Orthodromic Potentials Research Articles

Neurons of the A5 region are required for the tachycardia evoked by electrical stimulation of the hypothalamic defence area in anaesthetized rats

In order to assess the possible interactions between the pontine A5 region and the hypothalamic defence area (HDA), we have examined the pattern of double staining for c-Fos protein immunoreactivity (c-Fos-ir) and tyrosine hydroxylase, throughout the rostrocaudal extent of the A5 region in spontaneously breathing anaesthetized male Sprague-Dawley rats during electrical stimulation of the HDA. Activation of the HDA elicited a selective increase in c-Fos-ir with an ipsilateral predominance in catecholaminergic and non-catecholaminergic A5 somata (P < 0.001 in both cases). A second group of experiments was done to examine the importance of the A5 region in modulating the cardiorespiratory response evoked from the HDA. Cardiorespiratory changes were analysed in response to electrical stimulation of the HDA before and after ipsilateral microinjection of muscimol within the A5 region. Stimulation of the HDA evoked an inspiratory facilitatory response, consisting of an increase in respiratory rate (P < 0.001) due to a decrease in expiratory time (P < 0.01). The respiratory response was accompanied by a pressor response (P < 0.001) and tachycardia (P < 0.001). After muscimol microinjection within the A5 region, pressor and heart rate responses to HDA stimulation were reduced (P < 0.01 and P < 0.001, respectively). The respiratory response persisted unchanged. Finally, to confirm functional interactions between the HDA and the A5 region, extracellular recordings of putative A5 neurones were obtained during HDA stimulation. Seventy-five A5 cells were recorded, 35 of which were affected by the HDA (47%). These results indicate that neurones of the A5 region participate in the cardiovascular response evoked from the HDA. The possible mechanisms involved in these interactions are discussed.

Effects of Cholinergic Substances on Plasticity of Synapses in Olfactory Bulb of the Pike Esox lucius

An electrophysiological and morphometric study of effects of cholinergic substances on orthodromic potential (OP), induction of long-term post-tetanic potentiation (PTP), and potentiated OP in olfactory bulb (OB) of intact pike was carried out. The final effect of endogenous ACh on relay neurons of the OB was found to be inhibitory. Activation of M1-like cholinoreceptors (ChR) was shown to play the key role in induction of long-term PTP. In response to tetanization of olfactory nerve (ON) after pirenzepine-induced inhibition of M1-like ChR, no potentiation appears and the length of cross-section of axo-dendritic synapse active zone (AZ) does not change in the OB glomerular neuropil. Tetanization of ON after inhibition of M2-like ChR by gallamine leads to the appearance of short-term PTP transformed later into long-term PTP accompanied by a significant decrease of length of cross-sections of axo-dendritic synapse AZ. Effects of both increase of endogenous ACh concentration by eserine (0.1 μM) and blockade of M2-like ChR by gallamine (10 μM) on potentiated OP were manifested as a decrease of its amplitude to control level. The obtained data allow considering that endogenous ACh in the pike OB has a pronounced effect on induction, development, and stabilization of the long-term PTP. This holds equally true to both functional and morphological manifestations of plasticity of axo-dendritic synapses of the glomerular neuropil.

Inhibition of muscle spindle afferent activity during masseter muscle fatigue in the rat.

The influence of muscle fatigue on the jaw-closing muscle spindle activity has been investigated by analyzing: (1) the field potentials evoked in the trigeminal motor nucleus (Vmot) by trigeminal mesencephalic nucleus (Vmes) stimulation, (2) the orthodromic and antidromic responses evoked in the Vmes by stimulation of the peripheral and central axons of the muscle proprioceptive afferents, and (3) the extracellular unitary discharge of masseter muscle spindles recorded in the Vmes. The masseter muscle was fatigued by prolonged tetanic masseter nerve electrical stimulation. Pre- and postsynaptic components of the potentials evoked in the Vmot showed a significant reduction in amplitude following muscle fatigue. Orthodromic and antidromic potentials recorded in the Vmes also showed a similar amplitude decrease. Furthermore, muscle fatigue caused a decrease of the discharge frequency of masseter muscle spindle afferents in most of the examined units. The inhibition of the potential amplitude and discharge frequency was strictly correlated with the extent of muscle fatigue and was mediated by the group III and IV afferent muscle fibers activated by fatigue. In fact, the inhibitory effect was abolished by capsaicin injection in the masseter muscle that provokes selective degeneration of small afferent muscle fibers containing neurokinins. We concluded that fatigue signals originating from the muscle and traveling through capsaicin-sensitive fibers are able to diminish the proprioceptive input by a central presynaptic influence. In the second part of the study, we examined the central projection of the masseter small afferents sensitive to capsaicin at the electron-microscopic level. Fiber degeneration was induced by injecting capsaicin into the masseter muscle. Degenerating terminals were found on the soma and stem process in Vmes and on the dendritic tree of neurons in Vmot. This suggests that small muscle afferents may influence the muscle spindle activity through direct synapses on somata in Vmes and on dendrites of neurons in Vmot.

