Deep neurons in piriform cortex. I. Morphology and synaptically evoked responses including a unique high-amplitude paired shock facilitation

1989 ◽  
Vol 62 (2) ◽  
pp. 369-385 ◽  
Author(s):  
G. F. Tseng ◽  
L. B. Haberly
Keyword(s):  
Lucifer Yellow ◽  
Piriform Cortex ◽  
Afferent Fiber ◽  
Pyramidal Cells ◽  
Excitatory Postsynaptic Potential ◽  
Response Properties ◽  
Postsynaptic Potential ◽  
Association Fibers ◽  
Axonal Arbors ◽  
Stimulation Of

1. Synaptic responses of cells in layer III of the piriform cortex and the subjacent endopiriform nucleus (layer IV) were analyzed with intracellular recording techniques in a slice preparation from the rat, cut perpendicular to the pial surface. 2. Micropipettes containing Lucifer yellow (LY) were used to correlate response properties with morphology. An antiserum to LY was used to intensify staining and to prevent fading during detailed morphological study. Response properties were also examined with potassium acetate-containing electrodes. 3. Morphologically, two cell types were identified: pyramidal cells that were confined to layer III of the piriform cortex and multipolar cells that were in layer III and the endopiriform nucleus. 4. In morphology, deep pyramidal cells in layer III closely resembled superficial pyramidal cells in layer II, with the exception that primary apical dendritic trunks were longer and basal dendritic arborizations were more extensive than apical. Like superficial pyramidal cells, apical dendrites of all deep pyramidal cells stained extended through the afferent fiber termination zone in layer Ia and gave rise to local axonal arbors that were concentrated in layer III and the endopiriform nucleus. 5. Multipolar cells were morphologically indistinguishable in layer III and the endopiriform nucleus. All gave rise to nonvaricose spiny dendrites that never extended into layer II and local axonal arbors. 6. Response properties of deep pyramidal and multipolar cells were similar; responses of both of these populations were very different from those of superficial pyramidal cells. The primary difference between responses of deep pyramidal and multipolar cells was a shorter latency of postsynaptic potentials evoked in deep pyramidal cells by stimulation of afferent fibers, consistent with the extension of their dendrites into layer Ia. 7. Responses of most deep cells to stimulation of afferent and association fibers at sufficiently high strength consisted of an initial excitatory postsynaptic potential (EPSP), followed by a fast Cl- -mediated and a slow K+-mediated inhibitory postsynaptic potential (IPSP). 8. A characteristic feature of deep cells, which was only rarely observed in superficial pyramidal cells, was the presence of variable EPSPs evoked at long latencies (greater than 100 ms) by stimulation of afferent or association fibers. 9. A striking finding for deep pyramidal and multipolar cells, when studied with LY-containing pipettes, was a variable slowly rising depolarizing potential triggered at depolarized membrane potentials by stimulation of afferent or association fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of association fiber system in piriform cortex with intracellular recording and staining techniques

1984 ◽  
Vol 51 (1) ◽  
pp. 90-112 ◽  
Author(s):  
L. B. Haberly ◽  
J. M. Bower
Keyword(s):  
Intracellular Recording ◽  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Excitatory Postsynaptic Potential ◽  
Fiber System ◽  
Direct Stimulation ◽  
Postsynaptic Potential ◽  
Staining Techniques ◽  
Monosynaptic Epsp ◽  
Stimulation Of

