Evoked responses from an in vitro slice preparation of a primary gustatory nucleus: the vagal lobe of goldfish

The vagal lobe of goldfish (Carassius auratus) is a laminated structure in which primary gustatory afferents terminate in a stereotypical pattern. Because the afferent fibers enter and distribute within the lobe in the transverse plane, the structure appeared suitable for in vitro slice electrophysiology. Slices were cut on a vibratome at 400–800 μm thickness and placed in a fresh water teleost Ringer's solution. Following a recovery period, clear population responses were recorded following electrical stimulation of the incoming fiber bundle. The later two components of this evoked waveform were eliminated by removal of the calcium from the bathing solution indicating the synaptic origin of these potentials. Further, the waveform was highly dependent on the position of the recording electrode, both in terms of laminar and tangential position. Evoked response maxima corresponded to the layers in which the primary afferent fibers terminate. In addition, the maximal evoked response was limited to a tangential distance of approximately 100 μm. The spatial restriction of the evoked waveform therefore corresponds well with the known anatomical organization of the primary gustatory afferent fibers. The evoked waveforms are sensitive to stimulus repetition rate, being facilitated by stimulus trains less than 50 ms in duration and fatigued by stimulus repetitions as slow as 1 Hz. This in vitro preparation should provide a means for investigating the physiological and pharmacological properties of primary gustatory fibers and nuclei.     

Pharmacological uncoupling of activation induced increases in CBF and CMRO2

Neurovascular coupling provides the basis for many functional neuroimaging techniques. Nitric oxide (NO), adenosine, cyclooxygenase, CYP450 epoxygenase, and potassium are involved in dilating arterioles during neuronal activation. We combined inhibition of NO synthase, cyclooxygenase, adenosine receptors, CYP450 epoxygenase, and inward rectifier potassium (Kir) channels to test whether these pathways could explain the blood flow response to neuronal activation. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO₂) of the somatosensory cortex were measured during forepaw stimulation in 24 rats using a laser Doppler/spectroscopy probe through a cranial window. Combined inhibition reduced CBF responses by two-thirds, somatosensory evoked potentials and activation-induced CMRO₂ increases remained unchanged, and deoxy-hemoglobin (deoxy-Hb) response was abrogated. This shows that in the rat somatosensory cortex, one-third of the physiological blood flow increase is sufficient to prevent microcirculatory increase of deoxy-Hb concentration during neuronal activity. The large physiological CBF response is not necessary to support small changes in CMRO₂. We speculate that the CBF response safeguards substrate delivery during functional activation with a considerable ‘safety factor''. Reduction of the CBF response in pathological states may abolish the BOLD–fMRI signal, without affecting underlying neuronal activity.     

Physiological studies of brainstem reticular connectivity. I. Responses of mPRF neurons to stimulation of bulbar reticular formation

The connectivity between medial pontine reticular formation (mPRF) and bulbar reticular formation (BRF) was studied by intracellular recordings of mPRF neuronal responses to microstimulation of BRF in unanesthetized, undrugged cats. There was a very high percentage (75-90%) of monosynaptic latency postsynaptic potentials (PSPs) in mPRF neurons in response to microstimulation of 3 BRF areas: the magnocellular tegmental field (FTM), the bulbar gigantocellular tegmental field (BFTG), and bulbar lateral tegmental field (BFTL). The type of initial orthodromic response produced in mPRF neurons by BRF stimulation was predominantly (75-95%) a monosynaptic excitatory PSP (EPSP) which was characterized by a rapid rise time, a nearly constant latency, and often led to spike potential generation. In contrast, the percentage of initial monosynaptic inhibitory PSPs (IPSPs) was much lower for FTM (12.3%), for BFTG (12.5%) and was zero for BFTL. While microstimulation techniques alone cannot differentiate between excitation of fibers of passage and neuronal somata, the very high percentage of initial EPSPs in our data and the anatomical evidence for dense BRF to mPRF neuronal projections as compared with less dense projections from fibers passing through BRF to mPRF suggest that excitatory BRF-mPRF connections are predominant. The high degree of connectivity between BRF and mPRF may furnish an important substrate for functional interaction. Comparison of the mPRF neuronal population that was not antidromically activated by FTM microstimulation vs the mPRF neuronal population that was antidromically activated from FTM and also studied for orthodromic responsiveness showed no statistically significant differences between these populations on the parameters of percentage of monosynaptic input, monosynaptic initial EPSPs, monosynaptic initial IPSPs and presence of a PSP with a latency of less than 5 ms. For BRF connectivity this suggests an identity of mPRF input and output neurons with respect to synaptic response properties.     