Twitch interpolation in human muscles: mechanisms and implications for measurement of voluntary activation.

An electrical stimulus delivered to a muscle nerve during a maximal voluntary contraction usually produces a twitchlike increment in force. The amplitude of this "interpolated twitch" is widely used to measure voluntary "activation" of muscles. In the present study, a computer model of the human adductor pollicis motoneuron pool was used to investigate factors that affect the interpolated twitch. Antidromic occlusion of naturally occurring orthodromic potentials was modeled, but reflex effects of the stimulus were not. In simulations, antidromic collisions occurred with probabilities of between approximately 16% (in early recruited motoneurons) and nearly 100% (in late recruited motoneurons). The model closely predicted experimental data on the amplitude and time course of the rising phase of interpolated twitches over the full range of voluntary forces, except that the amplitude of interpolated twitches was slightly overestimated at intermediate contraction intensities. Small interpolated twitches (4.7% of the resting twitch) were evident in simulated maximal voluntary contractions, but were nearly completely occluded when mean peak firing rate was increased to approximately 60 Hz. Simulated interpolated twitches did not show the marked force drop that follows the peak of the twitch, and when antidromic collisions were excluded from the model interpolated twitch amplitude was slightly increased and time-to-peak force was prolonged. These findings suggest that both antidromic and reflex effects reduce the amplitude of the interpolated twitch and contribute to the force drop that follows the twitch. The amplitude of the interpolated twitch was related to "excitation" of the motoneuron pool in a nonlinear way, so that at near-maximal contraction intensities (>90% maximal voluntary force) increases in excitation produced only small changes in interpolated twitch amplitude. Thus twitch interpolation may not provide a sensitive measure of motoneuronal excitation at near-maximal forces. Increases in the amplitude of interpolated twitches such as have been observed in fatigue and various pathologies may reflect large reductions in excitation of the motoneuron pool.

Maintenance of muscimol-induced long-term depression by neurosteroids

1. 1. The present study was undertaken to expand investigations of the interaction between neurosteroids and long-term depression (LTD) induced by muscimol 10 μM. 2. 2. Extracellular recordings were made in the CA1 pyramidal cell layer of rat hippocampal slices following orthodromic stimulation of Schaffer collateral fibres in stratum radiatum (0.01 Hz). 3. 3. As previously reported, muscimol at 10 μM induced a time, frequency of stimulation and concentration-dependent LTD of the amplitude of orthodromic potentials. Alphaxalone, at concentrations that had no significant effect themselves on the population spike (0.5 and 1 μM), potentiated the inhibitory effect of muscimol on the population spike size. 4. 4. It is now reported that low concentrations of alphaxalone are able to potentiate the ability of muscimol to induce LTD. In addition, concentrations of muscimol as low as 1 μM which are not themselves able to induce LTD, as well as alphaxalone and 5α-pregnan-3αone 1μM were able to maintain the LTD induced by muscimol 10 μM. 5. It is suggested that the ability of such low concentrations of GABA receptor agonists to maintain LTD could be of physiological importance.

Induction of a novel form of hippocampal long‐term depression by muscimol: involvement of GABAA but not glutamate receptors

