Facilitation Of Reflex Research Articles

On the role of NK-2 tachykinin receptors in the mediation of spinal reflex excitability in the rat

The effects of intrathecal administration of neurokinin A, substance P and [Tyr 5, d-Trp, 6,8,9 Arg 10]neurokinin A-(4–10) (Men 10207), a specific NK-2 receptor antagonist, on the spinal nociceptive flexor reflex were studied in decerebrate, spinalized, unanesthetized rats. Intrathecal neurokinin A and substance P facilitate the flexor reflex in a similar manner. The reflex facilitation to intrathecal neurokinin A, but not substance P, is dose-dependently blocked by pretreatment with Men 10207. The NK-2 receptor antagonist by itself facilitates the flexor reflex with a potency about 10 times less than that of neurokinin A, indicating a partial agonistic property. Reversible depression of the flexor reflex, which is not due to nonspecific spinal blockade, is observed after 700 pmol Men 10207. Further increasing the dose of Men 10207 to 7 nmol totally and irreversibly blocks the flexor reflex. Conditioning stimulation of peripheral nerves at 1 Hz for 20 s at an intensity that activates unmyelinated (C) fibers facilitates the ipsilateral flexor reflex. The duration of the facilitation after conditioning stimulation to the cutaneous sural nerve is several minutes and about 1 h after conditioning stimulation of the gastrocnemius muscle nerves. Pretreatment with Men 10207 (70–700 pmol) has no effect on facilitation by the sural nerve conditioning stimulation, but effectively blocks the long-term reflex facilitation to the gastrocnemius nerve stimulation. The present results indicate a distinct role for NK-2 tachykinin receptors in mediation of spinal reflex excitability in the rat. Neurokinin A may be involved in the long-term increase of spinal reflex excitability after activation of unmyelinated fibers innervating muscle.

Facilitation of the acoustic startle reflex by ponto-geniculo-occipital waves: effects of PCPA

The relationship between ponto-geniculo-occipital (PGO) waves and motor activity during waking and non-rapid eye movement (non-REM) sleep stages was studied in cats treated with the serotonin synthesis inhibitor p-chlorephenylalanine (PCPA). PGO waves appeared in waking after daily treatment with PCPA. The magnitude of the acoustic startle elicited in the absence of prior PGO waves increased (by a mean of 555%) by the PCPA treatment as compared to that of the pre-drug level. When startle-eliciting stimuli were presented shortly after the occurrence of the PGO wave, the response amplitude was further enhanced as compared to that fo the baseline startle. The effects was maximal 50 ms following the peak of the PGGO wave (average 192% of the baseline level), with return to the baseline startle level within 200 ms. A similar effect could also be seen with waking eye-movement potentials (EMPs) in drug-naive animals. Over half of the spontaneous PGO waves were found to be precedded or followed by discrete head-body movements. After PCPA, the amplitude of auditory-evoked LGN PGO waves increased during quiet waking (QW) while those in non-REM and REM sleep states did not change. It was concluded that serotonergic systems produce a ttonic suppression of startle response and PGO amplitude in waking. PGO spikes in waking are associated with phasic facilitation of the sensorimotor mechanisms involved in startle.

The specific antagonistic effect of intrathecal spantide II on substance P- and C-fiber conditioning stimulation-induced facilitation of the nociceptive flexor reflex in rat

The effect of intrathecally (i.t.) applied tachkykin antagonist d-NicLys 1, 3-Pal 3, d-Cl 2Phe 5, Asn 6, d-Trp 7,9, Nle 11-substance P (SP), spantide II, on the nociceptive flexor reflex was studied in decerebrate, spinalized, unanaesthesized rats over the dose rangfe of 10 ng-10μg. I.lt. spantide II usually caused weak facilitation of the flexor reflex, especially at lower doses (10–100 ng) and at higher doses (1–10 μg) it sometimes depressed the reflex. Pre-treatment with spantide II (1, 3 or 10 μg) effectively antagonized the facilitatory effect of 10 ng i.t. SP on the flexor reflex for about 30 min. The facilitation of the reflex induced by i.t. administration of other neuropeptides present in primary afferents, somatostatin (SOM), vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP) and galanin (GAL), was not influenced by spantide II. This non-toxic antagonist also effectively blocked facilitation of the flexor reflex induced by C-fiber conditioning stimulation of the sural nerve. The present results indicate that spantide II is an effective tachykinin antagonist in the spinal cord. Furthermore, C-fiber stimulation facilitates the nociceptive flexor reflex through a mechanism involving the release of SP from the central terminals of primary afferents.

