Schaffer collateral

Nearly all mechanistic studies of LTP have been carried out in the CAl region of hippocampal slices, where Schaffer collateral/commissural fibres make monosynaptic contacts with the dendrites of CAl pyramidal cells. It is generally accepted that the... 

Ammonia has deleterious effects on brain function by direct and indirect mechanisms. Concentrations of ammonia in the 1-2 mmol/1 range, equivalent to those reported in the brain in liver failure, impair postsynaptic inhibition in cerebral cortex and brainstem by a direct effect on Cl extrusion from the postsynaptic neuron. Millimolar concentrations of ammonia also inhibit excitatory neurotransmission. Synaptic transmission from Schaffer collaterals to CA1 hippocampal neurons is reversibly depressed by 1 mmol/1 ammonia, and the firing of CA1 neurons by iontophoretic application of glutamate is inhibited by 2 mmol/1 ammonia [10],... 

It is well-established that the induction mechanism of LTP at the CA3-CA1 synapse of the Schaffer collateral pathway requires postsynaptic activation of the NMDA receptors (Ch. 15). The NMDA receptor seems to be a perfect cellular device to detect the synaptic coincidence between pre-synaptic and post-synaptic neurons, and to associate two events at the cellular level [8]. 

Figure 1. A. SimpMed diagram of the rodent hippocampal formation illustrating the major glutamatergic circuitry. The principal neuronal helds granule cells (GC) of the dentate gyrus and pyramidal cells of CAl and CA3 in Ammon s horn are shown. The main excitatory connections are also indicated the perforant path from entorhinal cortex to the granule cells, from there the mossy hbre (mf) axonal projections to CA3 and then the Schaffer collaterals (Sch) from CA3 to ipsilateral CAl and commissural (Comm) to contralateral CAl cells. Evoked responses in (B) were obtained by stimulating the afferent pathway from entorhinal cortex, the medial perforant path (Med), and recording the granule cell (GC) response in the hilus of the dentate gyrus.

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. 

Collingridge, G. L., Kehl, S. J. and McLennan, H. (1983) Excitatory amino acids in synaptic transmission in the Schaffer collateral-commissural pathway of the rat hippocampus. J Physiol (Lond) 334, 33-46. 

Endocannabinoids have also been suggested to participate in long-term synaptic potentiation (LTP), a widely recognized model of synaptic changes underlying learning and memory (Malenka and Bear 2004). Prior to discovery of the CB1 receptor, one study indicated that A9-THC alters hippocampal LTP (Nowicky et al. 1987). Activation of CB1 receptors by 2-AG was shown to prevent LTP induction at Schaffer collateral-CAl pyramidal cell synapses in hippocampus (Stella et al. 

Starke K (1981) Presynaptic receptors. Annu Rev Pharmacol Toxicol 21 7-30 Suarez LM, Solis JM (2006) Taurine potentiates presynaptic NMDA receptors in hippocampal Schaffer collateral axons. European Journal of Neuroscience 24 405-18... 

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). 

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).

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