1. Unlike long-term potentiation, long-term depression (LTD) in the central nervous system remains poorly understood. The present study was undertaken to investigate the role of GABAA receptors in LTD and synaptic plasticity. 2. Extracellular recordings were made in the CA1 pyramidal cell layer of rat hippocampal slices following orthodromic stimulation of Schaffer collateral fibres in stratum radiatum (0.01 Hz). 3. Muscimol induced a time- and concentration-dependent LTD of the amplitude of orthodromic potentials. Increasing the stimulation frequency from 0.01 Hz to 1 Hz for 10 s reversed the LTD induced by muscimol. Muscimol also induced LTD in the absence of electrical stimulation. 4. Adenosine decreased the spike size in a concentration-dependent manner, but failed to induce LTD. 5. Alphaxalone and 5 alpha-pregnan-3 alpha-ol-20-one at concentrations that did not have any effect themselves on the population spike (0.5 and 1 microM), potentiated the inhibitory effect of muscimol on the population spike size, including concentrations which were not effective by themselves. Both steroids were able to potentiate the ability of muscimol to induce LTD. 6. Bicuculline, 5 microM, reversed the LTD induced by muscimol, 10 microM. 7. The NMDA receptor antagonist (+/-)-2-amino-5-phosphonopentanoic acid (2-AP5), the NMDA/metabotropic antagonist 2-AP3 and selective metabotropic antagonist L-(+)-2-amino-3-phosphonopropionic acid (L(+)-AP3) failed to modify the LTD. Similarly, quisqualic acid and (1S, 3R)-aminocyclopentane dicarboxylic acid (ACPD) a selective agonist at metabotropic receptors did not induce LTD or short-term depression, whereas kynurenic acid prevented the reversal of the LTD obtained at 1 Hz. 8. It is concluded that LTD can be induced by the selective activation of GABAA receptors. The lack of involvement of glutamate receptors in our protocol confirms the unique nature of the LTD described here. The phenomenon of GABA-induced LTD and its reversal by 1 Hz stimulation may represent a novel type of long-lasting depression by which inhibitory interneurones can modulate pyramidal cell excitability in a frequency-dependent manner.

Changes in arterial blood pressure alter activity of electrophysiologically identified single units of the bed nucleus of the stria terminalis.

The bed nucleus of the stria terminalis may play a role in cardiovascular function by way of its connectivity to the diagonal band of Broca/ventral septal area. The present study sought to determine whether changes in systemic blood pressure affect the electrical activity of single units within the bed nucleus of the stria terminalis. Extracellular voltage recordings from neurons in the bed nucleus were performed in urethane-anaesthetized rats catheterized for arterial blood pressure measurements and for the intravenous administration of pressor and depressor drugs. Afferent or efferent connectivity of each recorded neuron was determined following electrical stimulation of nearby nuclei with and without known barosensitive regions. Of neurons demonstrating efferent connectivity (antidromically evoked potentials) with the diagonal band of Broca/ventral septal area or habenular nuclei, 24 and 20%, respectively, responded to changes in blood pressure with either increases or decreases in firing frequency. Paraventricular nucleus-projecting neurons were not affected by alterations in arterial blood pressure. Orthodromic potentials (inhibitory and/or excitatory) in the bed nucleus were also observed following stimulation of these nearby nuclei. Of these orthodromically activated neurons, changes in arterial pressure affected 31% of neurons receiving input from the diagonal band of Broca/ventral septal area, 33% of neurons with connectivity to the habenular nuclei and 60% of neurons with connectivity to the paraventricular nucleus. These data show that the bed nucleus of the stria terminalis contains a sub-population of cells that are sensitive to deviations in resting arterial pressure and that these cells receive synaptic modulation from several limbic/forebrain sources. Furthermore, the results are consistent with a role for the bed nucleus in the control of cardiovascular function and as a relay nucleus for modified baroreceptor input toward the diagonal band of Broca/ventral septal area.

The effect of calcium removal on the suppression by adenosine of epileptiform activity in the hippocampus: demonstration of desensitization.