Characterization of descending inhibition and facilitation from the nuclei reticularis gigantocellularis and gigantocellularis pars alpha in the rat

Descending influences on the spinal nociceptive tail-flick (TF) reflex produced by focal electrical stimulation and glutamate microinjection in the nuclei reticularis gigantocellularis (NGC) and gigantocellularis pars alpha (NGCα) were examined and characterized in rats lightly anesthetized with pentobarbital. Both inhibition and facilitation of the TF reflex were produced by electrical stimulation at identical sites in the NGC/NGCα; glutamate microinjection only inhibited the TF reflex. The chronaxie of stimulation for inhibition of the TF reflex was 169 ± 28 μsec. Inhibition of the TF reflex by stimulation was produced throughout the NGC and NGCα; intensities of stimulation for inhibition were least in the ventral NGC and in the NGCα. At threshold intensities of stimulation, inhibition of the TF reflex did not outlast the period of stimulation. Facilitation of the TF reflex was produced at many of the same sites at which stimulation inhibited the TF reflex, but always at lesser intensities of stimulation (mean, 10 μA vs. 43 μA for inhibition, n = 25). Stimulation in the NGC/NGCα at threshold intensities for facilitation or inhibition of the TF reflex did not significantly affect blood pressure. Strength-duration characterization of electrical stimulation and microinjection of glutamate into identical sites in the NGC and NGCα suggest that descending inhibition of the TF reflex results from activation of cell bodies in the NGC and NGCα.

On the Role of Galanin, Substance P and Other Neuropeptides in Primary Sensory Neurons of the Rat: Studies on Spinal Reflex Excitability and Peripheral Axotomy.

The interaction of intrathecally (i.t.) applied galanin (GAL) with substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), somatostatin (SOM) and C-fibre conditioning stimulation (CS) with regard to their effects on the spinal nociceptive flexor reflex was studied in decerebrate, spinalized, unanaesthetized rats with intact or sectioned sciatic nerves. SP, CGRP, VIP and SOM applied onto the surface of lumbar spinal cord or a brief CS train (1 Hz, 20 s) to the sural nerve facilitated the flexor reflex for several minutes in animals with intact or sectioned nerves. Pretreatment with GAL, which by itself had a biphasic effect on the flexor reflex in a dose-dependent manner, antagonized the reflex facilitation induced by sural CS before and after sciatic nerve section. SP-induced facilitation of the flexor reflex was antagonized by GAL in rats with intact sciatic nerves, but not after nerve section. In contrast, VIP-induced reflex facilitation was antagonized by GAL only after sectioning of the sciatic nerve. GAL was effective in antagonizing the facilitatory effect of CGRP under both situations, but had no effect on SOM-induced facilitation. A parallel immunohistochemical study revealed that after sciatic nerve section GAL-like immunoreactivity (LI) and VIP-LI are increased in the dorsal root ganglia and that these two peptides coexist in many cells. The present results indicate that GAL antagonizes the excitatory effect of some neuropeptides which exist in the spinal cord. This antagonism could explain the inhibitory effect of GAL on C-fibre CS-induced facilitation of the flexor reflex, which is presumably due to the release of some of these neuropeptides from the terminals of primary afferents. Furthermore, the interaction between GAL and other neuropeptides is altered by sciatic nerve section, paralleling changes in the levels of these neuropeptides in primary afferents and their pattern of coexistence after nerve section. It is proposed that SP and CGRP are important mediators of the spinal flexor reflex in intact rats. However, after axotomy VIP may replace SP in this capacity, paralleling the decrease in SP and marked increase in VIP levels. In general the study provides further support for involvement of peptides in sensory function.