Presynaptic modulation of synaptic effectiveness of afferent and ventrolateral tract fibers in the frog spinal cord

In the isolated frog spinal cord, antidromic stimulation of motor nerves produces intraspinal field potentials with a characteristic spatial distribution. When recording from the ventral horn, there is a short latency (1–2 msec) response corresponding to activity generated by antidromic activation of motoneuron cell bodies and proximal dendrites. In addition, in the dorsal horn, a delayed wave (12–13 msec latency) corresponding in time with the negative dorsal root potential is also recorded. This wave (VR-SFP) is positive at the dorsal surface of the cord and inverts to negativity at more ventral regions. The negative VR-SFP is maximum between 300–500 μm depth from the dorsal surface and decays with increasing depth towards the motor nucleus. Six days after chronic section of the dorsal roots L7 to L9 in one side of the spinal cord, stimulation of the motor nerves on the deafferented side produces only the early response attributable to antidromic activation of motoneurons. No distinctive VR-SFPs are recorded at any depth within the cord. These findings are consistent with the interpretation that afferent fiber terminals are the current generators of the VR-SFP. The presynaptic and postsynaptic focal potentials recorded in the motor nucleus after stimulation of the ventrolateral tract, as well as the corresponding synaptic potentials electrotonically recorded from the ventral roots, are not depressed during conditioning stimulations which produce primary afferent depolarization. This contrasts with the depression of the presynaptic and post-synaptic focal potentials and synaptic potentials produced by stimulation of sensory fibers. It is concluded that, unlike the afferent fiber terminals, the terminals of the ventrolateral tract are not subjected to a presynaptic modulation of the type involving primary afferent depolarization.     

Nonlinear neurovascular coupling in rat sensory cortex by activation of transcallosal fibers.

Functional neuroimaging and normal brain function rely on the robust coupling between neural activity and cerebral blood flow (CBF), that is neurovascular coupling. We examined neurovascular coupling in rat sensory cortex in response to direct stimulation of transcallosal pathways, which allows examination of brain regions inaccessible to peripheral stimulation techniques. Using laser-Doppler flowmetry to record CBF and electrophysiologic recordings of local field potentials (LFPs), we show an exponential relation between CBF responses and summed LFP amplitudes. Hemodynamic responses were dependent on glutamate receptor activation. CNQX, an AMPA receptor blocker, strongly attenuated evoked CBF responses and LFP amplitudes at all stimulation frequencies. In comparison, N-methyl D-aspartate (NMDA) receptor blockade by MK801 attenuated CBF responses at high (>7 Hz) but not low (<7 Hz) stimulation frequencies, without affecting evoked LFP amplitudes. This shows the limitation of using LFP amplitudes as indicators of synaptic activity. 7-Nitroindazole, a neuronal nitric oxide synthase inhibitor, and indomethacin, a nonspecific cyclooxygenase inhibitor, attenuated the hemodynamic responses by 50%+/-1% and 48%+/-1%, respectively, without affecting LFP amplitudes. The data suggest that preserved activity of both AMPA and NMDA receptors is necessary for the full CBF response evoked by stimulation of rodent interhemispheric connections. AMPA receptor activation gives rise to a measurable LFP, but NMDA receptor activation does not. The lack of a measurable LFP from neural processes that contribute importantly to CBF may explain some of the difficulties in transforming extracellular current or voltage measurements to a hemodynamic response.     