1. Previous work has suggested that presynaptic effects of adenosine may be dependent on divalent cations. The present study was undertaken to determine whether a similar requirement existed at postsynaptic sites. 2. Extracellular recordings were made in the CA1 pyramidal cell layer of rat hippocampal slices following orthodromic stimulation of Schaffer collateral fibres in stratum radiatum or antidromic stimulation of the alveus. In antidromic stimulation experiments, CaCl2 was omitted (calcium-free medium) or reduced to 0.24 mM (low calcium medium) and in some experiments MgSO4 was increased to 2 mM. Kynurenic acid at concentrations of 1 and 5 mM in calcium-free medium and 1 mM in low calcium medium had no effect on secondary spike size. 3. Adenosine and baclofen induced a concentration-dependent reduction in the amplitude of orthodromic potentials with maximum effects at 20 and 5 microM respectively. 4. In nominally calcium-free medium, bursts of multiple population spikes were obtained in response to antidromic stimulation. Adenosine had little effect in reducing the secondary spike amplitude. At high concentration (2 mM) an initial depression was seen which declined within 3-5 min. 5. Sensitivity to adenosine was restored in low calcium medium or by raising magnesium. Although raising the divalent cation concentration increased the inhibitory effect of adenosine, desensitization was still seen. 6. 2-Chloroadenosine (100-500 microM) and R-PIA (50 microM), which are not substrates for either the nucleoside transporters or adenosine deaminase, were inactive in the absence of calcium. S-(2-hydroxy-5 nitrobenzyl)-6-thioinosine, an adenosine uptake blocker, at a concentration 100 MicroM had no effect on secondary potential size and did not restore adenosine sensitivity in calcium-free medium.7. Thapsigargin, which discharges intracellular calcium stores, had no significant effect at 1 MicroM on the bursts of action potentials and did not change the effect of 0.5 mM adenosine in calcium-free medium.8. Unlike adenosine, baclofen concentration-dependently reduced the secondary spike size in calcium free medium and no sign of recovery was observed during maintained superfusion for up to 45 min. No cross-desensitization was seen between baclofen and adenosine.9. Applications of adenosine locally by pressure to neuronal somata or dendrites still resulted in desensitized responses in calcium-free medium.10. It is concluded that the postsynaptic sensitivity to adenosine is dependent on the concentration of divalent cations in the extracellular space implying an effect of cations on adenosine receptor activation or transduction processes.

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

Percent reduction profiles of cytochromes (cyt.) aa 3, 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. aa 3, bandc were almost the same as at 37 °C. Moreover, the orthodromic field potential was not evoked.

Functional connections of the rat medial cortex and basal forebrain: An in vivo intracellular study

Projections between the medial cortex and basal forebrain in the rat were demonstrated by intracellular recordings and the anterograde tracer Phaseolus vulgaris leucoagglutinin. Direct projections between these areas were indicated by antidromic action potentials, short latency ( < 5 ms) orthodromic potentials, and labeled axon terminals in the basal forebrain subsequent to iontophoresis of Phaseolus vulgaris leucoagglutinin into posterior cingulate cortex. High proportions of antidromic action potentials were encountered in responsive cortical neurons (66%) and basal forebrain neurons (97%). Antidromic latencies recorded in the basal forebrain (< 1.0ms) revealed fast ascending projections; cortical neurons showed both fast and slow descending projections (latencies of 0.32–3.7 ms). Relatively few synaptic potentials (none in the diagonal band of Broca) and sparse labeling of axon terminals observed in the basal forebrain indicated that the ascending projections may be the more physiologically important or, at least, densest pathway. Polysynaptic feedforward pathways were suggested through long latency ( < 20 ms) inhibitory and excitatory postsynaptic potentials, the former being the more common response. Candidate inhibitory neurons were identified in both cortex and basal forebrain. Possible monosynaptic ( < 5 ms) inhibitory postsynaptic and antidromic responses in these cells provided evidence that candidate inhibitory neurons participate in the reciprocal pathways.

NMDA-receptor-independent effects of low magnesium: involvement of adenosine

Perfusion of hippocampal slices with magnesium-free media elicits epileptiform activity attributable partly to the activity of N-methyl- D-aspartate (NMDA) receptors, but recent reports have documented an NMDA-independent enhancement of orthodromic potentials by moderate reductions in magnesium concentration. The present experiments indicate that this enhancement is comparable with that produced by perfusion with an adenosine antagonist, 8-phenyltheophylline, and that superfusion with this compound or adenosine deaminase precludes any enhancement of potential size in low magnesium solutions. The low magnesium enhancement is probably attributable to the recently described magnesium dependency of presynaptic inhibition by adenosine.

O-phosphohomoserine, a naturally occurring analogue of phosphonate amino acid antagonists, is an N-methyl-D-aspartate (NMDA) antagonist in rat hippocampus.

O-Phosphohomoserine, an analogue of the excitatory amino acid antagonist 2-amino-phosphonovalerate, has been synthesized and tested for activity as an excitatory amino acid antagonist. The tests were carried out on 500 micron thick slices of rat hippocampus superfused in vitro at 30 degrees C. Antidromic and orthodromic potentials were studied in the CA1 region, recording from the pyramidal cell layer. At concentrations of 0.5 and 1 mM the compound produced a weak but significant antagonism of the depression of evoked potentials produced by N-methyl-D-aspartate with no effect on the responses produced by kainic or quisqualic acids. O-Phosphohomoserine was not metabolised by brain homogenates or by alkaline phosphatases. Since O-phosphohomoserine is known to occur naturally in lower organisms, it would be of interest to seek its existence in the animal nervous system.