Ipsilateral and contralateral effects on cutaneous reflexes in a back muscle of the female rat: modulation by steroids relevant for reproductive behavior

1. Multiunit EMG recordings of cutaneous reflexes--evoked in the back extensor, lateral longissimus (LL), by bilateral stimulation of nerves to dorsal flank skin--were studied in ovariectomized female rats with and without estrogen pretreatment. 2. Poststimulus time (PST) histograms of data from rats with and without estrogen pretreatment show that the axial EMG response (10-30 ms) to ipsilateral (ipsi) flank skin nerve stimulation is significantly shorter in latency (1.4 ms) and 67% larger than the response to contralateral (contra) flank skin nerve stimulation recorded at the same site (n = 29 pairs). 3. When late EMG responses were also evoked at 50-120 ms in 37% of ipsi and 29% of contra cutaneous reflexes, the incidence of multiunit activity in the late peak was significantly greater in rats pretreated with silastics containing 100% estradiol (E) compared with 10% E or cholesterol controls. 4. When an ipsi cutaneous reflex in LL was conditioned by a stimulus to the contra flank skin nerve at a condition-test interval of 30 ms (C-T 30 ms), the average number of discharges in the early peak of the histogram was double that in the histogram obtained from the unconditioned ipsi reflex, independent of estrogen pretreatment. 5. In 12 out of 19 cases in which a contra cutaneous reflex was conditioned by a stimulus to the ipsi flank skin nerve (C-T 30 ms), the number of discharges in the early peak of the histogram was less than that in the early peak of the histogram derived from the unconditioned contra response, independent of estrogen pretreatment. 6. Intravenous injections of progesterone (P) or its metabolite 5 alpha-pregnane-3 alpha-ol-20-one (tetrahydraprogesterone, THP) decreased the magnitude of the early peak of the ipsi cutaneous reflex and the contra cutaneous reflex in LL, independent of estrogen pretreatment. At the same time, it did not reduce the magnitude of the early peak evoked by either ipsi or contra nerves after conditioning from the other side at C-T 30 ms. 7. As a consequence, the percentage facilitation of ipsi cutaneous reflexes by contra cutaneous conditioning was significantly increased after P or THP. This suggests that these steroids can selectively enhance behaviors involving bilateral inputs. 8. An unchanged axial motoneuron pool output to bilateral cutaneous inputs after P and THP, in spite of reduced motoneuron responses to cutaneous inputs from each side of the body, implies an increased gain in the reflex circuit.(ABSTRACT TRUNCATED AT 400 WORDS)

Plasticity of the peptidergic mediation of spinal reflex facilitation after peripheral nerve section in the rat

The effects of the tachykinin antagonist Spantide II ( d-Nic-Lys 1,3-Pal 3, d-Cl 2Phe 5,Asn 6 d-Trp 7,9,Nle 11)-substance P (SP) and the vasoactive intestinal peptide (VIP) antagonist (Ac-Tyr 1, d-Phe 2)-GRF(1–29)-NH 2 on the excitability of the spinal nociceptive flexor reflex to intrathecally (i.t.) applied SP and VIP, respectively, as well as the facilitation evoked by activation of cutaneous C-afferent was examined. Both antagonists blocked the effects of the respective neuropeptides in rats with both intact and sectioned sciatic nerves. Spantide II antagonised C-afferent induced reflex facilitation in rats with intact nerves, but the degree of antagonism declined after axotomy. In contrast, the VIP antagonist did not block C-afferent induced facilitation in rats with intact nerves, but did so after axotomy. The results indicate that the role of tachykinins in mediating C-afferent-induced reflex facilitation is taken over by VIP after axotomy.

Effects of flexor reflex afferent stimulation on the soleus H reflex in patients with a complete spinal cord lesion: evidence for presynaptic inhibition of Ia transmission

The effects of electrically stimulating the Flexor Reflex Afferent (FRA) on the soleus H reflexes were investigated in 34 paraplegic patients having a clinically complete spinal cord lesion. Conditioning stimuli (5-50 mA) were applied to the ipsilateral or contralateral sural nerve. The conditioning-test interval ranged from 20 to 1000 ms. A late ipsilateral flexor reflex (EMG) was found in all patients. A late contralateral extension reflex was sporadically observed in only 3 patients. The excitability curves usually showed two phases of ipsilateral H reflex inhibition and contralateral H reflex facilitation, one between 50 and 130 ms and the other after over 200 ms. These intervals correspond to early and late flexion reflexes. With high intensity stimulation the early and late ipsilateral inhibition fused. An early low threshold ipsilateral facilitation occurred in 9 patients. The contralateral late facilitation was followed by prolonged inhibition in 10 patients. Changes in presynaptic inhibition were assessed by measuring the heteronymous monosynaptic Ia facilitation from quadriceps to soleus. For methodological reasons, it was only possible to investigate the effect of contralateral conditioning volleys which was performed in 5 patients. A significant and regular reduction of the heteronymous Ia facilitation was found in 4 patients. The reduction is taken to indicate that the FRA evokes presynaptic inhibition of Ia transmission to alpha motoneurones. Presynaptic inhibition was also indicated by the enhancement of a vibratory stimulus induced inhibition in 2 subjects. These results are consistent with the hypothesis that the reflex organization in patients with a spinal cord section is similar to that of the acute spinal cat injected with DOPA.

