Role Of Hco3- Ions In Depolarizing Gaba-a Receptor-mediated Responses In Pyramidal Cells Of Rat Hippocampus
central-nervous-system; cl-channels; cortical-neurons; cultured astrocytes; dendritic inhibition; gamma-aminobutyric acid; glial-cells; guinea-pig hippocampus; long-term potentiation; mammalian; Neurosciences & Neurology; Physiology; synaptic responses
1. Activation of GABA(A) receptors can produce both hyperpolarizing and depolarizing responses in CA1 pyramidal cells. The hyperpolarizing response is mediated by a Cl- conductance, but the ionic basis of the depolarizing response is not clear. We compared the GABA(A) receptor-mediated depolarizations induced by synaptically released gamma-aminobutyric acid [GABA; depolarizing inhibitory postsynaptic potentials (dIPSPs)] with those produced by exogenous GABA (depolarizing GABA responses). Short trains of high-frequency (200 Hz) stimuli were used to generate dIPSPs. We found that dIPSPs generated by trains of stimuli and depolarizing responses to exogenous GABA were accompanied by a conductance increase and had a similar reversal potential, indicating a similar ionic basis for both responses. 2. We wished to determine whether an HCO3- current contributed to the GABA(A)-mediated depolarizations. We found that dIPSPs and depolarizing GABA responses were sensitive to perfusion with HCO3--free medium. Interpretation of these data was complicated by the mixed nature of the responses: dIPSPs were invariably accompanied by conventional, Cl--mediated fast hyperpolarizing IPSPs (fIPSPs), and response to exogenous GABA usually consisted of biphasic hyperpolarizing and depolarizing responses. However, it was sometimes possible to elicit responses to GABA that appeared purely depolarizing (monophasic depolarizing GABA responses). 3. We analyzed monophasic depolarizing GABA responses and found no change in reversal potential when slices were perfused with HCO3--free medium. We also made whole-cell recordings from CA1 pyramidal cells, attempting to reduce [HCO3-]i, and compared the reversal potential for monophasic depolarizing GABA responses with similar responses recorded with fine intracellular microelectrodes. We found no difference in reversal potential. We also examined effects of the carbonic anhydrase inhibitor acetazolamide (ACTZ) on depolarizing GABA responses. ACTZ reduced these responses but did not change their reversal potential. 4. Effects of HCO3--free medium were not specific to GABA(A) receptor-mediated responses. GABA(B) receptor-mediated slow IPSPs (sIPSPs) were also reduced, as were excitatory postsynaptic potentials (EPSPs). Analyses of field potentials and spontaneous fIPSPs suggested a decrease in presynaptic excitability during perfusion with HCO3--free medium. In addition, pyramidal cells showed decreased input resistance when perfused with HCO 3--free medium. 5. The sensitivity of GABA(A) receptor-mediated depolarizations to HCO3--free medium can be explained by a decrease in presynaptic excitability and an increased resting conductance in postsynaptic neurons. Reduced presynaptic excitability and resting input resistance are also likely causes of the reduction in fast IPSPs, slow IPSPs, and EPSPs in HCO3--free medium. We suggest that these nonspecific effects of HCO3--free medium may be a consequence of an extracellular acidification. These data do not provide convincing evidence for involvement of an HCO3- conductance in the generation of dIPSPs and depolarizing GABA responses.