Two types of GABA receptors in the intact olfactory bulb and primordial hippocampus of the frog: Pharmacologic data

The in vivo effects of (+/-) baclofen (10(-6)-10(-4) M), muscimol (10(-5)-10(-4) M), and (+) bicuculline (10(-4)-10(-3) M) applications on evoked potentials in the olfactory bulb (OB) and primordial hippoccamp (PH) were studied in frogs. Baclofen was found to decrease drastically postsynaptic components of OB orthodromic potential and to slightly increase OB antidromic potential. Muscimol decreased only the second component of OB orthodromic potential and OB antidromic potential. Baclofen and muscimol decreased all the components of PH orthodromic potential, but for the first positive one. All the effects were reversible and dose-dependent. Bicuculline antagonized muscimol effects, without affecting baclofen effects in both structures under study. The results suggest the presence of two types of GABA-receptors in OB and PH of frogs. GAGAB-receptors are shown to be located on the primary olfactory afferents and to be responsible for presynaptic inhibition in OB.

Electrophysiological analysis of potential arginine vasopressin projections to the ventral septal area of the rat

Extracellular electrophysiological studies of neurons in the ventral septal region of the rat have examined afferent input from the paraventricular nucleus, bed nucleus of the stria terminalis and suprachiasmatic nucleus. Short latency excitatory or inhibitory orthodromic potentials were obtained following electrical stimulation of each nucleus, thereby providing evidence for these areas as a possible source of arginine vasopressin (AVP) fibers to the ventral septal region. These projections may mediate the reported antipyretic action of arginine vasopressin in the ventral septal region.

Effect of destruction of basolateral nuclei of the amygdala on the character of electrical activity of the dorsomedial thalamic nucleus in rats

Characteristics of slow global and of unit activity in the dorsomedial thalamic nucleus were studied at various times after destruction of nuclei of the basolateral amygdala in semichronic experiments on anesthetized rats. Destruction of this kind was found to cause periodic transformation of the neuronal discharge into rhythmic bursts of spikes, and into the development of bursts of paroxysmal activity in the form of groups of four to six pointed waves with a mean duration of 60.5±20.6 msec, appearing with a frequency of 1.5±0.3 Hz. A change in the coefficient of correlation was found between the duration of bursts and their frequency during the 20–22-sec period of their generation. Interference was demonstrated between bursts and orthodromic focal potentials, evoked by stimulation of the anterior periamygdalar cortex and anterior amygdalar region. Neurons were described with long (up to 1 sec) responses to stimulation of the periamygdalar cortex and amygdalar region, in the form of regular bursts of spikes or tonic activation, correlating with the appearance of a rhythmic after-discharge. Bursts of this kind, which were most marked during the first 3 or 4 days after destruction of the basolateral amygdala, were observed to begin to disappear toward the end of the first postoperative week. It is suggested that one mechanism of the change in the adaptive behavior of animals with destruction of the amygdala is a disturbance, linked with the bursts, of the relay and integrative functions of the dorsomedial thalamic nucleus.

Facilitation of synaptic transmission by general anaesthetics.

1. The actions of five structurally different intravenous and inhalation anaesthetics (alphaxalone/alphadolone, halothane, ketamine, methohexitone, and pentobarbitone) have been studied on synaptic transmission through the cuneate nucleus of the dorsal column-lemniscal afferent pathway in the decerebrate cat. 2. Synaptic input and output were estimated from antidromic and orthodromic potentials, which were evoked by either afferent volleys from the periphery or micro-electrode excitation of the presynaptic fibre terminals in the cuneate and recorded at forelimb nerves and the medial lemniscus. 3. Each of the anaesthetic agents potentiated the efficiency of synaptic transmission, as shown by the elevation of input-output curves constructed from the integrals of the potentials evoked by varying intensities of either peripheral or cuneate stimulation. 4. The excitability of the afferent terminals, as measured at the peripheral nerves by the antidromic responses to micro-electrode stimulation, was depressed by the anaesthetics. Post-synaptic excitability, which was assessed from the direct lemniscal response to intra-nuclear stimulation, did not appear to change. 5. Hypotensive states (mean arterial levels less than 60 torr) produced depolarization of presynaptic terminals and depression of synaptic efficiency and transmission; these changes opposed the primary effects of the general anaesthetics. 6. It is concluded that anaesthetics do not depress activity at all synapses of the central nervous system. Their facilitatory action on cuneate transmission is attributed to an enhanced release of excitatory transmitter; the underlying mechanism may be hyperpolarization of the primary afferent terminals, secondary to an increase in K+ conductance.