The piriform cortex of the opossum has been studied with intracellular recording and staining techniques. The experiments were designed to investigate the association fiber system, but the results have also revealed new properties of the afferent fiber system from the olfactory bulb and the inhibitory systems within the piriform cortex. Following shock stimulation of the lateral olfactory tract (LOT), the response of pyramidal cells consists of an initial excitatory postsynaptic potential (EPSP) followed by a long-lasting inhibitory postsynaptic potential (IPSP). The LOT-evoked EPSP consists of two components: an initial monosynaptic followed by a disynaptic component. The monosynaptic EPSP can be isolated by the use of conditioning LOT shocks to block the IPSP and disynaptic EPSP. The disynaptic EPSP can be demonstrated by cutting LOT fibers at the surface of the cortex to eliminate the monosynaptic EPSP and by the use of bicuculline to block the IPSP. The latency of the IPSP is sufficiently brief so that the disynaptic EPSP is blocked at presumed intrasomatic recording sites unless these experimental manipulations are carried out. In all histologically verified pyramidal cells in both layers II and III in which the appropriate tests were carried out, both mono- and disynaptic EPSP components were present. It was concluded on the basis of anatomical considerations, however, that a small number of pyramidal cells would be expected to receive only a disynaptic EPSP. Evidence that the LOT-evoked disynaptic EPSP is mediated, at least in part, by association axons was provided by direct stimulation of these fibers in layer III and by demonstrating that the EPSP is present distal to cuts that sever LOT axons. Direct stimulation of association axons in layer III evokes both a monosynaptic EPSP and a disynaptic IPSP in pyramidal cells at similar latencies. This IPSP is indistinguishable in properties from that evoked by LOT stimulation. Indirect evidence indicates that it is mediated via both feedforward and feedback mechanisms. In most neurons the association fiber-evoked EPSP is masked by the IPSP in response to single deep shocks but can be demonstrated by blocking the IPSP with a preceding LOT shock or by application of bicuculline. Intracellular injection of horseradish peroxidase (HRP) revealed that pyramidal cell axons give rise to an extensive system of local collaterals with a large number of synaptic terminal-like swellings in layer III. It is postulated that these collaterals synapse on both pyramidal and nonpyramidal cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Characterization of synaptically mediated fast and slow inhibitory processes in piriform cortex in an in vitro slice preparation

1988 ◽  
Vol 59 (5) ◽  
pp. 1352-1376 ◽  
Author(s):  
G. F. Tseng ◽  
L. B. Haberly
Keyword(s):  
Membrane Potential ◽  
Piriform Cortex ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Membrane Depolarization ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Pentobarbital Sodium ◽  
Postsynaptic Potential ◽  
Conductance Increase

1. Intracellular recordings were obtained from anatomically verified layer II pyramidal cells in slices from rat piriform cortex cut perpendicular to the surface. 2. Responses to afferent and association fiber stimulation at resting membrane potential consisted of a depolarizing potential followed by a late hyperpolarizing potential (LHP). Membrane polarization by current injection revealed two components in the depolarizing potential: an initial excitatory postsynaptic potential (EPSP) followed at brief latency by an inhibitory postsynaptic potential (IPSP) that inverted with membrane depolarization and truncated the duration of the EPSP. 3. The early IPSP displayed the following characteristics suggesting mediation by gamma-aminobutyric acid (GABA) receptors linked to Cl- channels: associated conductance increase, sensitivity to increases in internal Cl- concentration, blockage by picrotoxin and bicuculline, and potentiation by pentobarbital sodium. The reversal potential was in the depolarizing direction with respect to resting membrane potential so that the inhibitory effect was exclusively via current shunting. 4. The LHP had an associated conductance increase and a reversal potential of -90 mV in normal bathing medium that shifted according to Nernst predictions for a K+ potential with changes in external K+ over the range 4.5-8 mM indicating mediation by the opening of K+ channels and ruling out an electrogenic pump origin. 5. Lack of effect of bath-applied 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) or internally applied ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) on the LHP and failure of high amplitude, direct membrane depolarization to evoke a comparable potential, argue against endogenous mediation of the LHP by a Ca2+ activated K+ conductance [gK(Ca)]. However, an apparent endogenously mediated gK(Ca) with a duration much greater than the LHP was observed in a low percent of layer II pyramidal cells. Lack of effect of 8-Br-cAMP also indicates a lack of dependence of the LHP on cAMP. 6. Other characteristics of the LHP that were demonstrated include: a lack of blockage by GABAA receptor antagonists, a probable voltage sensitivity (decrease in amplitude in the depolarizing direction), and an apparent brief onset latency (less than 10 ms) when the early IPSP was blocked by picrotoxin. The LHP was unaffected by pentobarbital sodium when the early IPSP was blocked by picrotoxin. 7. Both the LHP and early IPSP were blocked by low Ca2+/high Mg2+, consistent with disynaptic mediation.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent and association fiber differences in short-term potentiation in piriform (olfactory) cortex of the rat