Blockade of the spinal excitatory effect of cAMP on the startle reflex by intrathecal administration of the isoquinoline sulfonamide H-8: comparison to the protein kinase C inhibitor H-7

Drugs thought to inhibit the actions of protein kinase C (PKC) and cAMP dependent protein kinase (A-kinase) were infused intrathecally into the subarachnoid space of the lumbar region of the spinal cord, and the effects on acoustic startle were measured. Previous work has shown that intrathecal infusion of drugs thought to increase cAMP increase the startle response. The present experiment evaluated whether inhibition of A-kinase would prevent this effect. Rats were infused with the isoquinoline sulfonamide, H-8 (360 nmol) or vehicle (50% dimethyl sulfoxide), 30 min prior to infusion of 100 nmol of dibutyryl cAMP. By itself, H-8 had little effect on startle, but completely blocked the normal excitatory effect of dibutyryl cAMP on startle. In contrast, the isoquinoline sulfonamide, H-7, which is less active in blocking A-kinase, but more active in blocking PKC, did not block dibutyryl cAMP. Moreover, H-8 did not block the excitatory effect of intrathecal infusion of the 5-HT 1A receptor agonist, 8-OH-dipropylaminotetraline (8-OH-DPAT). Thus, the blockade of dibutyryl cAMP by H-8 appears somewhat specific and suggests an involvement of A-kinase in the excitatory effects of dibutyryl cAMP on the acoustic startle response. In a second experiment, it was found that administration of the isoquinoline sulfonomide H-7 caused a marked, dose-dependent (150–800 nmol) facilitation of the startle reflex in comparison with its vehicle, Tris buffer (0.1 M). Like H-7, another PKC inhibitor, GT 1b (20 nmol) produced a marked increase in the startle reflex versus its vehicle, 0.01 M phosphate buffer. Other isoquinoline sulfonamides, HA1004 (400 nmol) and H-8 (360 nmol), which have less PKC inhibitory activity than H-7, caused only modest increases in startle. Thus, the increases in startle caused by intrathecal infusions of the isoquinoline sulfonamides and the ganglioside GT 1b indicate that spinal PKC inhibition elevates startle, perhaps because PKC tonically inhibits startle at the spinal level.

Spinal motoneuronal excitability in hyperkinesis: effects of the Jendrassik manoeuvre

H-reflex recovery functions and homosynaptic depression curves were studied in unmedicated hyperkinetic and control children in the presence and absence of the Jendrassik manoeuvre. The Jendrassik manoeuvre failed to affect recovery function reflex amplitude across or within groups, but reflex amplitude was augmented in the homosynaptic depression procedure for hyperkinetic children who failed to show recovery function facilitation. The absence of Jendrassik-associated reflex facilitation in children during the recovery function and during selective homosynaptic depression rates may reflect developmental influences on processes underlying this phenomenon. However, reflex augmentation in non-facilitating hyperkinetic subjects suggests that these processes are present in children and can be revealed under conditions of decreased motoneuronal excitability. These findings suggest that reduced gamma-efferent drive may contribute to decreased motoneuronal excitability observed in hyperkinetic children, but the possible role of other Jendrassik-activated influences, such as coactivation of alpha and gamma motoneurons or selective activation of alpha motoneurons by processes independent of increased gamma-efferent drive, cannot be excluded.