Properties and tectal projections of monkey retinal ganglion cells

Page 432: Peter H. Schiller and Joseph G. Malpeli, “Properties and tectal projections of monkey retinal ganglion cells.” The legend to the figure at the bottom of page 432 should read: fig. 3. A: orthodromic potential of single cell in retina. B: antidromic response of same cell. Two components of the response evident which show considerable variation with antidromic activation. The second component is absent in the fifth trace. Time marker represents 1 ms.

Electrophysiological investigation of the conduction of excitation in the pterygopalatine ganglion of the cat

When responses in some nerves of the pterygopalatine ganglion of the cat in situ to stimulation of its other nerves were recorded it was found that most fibers passing through the ganglion are continuous sympathetic postganglionic fibers (at least three groups). Most of the parasympathetic preganglionic fibers forming synapses on neurons of the ganglion constitute a group of fibers with the same threshold of excitation. Intracellular recording from single neurons of the pterygopalatine ganglion showed that stimulation of the Vidian nerve evokes orthodromic spike potentials in some neurons of the ganglion with a short latent period, and in others with a long latent period (2.5–6.0 and 10–44 msec, respectively). Evidently only fast-conducting fibers terminate synaptically on most neurons of the ganglion and only slow-conducting fibers on some of them. Recording from intact nerves of the pterygopalatine ganglion revealed no tonic activity in them. Microelectrode recording from single neurons of the ganglion showed that either the frequency of generation of spike potentials is relatively low (1–3/sec) or such potentials are absent altogether.

Caudate evoked synaptic activities in nigral neurons

Intracellular recordings from neurons in the substantia nigra have revealed three varieties of monosynaptic PSPs in response to stimulation of the ipsilateral head of the caudate nucleus: short (3–5 msec) latency EPSPs; short (3–5 msec) latency IPSPs; and long (15–20 msec) latency IPSPs. The data indicate that at least three efferent fiber systems link the caudate to the nigra: two fast conducting axonal systems of comparable diameters mediate the short-latency PSPs whereas a slow conducting axonal system mediates the long-latency PSPs. The caudate evoked long-latency IPSPs in nigral neurons were preceded by antidromic and orthodromic potentials in the motor cortex; these cortical potentials are regarded as epiphenomena. The dual, facilitatory-inhibitory control of caudate on nigral neurons is consonant with the proposal that the caudate self-regulates its input from the nigra. The caudate-evoked EPSPs in nigral neurons are sine qua non for the operation of the caudato-nigrothalamic projection system.

An electrophysiological dissection of the hypothalamic regions which regulate the pre-ovulatory secretion of luteinizing hormone in the rat.

1. Extracellular action potentials were recorded from 299 single units in the preoptic and anterior hypothalamic areas of fifty-two female rats anaesthetized with urethane. The units were categorized by their response to single biphasic pulses (ca. 1 mA; 1 msec duration) applied to the ventromedial/arcuate region of the hypothalamus.2. Experiments with five lactating rats demonstrated that the effective zone of stimulation was confined within the ventromedial/arcuate region. This observation was supported by further evidence obtained during unit recording sessions.3. Antidromic action potentials were recorded from 122 (41%) of the neurones monitored in preoptic and anterior hypothalamic areas. These Type A cells were characterized by their very slow discharge rate (median for spontaneously active units 1.2 spikes/sec) when contrasted with adjacent cells (median 3.9 spikes/sec). Orthodromic action potentials were not observed in thirty-six Type A cells. The antidromically identified neurones had an average conduction rate of 0.32 m/sec. The absolute refractory period of the soma, computed by separation of the IS and SD components of the antidromic action potentials recorded from forty-four neurones, ranged from < 3.0 to > 100 msec. With ten units it was not possible to obtain a soma dendritic (SD) wave by antidromic activation even though the initial segment (IS) wave was seen clearly and the orthodromic potentials consisted of both IS and SD waves.4. Type B cells (32% of population) were excited and/or inhibited by the ventromedial/arcuate stimulation but were not antidromically activated. This post-stimulatory change in discharge rate lasted for up to 400 msec.5. Type C cells (27% of population) showed no change in spontaneous activity after stimulation of the ventromedial arcuate area. These neurones had discharge rates similar to Type B cells.6. The previously reported prooestrous increase in firing rate, recorded from neurones in the ventral part of the preoptic/anterior hypothalamic area was restricted to cell Types B and C.