1990 ◽  
Vol 64 (1) ◽  
pp. 179-190 ◽  
Author(s):  
M. E. Hasselmo ◽  
J. M. Bower
Keyword(s):  
Time Constant ◽  
Piriform Cortex ◽  
Low Frequency ◽  
Pyramidal Cells ◽  
Olfactory Cortex ◽  
Short Term ◽  
Term Potentiation ◽  
Association Fibers ◽  
Stimulation Of

1. The effects of low-frequency stimulus trains on synaptically evoked responses in piriform cortex pyramidal cells were studied by the use of intracellular recording techniques in an in vitro slice preparation. Afferent and association fiber systems were differentially stimulated with electrodes placed in layer 1a or layer 1b, respectively. To quantify synapse modifiability, the heights of postsynaptic potentials (PSPs) elicited by paired-pulse stimulation (100-ms interval) were averaged over a 50-s period before and after a set of 10 stimulus trains (10 pulses each, 20 Hz, 5-s interpulse interval). 2. Afferent and association fibers showed consistent differences in their response to stimulation during the period lasting from approximately 10 to 200 s after presentation of trains. During this time period, the responses to stimulation of association fibers in layer 1b displayed a short-term potentiation, which over the 10 posttrain trials, produced an average increase in PSP height of 23.2 +/- 3.7% (mean +/- SE). On the other hand, responses to layer 1a stimulation showed an average depression of 10.9 +/- 3.6%. Layer 1b potentiation decayed with time constant roughly estimated at 79 s. Layer 1b potentiation appeared even at very low stimulus voltages and after local association fiber input had been cut, suggesting that it was largely a monosynaptic effect. 3. In the period immediately after train presentations, responses evoked by both layers showed a short-term augmentation with a time constant around 3 s. In layer 1a, this augmentation was superimposed on a depression with slow recovery. At longer times after train presentation (greater than 5 min), 2 cells out of 46 showed changes (increases) in synaptic efficacy in response to layer 1b stimulation. 4. In the current experiments both layers 1a and 1b showed statistically significant facilitation before the presentation of stimulus trains. However, layer 1b facilitation decreased from 22.7 +/- 3.5% to a statistically insignificant 3.9 +/- 3.3% after the presentation of trains, whereas layer 1a facilitation remained at a statistically significant level of 23.1 +/- 5.7%. 5. These experiments show that pyramidal cell responses to stimulation of the afferent and association fiber systems are affected differently by the previous presentation of trains of stimuli. This suggests that mechanisms of synaptic modification may differ between the afferent and intrinsic association synaptic projections onto single pyramidal cells in olfactory cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Sensory, interneuronal, and motor interactions within Hermissenda visual pathway

1984 ◽  
Vol 52 (1) ◽  
pp. 156-169 ◽  
Author(s):  
Y. Goh ◽  
D. L. Alkon
Keyword(s):  
Hair Cells ◽  
Lucifer Yellow ◽  
Type A ◽  
Visual Pathway ◽  
Excitatory Input ◽  
Excitatory Postsynaptic Potential ◽  
Type B ◽  
Postsynaptic Potential ◽  
Chemical Synapses ◽  
Stimulation Of

The visual pathway of Hermissenda was identified by means of intracellular recordings and iontophoretic injection of the fluorescent dye lucifer yellow. This pathway consisted of five neuron types, namely, type B photoreceptors and the medial type A photoreceptor within each of the two eyes, hair cells in the two statocysts, a group of interneurons in the cerebropleural ganglia, and a putative motor neuron (MN1) in each pedal ganglion. The MN1 cells responded during illumination of the eye with increased impulse and excitatory postsynaptic potential (EPSP) activity. This response was often followed by bursting activity for higher light intensities. The medial type A photoreceptor, which was found to be inhibited by medial and intermediate type B photoreceptors, was demonstrated to excite the MN1 cell indirectly via a group of identified interneurons. Hair cells were also found to excite the MN1 cell indirectly via these interneurons. Among the ipsilateral hair cells, cephalic hair cells were least frequently found to excite the MN1 cell. Among the contralateral hair cells, on the other hand, lateral hair cells were most often found to excite the MN1 cell. Interneurons that were shown to excite the MN1 cell received excitatory input from the medial type A photoreceptor and hair cells. Our observations are consistent with the interpretation that these interactions are mediated by monosynaptic chemical synapses. Electrical stimulation of the MN1 cell with positive-current injection produced turning of the posterior half of the animal's foot to the ipsilateral direction consistent with the animal's turning behavior toward light. The visual pathway identified in this experiment was considered to have some significance in explaining, at least in part, a causal role for changes within type B photoreceptors in producing Hermissenda's modified behavior following associative conditioning.

