Introduction to slow synaptic potentials and their neuromodulation by dopamine

1992 ◽  
Vol 70 (S1) ◽  
pp. S3-S11 ◽  
Author(s):  
Benjamin Libet
Keyword(s):  
Cyclic Gmp ◽  
Long Term Potentiation ◽  
Superior Cervical Ganglia ◽  
Postsynaptic Potential ◽  
Term Potentiation ◽  
Fluorescent Cells ◽  
Cervical Ganglia ◽  
The 1960S ◽  
Post Synaptic Potential

The existence of two muscarinically mediated slow postsynaptic potentials (PSPs) and a noncholinergic (peptidergic) late-slow PSP was established in the 1960s. These have synaptic delays and PSP durations 100–10 000 times those for the nicotinic (fast) excitatory post-synaptic potential (EPSP). Evidence is reviewed for and against the proposal that, in rabbit superior cervical ganglia, the slow (s-) inhibitory postsynaptic potential requires a second transmitter, dopamine, released by muscarinic action on interneurones (the small, intensely fluorescent cells). The s-EPSP in frog ganglia appears only in already depolarized cells by a muscarinic closure of the M (voltage-sensitive K+) channels. But the large s-EPSP in mammalian neurones, not depolarized, is generated largely via other mechanisms, especially one involving cyclic GMP. Dopamine also produces a long-term enhancement (LTE) of the muscarinic slow PSPs in rabbit superior cervical ganglia, whether dopamine is applied exogeneously or released intraganglionically by preganglionic nerve impulses at 10 s−1. LTE is producible heterosynaptically, and it persists well over 3 h; a noncholinergic (peptide?) transmitter may contribute to the initial 30 min of LTE. LTE is mediated by a D1 receptor coupled to cyclic AMP; it is blocked by cyclic GMP or low Ca2+ or calmidazolium (a calmodulin inhibitor). The modulatory process of LTE has certain similarities to, but also fundamental differences from, the long-term potentiation known in the hippocampus.Key words: muscarinic synapses, peptidergic synapses, dopamine actions, neuromodulation, postsynaptic long-term enhancement.

Induction of long-term potentiation without participation of N-methyl-D-aspartate receptors in kitten visual cortex

1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama
Keyword(s):  
Nmda Receptors ◽  
Stimulus Frequency ◽  
Low Frequency ◽  
Nmda Antagonist ◽  
Long Term Potentiation ◽  
Conditioning Stimulation ◽  
Postsynaptic Potential ◽  
Term Potentiation ◽  
Stimulation Of

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.

scholarly journals Differential expression of long-term potentiation among identified inhibitory inputs to dopamine neurons

2017 ◽  
Vol 118 (4) ◽  
pp. 1998-2008 ◽  
Author(s):  
DeNard V. Simmons ◽  
Alyssa K. Petko ◽  
Carlos A. Paladini
Keyword(s):  
Nucleus Accumbens ◽  
Adenylyl Cyclase ◽  
Ventral Tegmental Area ◽  
Cyclic Gmp ◽  
Long Term Potentiation ◽  
Dopamine Neurons ◽  
Gaba Neurons ◽  
Tegmental Nucleus ◽  
Term Potentiation