An in vitro analysis of sound localization mechanisms in the gerbil lateral superior olive

One way in which animals localize sounds along the horizon is by detecting the level differences at the 2 ears. Neurons in the lateral superior olive (LSO) encode this cue by integrating the synaptic drive from ipsilateral excitatory and contralateral inhibitory connections. This synaptic integration was analyzed in 400-500-microns brain slices through the gerbil superior olive. Intracellular recordings from LSO neurons were obtained during the application of independent or conjoint electrical stimuli to the excitatory afferent and inhibitory afferent pathways. Stimulation of ascending fibers from the ipsilateral cochlear nucleus reliably evoked EPSPs and action potentials. Stimulation of the medial nucleus of the trapezoid body (MNTB) consistently evoked IPSPs. The evoked postsynaptic potentials differed in that IPSPs were 2 times the duration of EPSPs. An electrophysiological estimate of convergence indicated approximately 10 excitatory and 8 inhibitory afferents per LSO neuron. MNTB stimulation suppressed synaptically evoked action potentials. When stimulus amplitude was increased to the excitatory pathway, it was generally found that a greater MNTB stimulus was necessary to suppress the action potential. A similar commensurate rise in ipsilateral and contralateral acoustic stimulation was also found to be necessary to give the same criterion response. These results confirm that the LSO can integrate evoked action potentials and IPSPs to encode interaural level. Increasing stimulus voltage was found to decrease both action potential and IPSP latency, suggesting that intensity information may be encoded with temporal cues in the nervous system. It was also found that an evoked burst of action potentials could be inhibited in such a way as to yield intermediate discharge rates, dependent on contralateral stimulus level. Taken together, these results suggest that certain properties related to level-difference coding may be available for intracellular analysis using the brain-slice preparation. Several temporal characteristics of the synaptic potentials, including latency and duration, may play a critical role in this simple computation.     

Stellate neurons mediate functional hyperemia in the cerebellar molecular layer.

Mice lacking cyclin D2 have a profound reduction in the number of stellate neurons in the cerebellar molecular layer. We used cyclin D2-null mice to study the contribution of stellate neurons in the increase of cerebellar blood flow (BFcrb) produced by neural activation. Crus II, a region of the cerebellar cortex that receives trigeminal sensory afferents, was activated by stimulation of the upper lip (5-30 V; 10 Hz), and BFcrb was recorded at the activated site by the use of a laser-Doppler flow probe. In wild-type mice, upper lip stimulation increased BFcrb in crus II by 32 +/- 2%. The rise in BFcrb was attenuated by 19% in heterozygous mice and by 69% in homozygous mice. In contrast to the cerebellum, the increases in somatosensory cortex blood flow produced by upper lip stimulation was not attenuated in D2-null mice. The field potentials evoked in crus II by upper lip stimulation did not differ between wild-type and D2-null mice. Stellate neurons are a major source of nitric oxide (NO) in the cerebellar molecular layer. The neuronal NO synthase inhibitor 7-nitroindazole attenuated the vascular response to crus II activation in wild-type mice but not in D2-null mice, suggesting that stellate neurons are the major source of NO mediating the vascular response. The data provide evidence that stellate neurons are a critical link between neural activity and blood flow in the activated cerebellum and that NO is the principal effector of their vascular actions.     