Electrically coupled pacemaker neurons respond differently to same physiological inputs and neurotransmitters

1984 ◽  
Vol 51 (6) ◽  
pp. 1362-1374 ◽  
Author(s):  
E. Marder ◽  
J. S. Eisen
Keyword(s):  
Motor Neurons ◽  
Slow Wave ◽  
Lucifer Yellow ◽  
Electrical Coupling ◽  
Excitatory Postsynaptic Potential ◽  
Panulirus Interruptus ◽  
Bursting Neuron ◽  
Postsynaptic Potential ◽  
Pyloric Dilator ◽  
Muscarinic Cholinergic

The two pyloric dilator (PD) motor neurons and the single anterior burster (AB) interneuron are electrically coupled and together comprise the pacemaker for the pyloric central pattern generator of the stomatogastric ganglion of the lobster, Panulirus interruptus. Previous work (31) has shown that the AB neuron is an endogenously bursting neuron, while the PD neuron is a conditional burster. In this paper the effects of physiological inputs and neurotransmitters on isolated PD neurons and AB neurons were studied using the lucifer yellow photoinactivation technique (33). Stimulation of the inferior ventricular nerve (IVN) fibers at high frequencies elicits a triphasic response in AB and PD neurons: a rapid excitatory postsynaptic potential (EPSP) followed by a slow inhibitory postsynaptic potential (IPSP), followed by an enhancement of the pacemaker slow-wave depolarizations. Photoinactivation experiments indicate that the enhancement of the slow wave is due primarily to actions of the IVN fibers on the PD neurons but not on the AB neuron. Bath-applied dopamine dramatically alters the motor output of the pyloric system. Photoinactivation experiments show that 10(-4) M dopamine increases the amplitude and frequency of the slow-wave depolarizations recorded in the AB neurons but hyperpolarizes and inhibits the PD neurons. Bath-applied serotonin increases the frequency and amplitude of the slow-wave depolarizations in the AB neuron but has no effect on PD neurons. Pilocarpine, a muscarinic cholinergic agonist, stimulates slow-wave depolarization production in both PD neurons and the AB neuron, but the waveform and frequency of the slow waves elicited are quite different. These results show that although the electrically coupled PD and AB neurons always depolarize synchronously and act together as the pacemaker for the pyloric system, they respond differently to a neuronal input and to several putative neuromodulators. Thus, despite electrical coupling sufficient to ensure synchronous activity, the PD and AB neurons can be modulated independently.

scholarly journals Intracellular and Computational Characterization of the Intracortical Inhibitory Control of Synchronized Thalamic Inputs In Vivo

1997 ◽  
Vol 78 (1) ◽  
pp. 335-350 ◽  
Author(s):  
Diego Contreras ◽  
Alain Destexhe ◽  
Mircea Steriade
Keyword(s):  
Inhibitory Control ◽  
Computational Models ◽  
Pyramidal Cells ◽  
Excitatory Postsynaptic Potential ◽  
Thalamic Stimulation ◽  
Postsynaptic Potential ◽  
Spike Wave