The in vivo firing pattern of ventral tegmental area (VTA) dopamine neurons is controlled by GABA afferents originating primarily from the nucleus accumbens (NAc), rostromedial tegmental nucleus (RMTg), and local GABA neurons within the VTA. Although different forms of plasticity have been observed from GABA inputs to VTA dopamine neurons, one dependent on cyclic GMP synthesis and the other on adenylyl cyclase activation, it is unknown whether plasticity is differentially expressed in each. Using an optogenetic strategy, we show that identified inhibitory postsynaptic currents (IPSCs) from local VTA GABA neurons and NAc afferents exhibit a cyclic GMP-dependent long-term potentiation (LTP) that is capable of inhibiting the firing activity of dopamine neurons. However, this form of LTP was not induced from RMTg afferents. Only an adenylyl cyclase-mediated increase in IPSCs was exhibited by all three inputs. Thus discrete plasticity mechanisms recruit overlapping but different subsets of GABA inputs to VTA dopamine neurons. NEW & NOTEWORTHY We describe a mapping of plasticity expression, mediated by different mechanisms, among three distinct GABA afferents to ventral tegmental area (VTA) dopamine neurons: the rostromedial tegmental nucleus, the nucleus accumbens, and the local GABA neurons within the VTA known to synapse on VTA dopamine neurons. This work is the first demonstration that discrete plasticity mechanisms recruit overlapping but different subsets of GABA inputs to VTA dopamine neurons.

Synaptic plasticity in sympathetic ganglia from acquired and inherited forms of ouabain-dependent hypertension

2001 ◽  
Vol 281 (2) ◽  
pp. R635-R644 ◽  
Author(s):  
Azeez A. Aileru ◽  
Aline De Albuquerque ◽  
John M. Hamlyn ◽  
Paolo Manunta ◽  
Jui R. Shah ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Neurons ◽  
Long Term Potentiation ◽  
Sympathetic Ganglia ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Term Potentiation ◽  
Compound Action Potentials ◽  
Cervical Ganglia

Altered sympathetic nervous system activity has been implicated often in hypertension. We examined short-term potentiation [posttetanic potentiation (PTP)] and long-term potentiation (LTP) in the isolated superior cervical ganglia (SCG) from Sprague-Dawley (SD) rats given vehicle, digoxin, or ouabain by subcutaneous implants as well as in animals with ouabain-induced hypertension (OHR), and inbred Baltimore ouabain-resistant (BOR) and Baltimore ouabain-sensitive (BOS) strains of rats. Postganglionic compound action potentials (CAP) were used to determine PTP and LTP following a tetanic stimulus (20 Hz, 20 s). Baseline CAP magnitude was greater in ganglia from OHR than in vehicle-treated SD rats before tetanus, but the decay time constant of PTP was significantly decreased in OHR and in rats infused with digoxin that were normotensive. In hypertensive BOS and OHR, the time constants for the decay of both PTP and LTP ( t L) were increased and correlated with blood pressure (slope = 0.15 min/mmHg, r = 0.52, P < 0.047 and 6.7 min/mmHg, r = 0.906, P < 0.0001, respectively). In BOS and OHR, t L (minutes) was 492 ± 40 ( n = 7) and 539 ± 41 ( n = 5), respectively, and differed ( P < 0.05) from BOR (257 ± 48, n = 4), SD vehicle rats (240 ± 18, n = 4), and captopril-treated OHR (370 ± 52, n = 5). After the tetanus, the CAP at 90 min in BOS and OHR SCG declined less rapidly vs. SD vehicle rats or BOR. Captopril normalized blood pressure and t L in OHR. We conclude that the duration of ganglionic LTP and blood pressure are tightly linked in ouabain-dependent hypertension. Our results favor the possibility that enhanced duration of LTP in sympathetic neurons contributes to the increase in sympathetic nerve activity in ouabain-dependent hypertension and suggest that a captopril-sensitive step mediates the link of ouabain with LTP.

scholarly journals Ganglionic Long-Term Potentiation in Prehypertensive and Hypertensive Stages of Spontaneously Hypertensive Rats Depends on GABA Modulation

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Luis A. Martínez ◽  
Fredy Cifuentes ◽  
Miguel A. Morales
Keyword(s):  
Synaptic Plasticity ◽  
Spontaneously Hypertensive Rats ◽  
Long Term Potentiation ◽  
Hypertensive Rats ◽  
Gaba A ◽  
Spontaneously Hypertensive ◽  
Term Potentiation ◽  
Cervical Ganglia ◽  
Wistar Kyoto

