber potential amplitude recorded from young ( ) and old (O) rat slices. (From Barnes and McNaughton, 1980.)... Fig. 13. (A) The effect of increasing the stimulus intensity on the intracellularly recorded granule cell response, and on the extracellular response recorded simultaneously in the molecular layer. Note from this record that the latency of the action potential in the intracellular record corresponds well with the latency of the population spike in the extracellular record. Note also that the fiber potential (arrow) is not contaminated by directly activated action potentials in the granule cells. The dashed lines indicate the points from which the epsp amplitude measures were taken. (B) Relationship between intracellular epsp amplitude and the extracellularly recorded fiber potential amplitude recorded from young ( ) and old (O) rat slices. (From Barnes and McNaughton, 1980.)...

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