Postsynaptic potentials evoked in spiny neostriatal projection neurons by stimulation of ipsilateral and contralateral neocortex

Postsynaptic potentials were evoked in neostriatal neurons by stimulation of the ipsilateral and contralateral medial agranular frontal cortical field (AGm) in the rat. This cortical region is known to project bilaterally to the dorsal lateral head of the caudate-putamen of rats. Ipsilateral stimulation of AGm should excite all types of corticostriatal neurons projecting to neostriatal neurons in the corresponding area in neostriatum, while stimulation of the same cortical area on the side contralateral to the recording should evoke synaptic potentials from a more restricted subpopulation of crossed corticostriatal neurons. Neostriatal neuronal responses were recorded intracellularly and spiny projection neurons identified by intracellular staining with horseradish peroxidase. The initial EPSP response to contralateral stimulation was similar to that evoked from the ipsilateral side, except for the absence of a relatively small short latency component responsible for the earliest part of the response to ipsilateral cortical stimulation. Comparison with previous findings indicated that this earliest EPSP component was due to activation of fast-conducting descending cortical efferents with collateral projections exclusively to the ipsilateral neostriatum. Stimulation of contralateral neostriatum evoked responses identical to those obtained using stimulation of contralateral neocortex. Analyses of these responses indicated that both EPSPs arise from activation of the same population of fibers. Stimulation of the contralateral internal capsule just caudal to neostriatum was not effective in evoking the EPSP. Chronic hemidecortication did not change the shape of the EPSP evoked from the intact contralateral side, but reduced its amplitude by approximately one half. These observations indicate that contralaterally projecting corticostriatal neurons in the rat project bilaterally in neostriatum, have axonal branches to the contralateral cerebral cortex as well as neostriatum, and converge onto neostriatal neurons that also receive input from the corresponding cortical region on the ipsilateral side.     

Evidence forN-methyl-d-aspartic acid receptor-mediated modulation of the commissural input to central vestibular neurons of the frog

We have investigated the role ofN-methyl-d-asparte (NMDA) receptors in the excitatory synaptic transmission to central vestibular neurons in the isolated superfused brainstem of the frog. In superfusate containing 1 mM Mg²⁺ field potentials in the vestibular nuclei evoked by electrical stimulation of either the ipsi- or the contralateral VIIIth nerve were not affected by bath-appliedd-2-amino-5-phosphonovaleric acid (D-APV, 25–50 μM), a selective NMDA antagonist. In a low Mg²⁺ solution postsynaptic field potential components were larger than control but still unaffected by D-APV. Ipsi- and contralaterally evoked excitatory postsynaptic potentials (EPSPs) differed in their shape parameters as well as their pharmacological sensitivity. Ipsilaterally evoked EPSPs were not affected by D-APV and had a rise time that was faster than that of contralaterally evoked EPSPs. The peak amplitude of the latter was reduced by D-APV (25–50 μM) to about 65% of the control value in the presence of 1 mM Mg²⁺. During bath application of NMDA (100 μM) an increased input resistance and repetitive de- and hyperpolarizing membrane potential shifts were observed. Similar events were observed during a reduction of the Mg²⁺ concentration. Bath application of NMDA (0.1–1 μM) resulted in an enhanced size of the recorded EPSPs. Dendritic and somatic EPSPs were stimulated on a computer with the assumption of a constant NMDA receptor activation and a pulse-like non-NMDA receptor activation. The results of these stimulations are consistent with the hypothesis that the efficacy of non-NMDA-mediated vestibular commissural synaptic transmission is modulated through tonically activated NMDA receptors.     

Pyramidal cells and cytochrome P450 epoxygenase products in the neurovascular coupling response to basal forebrain cholinergic input

Activation of the basal forebrain (BF), the primary source of acetylcholine (ACh) in the cortex, broadly increases cortical cerebral blood flow (CBF), a response downstream to ACh release. Although endothelial nitric oxide and cholinoceptive GABA (γ-aminobutyric acid) interneurons have been implicated, little is known about the role of pyramidal cells in this response and their possible interaction with astrocytes. Using c-Fos immunohistochemistry as a marker of neuronal activation and laser-Doppler flowmetry, we measured changes in CBF evoked by BF stimulation following pharmacological blockade of c-Fos-identified excitatory pathways, astroglial metabolism, or vasoactive mediators. Pyramidal cells including those that express cyclooxygenase-2 (COX-2) displayed c-Fos upregulation. Glutamate acting via NMDA, AMPA, and mGlu receptors was involved in the evoked CBF response, NMDA receptors having the highest contribution (~33%). In contrast, nonselective and selective COX-2 inhibition did not affect the evoked CBF response (+0.4% to 6.9%, ns). The metabolic gliotoxins fluorocitrate and fluoroacetate, the cytochrome P450 epoxygenase inhibitor MS-PPOH and the selective epoxyeicosatrienoic acids (EETs) antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE) all blocked the evoked CBF response by ~50%. Together, the data demonstrate that the hyperemic response to BF stimulation is largely mediated by glutamate released from activated pyramidal cells and by vasoactive EETs, likely originating from activated astrocytes.     