Grover L M; Lambert N A; Schwartzkroin P A; Teyler T J
Journal of Neurophysiology
1993
1993-05
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1152/jn.1993.69.5.1541" target="_blank" rel="noreferrer noopener">10.1152/jn.1993.69.5.1541</a>
Haploinsufficiency In Peptidylglycine Alpha-amidating Monooxygenase Leads To Altered Synaptic Transmission In The Amygdala And Impaired Emotional Responses
acoustic startle; central-nervous-system; conditioned fear; consolidation; cytosolic domain; gastrin-releasing-peptide; lateral amygdala; long-term potentiation; memory; Neurosciences & Neurology; parvalbumin-immunoreactive interneurons; rat basolateral amygdala
Gaier E D; Rodriguiz R M; Ma X M M; Sivaramakrishnan S; Bousquet-Moore D; Wetsel W C; Eipper B A; Mains R E
Journal of Neuroscience
2010
2010-10
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1523/jneurosci.2200-10.2010" target="_blank" rel="noreferrer noopener">10.1523/jneurosci.2200-10.2010</a>
The Invitro Hippocampal Slice Preparation As A Screen For Neurotoxicity
area ca1; brain; long-term potentiation; memory; metabolite; mptp; neurons; pyramidal cells-invitro; synaptic transmission; Toxicology; trimethyltin
Fountain S B; Ting Y L T; Teyler T J
Toxicology in Vitro
1992
1992-01
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/0887-2333(92)90088-9" target="_blank" rel="noreferrer noopener">10.1016/0887-2333(92)90088-9</a>
Role of voltage-dependent calcium channel long-term potentiation (LTP) and NMDA LTP in spatial memory
hippocampus; rat; learning; verapamil; Neurosciences & Neurology; expression; neurons; long-term potentiation; environment; NMDA; MK-801; 2 forms; voltage-dependent calcium channel; nmdaLTP; spatial memory; vdccLTP; antagonist mk-801; working
This experiment explores the role of two forms of long-term potentiation (LTP) in behavioral memory. NMDA and/or voltage-dependent calcium channels (VDCCs) were antagonized pharmacologically at levels that block nmdaLTP and vdccLTP, respectively, in rats learning an eight-arm radial maze task. Animals were trained twice a day for 11 d under the systemic influence of MK-801, verapamil, both drugs, or saline. During acquisition, the mixed drug group displayed significantly more working memory errors and reference memory errors than all other groups. The mixed drug group was markedly impaired on the first daily trial but improved dramatically on their second daily trial. After a 7 d delay, saline and MK-801 animals maintained their predelay level of performance. The performance of the verapamil groups declined significantly over the delay. These results demonstrate that: (1) vdccLTP is necessary for the retention of information over a 7 dperiod, (2) the blockade of both forms of LTP prevents the retention of information over a 21 hr period, and (3) blockade of both forms of LTP does not prevent the storing of information over a short period of time (3 hr).
Borroni A M; Fichtenholtz H; Woodside B L; Teyler T J
Journal of Neuroscience
2000
2000-12
Journal Article or Conference Abstract Publication
n/a
VISUAL DEPRIVATION DECREASES LONG-TERM POTENTIATION IN RAT VISUAL CORTICAL SLICES
cortex; rat; plasticity; depression; period; Neurosciences & Neurology; pathways; induction; long-term potentiation; organization; nmda receptors; evoked-potentials; visual cortex; critical; current source density; dark rearing; monocular deprivation; source density analysis
A major finding in the visual plasticity literature is that visual deprivation is effective only during an early 'sensitive' period, which is lengthened by dark rearing. Unresolved is whether the visual cortex is in a normally plastic state prior to light stimulation. This cannot be addressed using paradigms employing light exposure to assess plasticity. Several developmental studies have investigated a plastic phenomenon termed long-term potentiation (LTP) in slices from cat (J. Neurophysiol., 59 (1988) 124-141) and rat (Brain Res., 439 (1988) 222-229) visual cortex. Susceptibility to the induction of LTP parallels the period of sensitivity to visual deprivation. This suggests that slices can be used to assay visual cortical plasticity, avoiding light exposure. In the present study, field potentials were recorded from slices of the primary visual cortices of dark-reared (DR) and control (CONT) Long Evans hooded rats (17 to 21 days). Field potential profiles recorded before and 90 min following tetanic electrical stimulation were subjected to current source density analysis, yielding extracellular current sink amplitudes. Tetanus resulted in LTP in both CONT and DR slices, but DR slices were significantly less potentiated. These results indicate that the primary visual cortex of DR animals is not fully plastic, indicating a role for light stimulation in inducing visual cortical plasticity.
