Investigation of β-adrenergic modulation of synaptic transmission and postsynaptic induction of associative LTP in layer V neurones in slices of rat sensorimotor cortex

1992 ◽  
Vol 137 (2) ◽  
pp. 270-273 ◽  
Author(s):  
Alex V. Nowicky ◽  
Geri Christofi ◽  
Lynn J. Bindman
1998 ◽  
Vol 79 (2) ◽  
pp. 937-946 ◽  
Author(s):  
B. D. Bennett ◽  
J. R. Huguenard ◽  
D. A. Prince

Bennett, B. D., J. R. Huguenard, and D. A. Prince. Adrenergic modulation of GABAA receptor-mediated inhibition in rat sensorimotor cortex. J. Neurophysiol. 79: 937–946, 1998. The effect of adrenoceptor activation on pharmacologically isolated monosynaptic inhibitory postsynaptic currents (IPSCs) detected in layer V pyramidal neurons was examined by using whole cell voltage-clamp in a slice preparation of rat sensorimotor cortex. Epinephrine (EPI; 10 μM) reversibly altered the amplitude of evoked IPSCs (eIPSCs) in slices from postnatal day 9–12 (P9–12) and P15–18 rats. The effects of EPI were heterogeneous in both age groups, and in individual cases an enhancement, a depression or no effect of eIPSCs was observed, although depression was observed more commonly in the younger age group. The effects of EPI on eIPSC amplitude were likely mediated through presynaptic mechanisms because they occurred in the absence of any alteration in the current produced by direct application of γ-aminobutyric acid (GABA), or in input resistance. EPI always elicited an increase in the frequency of spontaneous IPSCs (sIPSCs) irrespective of whether or not it induced any change in the amplitude of eIPSCs in the same neuron. The increase in sIPSC frequency was blocked by phentolamine (10 μM) but not by propranolol (10 μM), supporting the conclusion that EPI-mediated effects on sIPSC frequency result from activation of α-adrenoceptors located on presynaptic inhibitory interneurons. In a subpopulation of neurons (3/9) from P15–18 rats, EPI increased both the amplitude and frequency of miniature IPSCs (mIPSCs) recorded in the presence of tetrodotoxin (TTX) and under conditions where postsynaptic EPI effects were blocked, suggesting activation of adrenoceptors on presynaptic terminals in these cells. Results of these experiments are consistent with an action of EPI at adrenoceptors located on presynaptic GABAergic interneurons. Adrenergic activation thus has multiple and complex influences on excitability in cortical circuits, some of which are a consequence of interactions that regulate the strength of GABAergic inhibition.


2010 ◽  
Vol 103 (5) ◽  
pp. 2876-2888 ◽  
Author(s):  
Yuko Koyanagi ◽  
Kiyofumi Yamamoto ◽  
Yoshiyuki Oi ◽  
Noriaki Koshikawa ◽  
Masayuki Kobayashi

β-Adrenoceptors play a crucial role in the regulation of taste aversion learning in the insular cortex (IC). However, β-adrenergic effects on inhibitory synaptic transmission mediated by γ-aminobutyric acid (GABA) remain unknown. To elucidate the mechanisms of β-adrenergic modulation of inhibitory synaptic transmission, we performed paired whole cell patch-clamp recordings from layer V GABAergic interneurons and pyramidal cells of rat IC aged from postnatal day 17 (PD17) to PD46 and examined the effects of isoproterenol, a β-adrenoceptor agonist, on unitary inhibitory postsynaptic currents (uIPSCs). Isoproterenol (100 μM) induced facilitating effects on uIPSCs in 33.3% of cell pairs accompanied by decreases in coefficient of variation (CV) of the first uIPSC amplitude and paired-pulse ratio (PPR) of the second to first uIPSC amplitude, whereas 35.9% of pairs showed suppressive effects of isoproterenol on uIPSC amplitude obtained from fast spiking (FS) to pyramidal cell pairs. Facilitatory effects of isoproterenol were frequently observed in FS–pyramidal cell pairs at ≥PD24. On the other hand, isoproterenol suppressed uIPSC amplitude by 52.3 and 39.8% in low-threshold spike (LTS)–pyramidal and late spiking (LS)–pyramidal cell pairs, respectively, with increases in CV and PPR. The isoproterenol-induced suppressive effects were blocked by preapplication of 100 μM propranolol, a β-adrenoceptor antagonist. There was no significant correlation between age and changes of uIPSCs in LTS–/LS–pyramidal cell pairs. These results suggest the presence of differential mechanisms in presynaptic GABA release and/or postsynaptic GABAA receptor-related assemblies among interneuron subtypes. Age- and interneuron subtype-specific β-adrenergic modulation of IPSCs may contribute to experience-dependent plasticity in the IC.