The sympathetic nervous system (SNS) regulates body functions in normal and pathological conditions and is characterized by the presence of a neuroplastic phenomenon, termed ganglionic long-term potentiation (gLTP). In hypertension, either in spontaneously hypertensive rats (SHR) or in humans, sympathetic hyperfunction, such as elevated SNS outflow and changes in synaptic plasticity have been described. Because enhanced SNS outflow is detected in the hypertensive stage and, more importantly, in the prehypertensive phase of SHR, here we explored whether synaptic plasticity, particularly gLTP, was modified in the superior cervical ganglia (SCG) of prehypertensive SHR. Furthermore, considering that GABA modulates sympathetic synaptic transmission and gLTP in Wistar rats, we studied whether GABA might modulate gLTP expression in SHR. We characterized gLTP in the SCG of young prehypertensive 6-week-old (wo) and adult hypertensive (12 wo) SHR and in the SCG of Wistar Kyoto (WKy) normotensive control rats of the same ages. We found that gLTP was expressed in 6 wo SHR, but not in 12 wo rats. By contrast, in WKy, gLTP was expressed in 12 wo, but not in 6 wo rats. We also found that gLTP depends on GABA modulation, as blockade of GABA-A subtype receptors with its antagonist bicuculline unmasked gLTP expression in adult SHR and young WKy. We propose that (1) activity-dependent changes in synaptic efficacy are altered not only during hypertension but also before its onset and (2) GABA may play a modulatory role in the changes in synaptic plasticity in SHR, because the blockade of GABA-A receptors unmasked the expression of gLTP. These early changes in neuroplasticity and GABA modulation of gLTP could be part of the sympathetic hyperfunction observed in hypertension.

Sevoflurane Blocks the Induction of Long-term Potentiation When Present during, but Not When Present Only before, the High-frequency Stimulation

2018 ◽  
Vol 128 (3) ◽  
pp. 555-563 ◽  
Author(s):  
Jinyang Liu ◽  
Lie Yang ◽  
Daisy Lin ◽  
James E. Cottrell ◽  
Ira S. Kass
Keyword(s):  
High Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Ca1 Region ◽  
Postsynaptic Potential ◽  
Artificial Cerebrospinal Fluid ◽  
Term Potentiation ◽  
Frequency Stimulation

Abstract Background This study tests the hypothesis that sevoflurane blocks long-term potentiation only if it is present during the high-frequency stimulation that induces long-term potentiation. Methods Long-term potentiation, an electrophysiologic correlate of memory, was induced by high-frequency stimulation and measured as a persistent increase in the field excitatory postsynaptic potential slope in the CA1 region. Results Long-term potentiation was induced in the no sevoflurane group (171 ± 58% vs. 96 ± 11%; n = 13, mean ± SD); when sevoflurane (4%) was present during the high-frequency stimulation, long-term potentiation was blocked (92 ± 22% vs. 99 ± 7%, n = 6). While sevoflurane reduced the size of the field excitatory postsynaptic potential to single test stimuli by 59 ± 17%, it did not significantly reduce the size of the field excitatory postsynaptic potentials during the 100 Hz high-frequency stimulation. If sevoflurane was removed from the artificial cerebrospinal fluid superfusing the slices 10 min before the high-frequency stimulation, then long-term potentiation was induced (185 ± 48%, n = 7); this was not different from long-term potentiation in the no sevoflurane slices (171 ± 58). Sevoflurane before, but not during, ⊖-burst stimulation, a physiologic stimulus, did not block the induction of long-term potentiation (151 ± 37% vs. 161 ± 34%, n = 7). Conclusions Sevoflurane blocks long-term potentiation formation if present during the high-frequency stimulation; this blockage of long-term potentiation does not persist if sevoflurane is discontinued before the high-frequency stimulation. These results may explain why short periods of insufficient sevoflurane anesthesia may lead to recall of painful or traumatic events during surgery.

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