Berry R L; Perkins A T; Teyler T J
Brain Research
1993
1993-11
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/0006-8993(93)90943-h" target="_blank" rel="noreferrer noopener">10.1016/0006-8993(93)90943-h</a>
Forms of associative synaptic plasticity
2 forms; apical dendrites; area ca1; glutamate; hippocampal ca1; in-vivo; long-term potentiation; ltp; nmda receptors; protein-phosphorylation; receptors
Teyler T J
2001
2001
Book/Monograph
n/a
NMDA receptors and voltage-dependent calcium channels mediate different aspects of acquisition and retention of a spatial memory task
2 forms; activation; anesthetized rats; antagonists cpp; area ca1; Behavioral Sciences; hippocampus; in-vivo; learning; long-term potentiation; ltp; ltp; Neurosciences & Neurology; nmdaLTP; Psychology; spatial; spatial memory; synaptic plasticity; vdccLTP
Activity dependent calcium entry into neurons can initiate a form of synaptic plasticity called long-term potentiation (LTP). This phenomenon is considered by many to be one possible cellular mechanism underlying learning and memory. The calcium entry that induces this phenomenon can occur when N-methyl-D-aspartate receptors (NMDARs) and/or voltage-dependent calcium channels (VDCCs) are activated. While much is known about synaptic plasticity and the mechanisms that are triggered by activation of these two Ca2+ channels, it is unclear what roles they play in learning. To better understand the role activation of these channels may play in learning we systemically administered pharmacological antagonists to block NMDARs, VDCCs, or both during training trials and retention tests in a radial arm maze task. Wistar rats injected with the NMDAR antagonist MK-801 (0.1 mg/kg) were impaired in the acquisition of this task. In contrast, rats injected with verapamil (10 mg/kg), an antagonist to VDCCs, acquired the task at the same rate as control animals, but were impaired on a 10-day retention test. A group of animals injected with both antagonists were unable to learn the task. The results suggest that each of the calcium channels and the processes they trigger are involved in a different stage of memory formation or expression. (C) 2003 Elsevier Inc. All rights reserved.
Woodside B L; Borroni A M; Hammonds M D; Teyler T J
Neurobiology of Learning and Memory
2004
2004-03
Journal Article
<a href="http://doi.org/10.1016/j.nlm.2003.10.003" target="_blank" rel="noreferrer noopener">10.1016/j.nlm.2003.10.003</a>
BDNF protects against stress-induced impairments in spatial learning and memory and UP
adult-rat; brain; central-nervous-system; hippocampal pyramidal neurons; hippocampus; in-vivo; knockout mice; long-term potentiation; neuroprotection; Neurosciences & Neurology; neurotrophic factor; neurotrophins; rat; synaptic plasticity; synaptic transmission
The present study investigated whether infusion of brain-derived neurotrophic factor (BDNF) could ameliorate stress-induced impairments in spatial learning and memory as well as hippocampal long-term potentiation (LTP) of rats. Chronic immobilization stress (2 h/day X 7 days) significantly impaired spatial performance in the Morris water maze, elevated plasma corticosterone, and attenuated LTP in hippocampal slices from these animals as compared with normal control subjects. BDNF was infused into the left hippocampus (0.5 mu l/h) for 14 days, beginning 7 days before the stress exposure. The BDNF group was protected from the deleterious effects of stress and performed at a level indistinguishable from normal control animals despite the presence of elevated corticosterone. BDNF alone and sham infusions had no effect on performance or LTP. These results demonstrate that spatial learning and memory, and LTP, a candidate neural substrate of learning and memory, are compromised during chronic stress, and may be protected by BDNF administration. (c) 2004 Wiley-Liss, Inc.
Radecki D T; Brown L M; Martinez J; Teyler T J
Hippocampus
2005
2005
Journal Article
<a href="http://doi.org/10.1002/hipo.20048" target="_blank" rel="noreferrer noopener">10.1002/hipo.20048</a>