2000 ◽  
Vol 83 (5) ◽  
pp. 2519-2525 ◽  
Author(s):  
D. Ieuan Evans ◽  
Roland S. G. Jones ◽  
Gavin Woodhall

The role of group III metabotropic glutamate receptors (mGluRs) in modulating excitatory synaptic transmission was investigated in the rat entorhinal cortex (EC) in vitro. AMPA receptor-mediated excitatory postsynaptic currents (EPSCs) were recorded in the whole cell configuration of the patch-clamp technique from visually identified neurons in layers V and II. In layer V, bath application of the specific group III mGluR agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4, 500 μM) resulted in a marked facilitation of both spontaneous and activity-independent “miniature” (s/mEPSC) event frequency. The facilitatory effect of L-AP4 (100 μM) on sEPSC frequency prevailed in the presence ofdl−2-amino-5-phosphonopentanoic acid (100 μM) but was abolished by the group III antagonist (RS)-cyclopropyl-4-phosphonophenylglycine (20 μM). These data confirmed that group III mGluRs, and not N-methyl-d-aspartate (NMDA) receptors were involved in the response to L-AP4. Bath application of the specific mGluR4a agonist (1S,3R,4S)-1-aminocyclopentane-1,2,4-tricarboxylic acid (20 μM) also had a facilitatory effect on sEPSC frequency, suggesting involvement of mGluR4a. In layer II neurons, L-AP4 caused a reduction in sEPSC frequency but did not affect mEPSCs recorded in the presence of tetrodotoxin. These findings suggest that a group III mGluR with mGluR4a-like pharmacology is involved in modulating synaptic transmission in layer V cells of the EC. The effect on mEPSCs suggests that this receptor is located presynaptically and that its activation results in a direct facilitation of glutamate release. This novel facilitatory effect is specific to layer V and, to our knowledge, is the first report of a direct facilitatory action of group III mGluRs on synaptic transmission. In layer II, L-AP4 had an inhibitory effect on glutamate release similar to that reported in other brain regions.


1983 ◽  
Vol 49 (3) ◽  
pp. 780-791 ◽  
Author(s):  
C. D. Woody ◽  
E. H. Kim ◽  
N. E. Berthier

1. The activity of single units of the coronal pericruciate (CPC) cortex was studied in 11 awake cats during sessions in which a click conditioned stimulus (CS) was repeatedly paired with glabella tap unconditioned stimulus (US) and hypothalamic stimulation (HS). Effects of HS on the activity of cortical units were also studied during sessions in which HS alone was delivered repeatedly every 10 s. 2. HS evoked an increase in spike activity of less than 60 ms latency in 89 of 116 units tested. 3. Repeated presentation of HS that was effective in producing rapid behavioral conditioning resulted in a characteristic reduction in the latency of discharge evoked by HS in cortical units. 4. Short-latency activation (less than 20 ms) of units of the sensorimotor cortex appeared to be characteristic of HS that led to enhanced rates of conditioned response (CR) acquisition. One of the cells responding in this way was identified as a pyramidal cell of layer V by intracellular injection of horseradish peroxidase (HRP). 5. Further analyses of activity were performed on 16 units of the CPC cortex that were followed through conditioning (or reconditioning) and extinction of the CR. After less than 10 CS-US-HS pairings, there was a selective augmentation of unit response to the CS but not of response to an explicitly unpaired discriminative stimulus (DS). Responses to the CS were not similarly augmented when presentations of HS preceded rather than followed the presentations of the CS and US. The rapid development of CS-evoked unit activity coincided with the rapid acquisition of discriminative CRs behaviorally. 6. During conditioning, the most conspicuous increases in CS-evoked unit response occurred at latencies 100 ms or more after onset of the click CS. This corresponded with the behavioral observation that the majority of eye blink CRs occurred with onset latencies longer than 100 ms.


1998 ◽  
Vol 10 (4) ◽  
pp. 821-835 ◽  
Author(s):  
Misha Tsodyks ◽  
Klaus Pawelzik ◽  
Henry Markram

Transmission across neocortical synapses depends on the frequency of presynaptic activity (Thomson & Deuchars, 1994). Interpyramidal synapses in layer V exhibit fast depression of synaptic transmission, while other types of synapses exhibit facilitation of transmission. To study the role of dynamic synapses in network computation, we propose a unified phenomenological model that allows computation of the postsynaptic current generated by both types of synapses when driven by an arbitrary pattern of action potential (AP) activity in a presynaptic population. Using this formalism, we analyze different regimes of synaptic transmission and demonstrate that dynamic synapses transmit different aspects of the presynaptic activity depending on the average presynaptic frequency. The model also allows for derivation of mean-field equations, which govern the activity of large, interconnected networks. We show that the dynamics of synaptic transmission results in complex sets of regular and irregular regimes of network activity.


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