Contreras, Diego, Alain Destexhe, and Mircea Steriade. Intracellular and computational characterization of the intracortical inhibitory control of synchronized thalamic inputs in vivo. J. Neurophysiol. 78: 335–350, 1997. We investigated the presence and role of local inhibitory cortical control over synchronized thalamic inputs during spindle oscillations (7–14 Hz) by combining intracellular recordings of pyramidal cells in barbiturate-anesthetized cats and computational models. The recordings showed that 1) similar excitatory postsynaptic potential (EPSP)/inhibitory postsynaptic potential (IPSP) sequences occurred either during spindles or following thalamic stimulation; 2) reversed IPSPs with chloride-filled pipettes transformed spindle-related EPSP/IPSP sequences into robust bursts with spike inactivation, resembling paroxysmal depolarizing shifts during seizures; and 3) dual simultaneous impalements showed that inhibition associated with synchronized thalamic inputs is local. Computational models were based on reconstructed pyramidal cells constrained by recordings from the same cells. These models showed that the transformation of EPSP/IPSP sequences into fully developed spike bursts critically needs a relatively high density of inhibitory currents in the soma and proximal dendrites. In addition, models predict significant Ca2+ transients in dendrites due to synchronized thalamic inputs. We conclude that synchronized thalamic inputs are subject to strong inhibitory control within the cortex and propose that 1) local impairment of inhibition contributes to the transformation of spindles into spike-wave-type discharges, and 2) spindle-related inputs trigger Ca2+ events in cortical dendrites that may subserve plasticity phenomena during sleep.

Duration of NMDA-Dependent Synaptic Potentiation in Piriform Cortex In Vivo Is Increased After Epileptiform Bursting

1998 ◽  
Vol 80 (4) ◽  
pp. 1623-1629 ◽  
Author(s):  
A. Kapur ◽  
L. B. Haberly
Keyword(s):  
Seizure Activity ◽  
Piriform Cortex ◽  
Long Term Potentiation ◽  
Excitatory Postsynaptic Potential ◽  
Synaptic Potentiation ◽  
Lateral Olfactory Tract ◽  
Afferent Fibers ◽  
Stimulation Of

Kapur, A. and L. B. Haberly. Duration of NMDA-dependent synaptic potentiation in piriform cortex in vivo is increased after epileptiform bursting. J. Neurophysiol. 80: 1623–1629, 1998. Stimulation of afferent fibers with current pulse trains has been reported to induce long-term potentiation (LTP) in piriform cortex in vitro but not in vivo. LTP has been observed in vivo only when trains are paired with behavioral reinforcement and as a consequence of kindled epileptogenesis. This study was undertaken in the urethan-anesthetized rat to determine if the reported failures to observe pulse-train evoked LTP in vivo may be related to a lesser persistence rather than lack of occurrence, if disinhibition might facilitate induction, and to examine the nature of the relationship between seizure activity and LTP. Stimulation of afferent fibers in the lateral olfactory tract with θ-burst trains under control conditions potentiated the monosynaptic field excitatory postsynaptic potential (EPSP) by approximately the same extent (20.3 ± 2%; n = 12) as reported for the slice. However, in contrast to the slice, potentiation in vivo decayed to a low level within 1–2 h after induction (70% loss in 1.5 h, on average). The N-methyl-d-aspartate (NMDA)-receptor antagonists d-APV and MK-801 blocked the induction of this decremental potentiation. Pharmacological reduction of γ-aminobutyric acid–mediated inhibition at the recording site did not increase the duration of potentiation. In contrast, θ-burst stimulation applied after recovery from a period of epileptiform bursting induced stable NMDA-dependent potentiation. Mean increase in the population EPSP was approximately the same as under control conditions (21 ± 2%; n = 6), but in five of six experiments there was little or no decay in potentiation for the duration of the monitoring period (≤6 h). It is concluded that seizure activity has an enabling action on the induction of persistent synaptic potentiation by stimulus trains that bypasses the need for behavioral reinforcement.

Mechanisms of Neuronal Hyperexcitability Caused by Partial Inhibition of Na+-K+-ATPases in the Rat CA1 Hippocampal Region

2002 ◽  
Vol 88 (6) ◽  
pp. 2963-2978 ◽  
Author(s):  
Cyrille Vaillend ◽  
Susanne E. Mason ◽  
Matthew F. Cuttle ◽  
Bradley E. Alger
Keyword(s):  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Burst Firing ◽  
Membrane Properties ◽  
Initial Slope ◽  
Excitatory Postsynaptic Potential ◽  
Neuronal Hyperexcitability ◽  
Partial Inhibition ◽  
Postsynaptic Potential ◽  
Bursting Activity