Extracellular fields influence transmembrane potentials and synchronization of hippocampal neuronal activity

The influence of extracellular fields on the transmembrane potential (TMP) of CA1 pyramidal neurons was investigated following both ortho- and antidromic stimulation in the in vitro hippocampal slice preparation. A short latency negative deflection on the intracellular potential coincided with the falling phase of the extracellular population spike. Subtraction of extracellular field potentials from ground referenced intracellular records revealed a sharp depolarizing wave of the TMP superimposed upon the underlying synaptic potential. This graded depolarization was capable of discharging CA1 cells and displayed a parallel shift in latency and amplitude with the extracellular population spike. A similar depolarizing wave was associated with the antidromically evoked population spike which persisted following blockade of synaptic activity. Finally, multiple population spike activity similar to that observed during epileptiform discharge was associated with repetitive depolarizing waves of the TMP. These data suggest that extracellular field potentials can ephaptically discharge CA1 neurons and may play a role in recruitment and synchronization of neuronal activity in the hippocampus.     

Hippocampal responses evoked by tooth pulp and acoustic stimulation: Depth profiles and effect of behavior

Averaged evoked potentials and unitary discharges in response to tooth pulp and acoustic click stimuli were recorded from the hippocampus of freely moving rats. The spatial distribution of evoked field responses to tooth pulp stimulation and acoustic clicks were identical. Averaged evoked potentials consisted of a large negative deflection (N1) preceded by a small positive potential (P1). The shortest latency N1 in response to tooth pulp stimulation was recorded from the middle third of the dentate molecular layer and the outer portion of apical dendrites of CA3 (27 ms). The peak latency of N1 was significantly longer (34 ms) in the stratum radiatum of CA1. Laminar profiles of N1 in the dentate gyrus and CA3 were similar to that evoked by electrical stimulation of the medial entorhinal afferents; in CA1 the depth profiles of the potentials were similar to the response profile evoked by the Schaffer collaterals. Largest amplitude P1 was obtained from above the pyramidal layer of CA1 and the hilus. Both sensory modalities were able to modify the discharge rate of neurons in all hippocampal regions. The amplitude of evoked field potentials and cellular responses were dependent upon both the ongoing behavior of the animal and the nature of its response to the stimulus. The largest amplitude evoked potentials were recorded during immobility and slow wave sleep. On the other hand, virtually no potentials were obtained during exploratory behaviors associated with theta EEG activity. The findings indicate that information about sensory stimuli can reach the hippocampus by two distinctive pathways: a short latency inhibitory input via the fimbria-fornix and a longer latency path via the entorhinal cortex. It is suggested that neuronal mechanisms involved in theta EEG block the sequential activation of the unidirectional entorhinal-hippocampal circuitry.     

A slim needle-shaped multiwire microelectrode for intracerebral recording

The construction of a needle-shaped multiwire microelectrode is described. It can be made with simple mechanical tools. The presented electrode assembly consists of 12 insulated nichrome wires (core diameter 25 μm) which are embedded in epoxylite resin. The straight-cut wire tips are aligned lengthwise and have a relative spacing of 150 μm. Outer dimensions vary from 100 × 180 μm at the level of the 1st electrode channel, to 100 × 100 μm at the level of the 12th channel at the tip. The configuration of this electrode was determined by its application: the laminar analysis of evoked potentials in the cortex of the rat. However, the number of channels, the diameter of the (nichrome) wire which determines the surface area of these channels, and the channel spacing can be easily adjusted during construction to meet other experimental requirements, such as the recording of single-unit activity. The electrode which is composed of biocompatible materials is suited for the study of field potentials and multiple-unit activity, in both acute and chronic experiments, and can be used repeatedly. To demonstrate the performance of the electrode assembly, a depth profile of field potentials is presented, accompanied by the corresponding current source density distribution. The potentials were recorded in the somatosensory cortex of the rat following stimulation of the median nerve under ketamine anesthesia.     