Extra- and intracellular records were made from rat acute hippocampal slices to examine the effects of partial inhibition of Na+-K+-ATPases (Na+-K+pumps) on neuronal hyperexcitability. Bath application of the low-affinity cardiac glycoside, dihydroouabain (DHO), reversibly induced interictal-like epileptiform bursting activity in the CA1 region. Burst-firing was correlated with inhibition of the pumps, which was assayed by changes in [K+]ouptake rates measured with K+-ion-sensitive microelectrodes. Large increases in resting [K+]odid not occur. DHO induced a transient depolarization (5–6 mV) followed by a long-lasting hyperpolarization (∼6 mV) in CA1 pyramidal neurons, which was accompanied by a 30% decrease in resting input resistance. Block of an electrogenic pump current could explain the depolarization but not the hyperpolarization of the membrane. Increasing [K+]ofrom 3 to 5.5 mM minimized these transient shifts in passive membrane properties without preventing DHO-induced hyperexcitability. DHO decreased synaptic transmission, but increased the coupling between excitatory postsynaptic potentials and spike firing (E-S coupling). Monosynaptic inhibitory postsynaptic potential (IPSP) amplitudes declined to ∼25% of control at the peak of bursting activity; however, miniature TTX-resistant inhibitory postsynaptic current amplitudes were unaffected. DHO also reduced the initial slope of the intracellular excitatory postsynaptic potential (EPSP) to ∼40% of control. The conductances of pharmacologically isolated IPSPs and EPSPs in high-Ca/high-Mg-containing saline were also reduced by DHO by ∼50%. The extracellular fiber volley amplitude was reduced by 15–20%, suggesting that the decrease in neurotransmission was partly due to a reduction in presynaptic fiber excitability. DHO enhanced a late depolarizing potential that was superimposed on the EPSP and could obscure it. This potential was not blocked by antagonists of NMDA receptors, and blockade of NMDA, mGlu, or GABAAreceptors did not affect burst firing. The late depolarizing component enabled the pyramidal cells to reach spike threshold without changing the actual voltage threshold for firing. We conclude that reduced GABAergic potentials and enhanced E-S coupling are the primary mechanisms underlying the hyperexcitability associated with impaired Na+-K+pump activity.

Laryngeal afferent inputs to the nucleus of the solitary tract

1993 ◽  
Vol 265 (2) ◽  
pp. R269-R276 ◽  
Author(s):  
S. W. Mifflin
Keyword(s):  
Stimulus Frequency ◽  
Time Dependent ◽  
Excitatory Postsynaptic Potential ◽  
Solitary Tract ◽  
Neuronal Responses ◽  
Epsp Amplitude ◽  
Postsynaptic Potential ◽  
Afferent Inputs ◽  
Inhibitory Interactions ◽  
Stimulation Of

The following study was undertaken to examine the integration of laryngeal afferent inputs within the nucleus of the solitary tract (NTS), the primary site of termination of laryngeal afferent fibers. Intracellular recordings were obtained from 63 cells that responded to electrical stimulation of the superior laryngeal nerve (SLN) with an excitatory postsynaptic potential (EPSP; n = 49), an excitatory-inhibitory postsynaptic potential (EPSP-IPSP) sequence (n = 13), or an IPSP (n = 1). Mechanical stimulation of laryngeal mechanoreceptors revealed a variety of response patterns (e.g., slowly and rapidly adapting depolarizations or hyperpolarizations). Two types of response to increasing SLN stimulus frequency were observed. In 11 cells SLN-evoked EPSP amplitude at 10 Hz was only 47 +/- 4% of the amplitude at 1 Hz, while in 6 cells EPSP amplitude at 10 Hz was virtually identical (93 +/- 3%) to that at 1 Hz. Time-dependent inhibitory interactions occurred between SLN inputs to NTS neurons at intervals between 50 and 400 ms and in the absence of any change in membrane potential. NTS neuronal responses to brief activation of laryngeal mechanoreceptors correspond well to discharge patterns described for individual laryngeal mechanoreceptors. Frequency-dependent filtering and time-dependent inhibitory interactions might modify NTS neuronal responses during more intense stimulation of laryngeal afferents.

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