Development of evoked potentials in specific brain systems after neonatal administration of estradiol

The effects of neonatal administration of estradiol on the development of the transcallosal response (TCR) and the thalamically evoked relayed pyramidal response (RPR) were studied in rats by analyzing evoked potentials at several ages. Estradiol-treated animals generally showed a lower threshold, shorter peak latency, and greater peak amplitude of the TCR at the younger ages studied, indicating accelerated development at these ages. The maximal effect on peak amplitude occurred at a different age than that of threshold and peak latency. The RPR was only slightly affected. The data also suggest that the effects of estradiol may be mediated by increased neuronal excitability, precocious myelination, and precocious development of synaptic connections. These findings extend those of other investigators by indicating that hormones act selectively upon specific systems as well as generally upon the whole brain.     

Presynaptic D2 dopaminergic receptors mediate inhibition of excitatory synaptic transmission in rat neostriatum

The effect of dopamine (DA) on excitatory synaptic transmission was studied in rat neostriatal neurons using intracellular- and whole-cell voltage clamp-recording methods. Depolarizing excitatory postsynaptic potentials (EPSPs) were evoked by cortical stimulation. Superfusion of DA (0.01–10 μM) reversibly decreases EPSP in a concentration-dependent manner and with a estimated IC₅ of 0.3 μM. In addition, the inhibitory effect induced by DA at a low concentratiion (0.1 μM) was antagonized by sulpiride (1–10 nM), a selective D₂ dopaminergic receptor antagonist. However, D₁ dopaminergic receptor antagonist SKF-83566 (1–5 μM) did not affect the blocking effect by DA 0.1 μM. Based on these findings, we conclude that DA at a low concentration ( 0.1 μM) reduced the excitatory response of neostriatal neurons following cortical stimulation via the activation of D₂, but not D₁ dopaminergic receptors, located on the terminals of corticostriatal neurons.     

Profiles of percent reduction of cytochromes in guinea pig hippocampal brain slices in vitro

Percent reduction profiles of cytochromes (cyt.) aa₃, bandc were investigated in bloodless guinea pig hippocampal brain slices of 400, 600 and 800 μm in thickness ranging in temperature from 22 to 37 °C. The extent of the percent reduction of cytochromes was compared with the generation of orthodromic potentials elicited by the stimulation of the stratum radiatum, and the cessation of the potentials was found to be correlated with the extent of the percent reduction of the cytochromes. In the case of 400 μm slices, they were found to be in normoxia both from the extent of the percent reduction levels of cytochromes and from the generation of orthodromic responses over a range in temperature. In the case of 600 μm slices, those incubated under temperatures of 22 to 32 °C were not in hypoxia from the levels of cytochrome reduction and the production of a field potential. However, slices at 37 °C were in hypoxia because of cyt. c levels approached those of cyt. b and the orthodromic response was suppressed. In 800 μm slices, those at 22–27 °C were in normoxia; however, slices maintained at 32–37 °C were in hypoxia because the levels of cyt. c reduction closely approximated those of cyt. b at 32 °C whereas those of cyt. aa₃, bandc were almost the same as at 37 °C. Moreover, the orthodromic field potential was not evoked.     

Flat and steep terminal negativity in the DC-potential after deprivation of oxygen and glucose in human neocortical slices

The so-called terminal negativity (TN) of the DC-potential is a characteristic reaction of neuronal tissue to hypoxia or ischemia. In a previous study on human neocortical slices, two types of TN with flat and steep slopes of rise (< or >10 mV/min) were found with hypoxia. The aim of the present study was to further investigate causes underlying the occurrence of flat and steep TN. Experiments were performed on 23 human neocortical slices (500 μm) resected from 13 patients (epilepsy and tumour surgery). DC-potential and evoked potentials (white matter stimulation) were recorded in layer III. The extracellular potassium concentration ([K⁺]_o) was measured by K⁺-sensitive microelectrodes. In an interface type chamber, ischemic episodes were induced by oxygen and glucose deprivation. They were terminated when TN had peaked. Both flat and steep TN also existed with ischemic conditions. There was a linear correlation between the slope of rise of TN and the associated slope of rise in [K⁺]_o, respectively, but none regarding latencies of TN or recovery of evoked potentials. Peak levels in [K⁺]_o were 13.9±0.9 mmol/l. Compared to control, the slope of rise and latency of TN were clearly increased by addition of dimethyl sulfoxide (DMSO, 0.4%) to the bath solution, whereas nimodipine (40 μmol/l) in 0.4% DMSO had neither an effect on slope of rise of TN nor on latency of TN. As a whole, our observations suggest, that the actual metabolic state determines the occurrence of flat or steep TN.     

Hypothalamic influences on the electrical activity of the olfactory pathway

By means of evoked potentials a direct efferent connection was found to run from the posterior hypothalamus and medial forebrain bundle to primary olfactory structures (olfactory bulb, olfactory tubercle and prepyriform cortex). The pathway from the hypothalamus to the olfactory bulb follows in the lateral olfactory tract at a conduction velocity 5–10 m/sec. The olfactory tubercle functions as a relay station for the efferent fibers from various sources, running to the olfactory bulb. In animals with electrodes chronically implanted in the olfactory structures, hypothalamic stimulation gives rise to a prolonged train of hypersynchronous bursts of activity (40–50 Hz), which resemble the arousal reaction. This response is modified by transecting the cervical sympathetic trunk. By pathways still to be defined, potentials are evoked in the olfactory bulb by stimulation of the cervical sympathetic trunk and the termination of these sympathetic fibers shows a common postsynaptic neuronal pool with axons of hypothalamic origin. Epinephrine topically applied to the olfactory mucosa induced hypersynchronous activity in olfactory structures, quite similar to that consequent to hypothalamic stimulation. These results suggest a multichanneled hypothalamic modulation of olfactory input.     

Frequency-dependent changes in cerebral blood flow and evoked potentials during somatosensory stimulation in the rat.

Contrary to the concept of neuronal-vascular coupling, cortical evoked potentials do not always correlate with blood flow responses during somatosensory stimulation at changing stimulus rates. The goal of this study is to clarify the effects of stimulus frequency on the relationship between somatosensory evoked potentials (SEPs) and cerebral blood flow. In rats anesthetized with alpha-chloralose, we measured SEPs by signal-averaging field potentials recorded with an electrode placed on dura overlying the hindlimb somatosensory cortex. Regional blood flow was simultaneously assessed in the same region with a laser-Doppler flow (LDF) probe. The contralateral sciatic nerve was stimulated with 0.1 A pulses at the frequencies of 1, 2, 5, 10 and 20 Hz. SEPs (both P1 and N1 components) declined with increasing frequency regardless whether stimulus duration (20 s) or number (100) were kept constant, suggesting that frequency is an important determinant of neuronal activity. In contrast, LDF responses increased to a maximum at 5 Hz, and do not correlate with SEPs. Because CBF should reflect integrated neuronal activity, we computed the sum of SEPS (summation operatorSEP = SEP x stimulus frequency) as an index of total neuronal activity at each frequency. Summation operatorSEP indeed correlates positively (P<0.001) with LDF responses. Thus, during somatosensory stimulation at various frequencies, cerebral blood flow is coupled to integrated neuronal activity but not to averaged evoked potentials.