The N-terminal 1–16, but not C-terminal 17–29, galanin fragment affects the flexor reflex in rats

The biological activity of two galanin (GAL) fragments, GAL-(1–16) and GAL-(17–29), was tested in vivo by using a spinal nociceptive flexor reflex model in the rat. Intrathecal (i.t.) GAL-(1–16) had a similar biphasic effect on the flexor reflex, with facilitation at lower doses and facilitation followed by depression at higher doses, as the full length peptide GAL-(1–29). GAL-(1–16) also effectively depressed the facilitation of the flexor reflex caused by i.t. substance P (SP) or C-fiber conditioning stimulation (CS) and potentiated the depressive effect of i.t. morphine on the reflex, both actions that have been reported earlier with GAL-(1–29). In contrast, i.t. GAL-(17–29), even at high doses, did not induce changes in the amplitude of the flexor reflex, nor did it interact with the effects of i.t. SP, morphine or C-fiber CS. It is concluded that the N-terminal portion of GAL-(1–29) is critical for the biological activity of the intact peptide in the dorsal horn of the rat spinal cord. The similarity between the effects GAL-(1–16) and GAL-(1–29) indicates that they probably act on the same GAL receptor.

Motor outflow to cervical motoneurons from raccoon motorsensory cortex

Motor outflow from forelimb motorsensory cortex (MsI) to forelimb muscle motoneurons in raccoon has been investigated using three approaches: 1) determination of latencies for cortically evoked efferent discharge in forelimb nerves; 2) determination of latencies for cortical facilitation of forelimb monosynaptic reflexes; and 3) intracellular recording of cortically evoked synaptic potentials. All three approaches indicated a major polysynaptic pathway (minimally disynaptic) for corticofugal facilitation or inhibition of cervical motoneurons. Suggestive evidence for a monosynaptic connection between forelimb MsI and cervical motoneurons was found for only one motoneuron. Nevertheless, the motor pathway between MsI and cervical motoneurons was shown to be more efficacious (defined on the basis of central delays) than in the cat under similar experimental conditions. The results are discussed in terms of organization changes in forelimb MsI which appear to be related to the extent to which certain mammals use their forelimbs for manipulating and exploring objects.

Enhancement and depression of tactile and acoustic startle reflexes with variation in background noise level

The amplitude ofthe acoustic startle reflex in the rat is related to the level ofbroadband background noise by an inverted-U-shaped function. We tested the hypotheses that (1) the initial increment, (2) the subsequent decrement, or (3) the entire function results from a nonspecific noise effect on reflex expression, as would be indicated by a common effect across reflexes elicited by acoustic and nonacoustic stimuli. Responses to electrotactile, airpuff, and acoustic startle stimuli were measured, each in aseparate group of rats, in noise levels varying from 60 to 100 dB. A biphasic effect of noise on the acoustic startle reflex was observed, with a modest increase from 60 to 70 or 80 dB, and a decline thereafter. In contrast, electrotactile startle provided a monotonie increase in amplitude to a maximum at 90 or 100 dB, whereas airpuff startle showed a progressive decline in amplitude, with an increase in background level beyond the optimal value at 60 to 70 dB. The latter effects demonstrated an unexpected division between facilitation versus reflex depression within the tactile modality, but subsequent data demonstrated that the effective component of the airpuff was acoustic, rather than tactile, in nature. The overall empirical conclusion is that facilitation by noise is nonspecific, whereas reflex depression that appears at noise levels beyond 70 to 80 dB is specific to acoustic stimuli. These findings suggest that reflex facilitation results from motor excitation and that reflex depression results from a partial masking of the eliciting stimulus.

Augmentation of muscle nociceptive respiratory reflex facilitation by vagal afferents.

Vagal influence on the facilitation of phrenic neural activity during respiratory phase-locked, gastrocnemius muscle nerve nociceptive electrical stimulation was examined in anesthetized, glomectomized, paralyzed, and artificially ventilated cats. (1) In the vagi-intact state, respiratory reflex facilitation was characterized by a sharp rise in peak amplitude, maximum rate of rise or slope, and mean rate of rise of integrated phrenic nerve activity. This was greater during inspiratory phase-locked (T1-locked) muscle nerve electrical stimulation than during expiratory phase-locked (TE-locked) muscle nerve electrical stimulation. "Evoked post-inspiratory phrenic activity" during the early expiratory phase was also observed during TE-locked muscle nerve electrical stimulation. (2) Bilateral vagotomy significantly attenuated the respiratory facilitation during both T1- and TE-locked muscle nerve electrical stimulation. In particular, the "evoked post-inspiratory phrenic activity" during TE-locked muscle nerve electrical stimulation was also attenuated or almost completely abolished. (3) Conditioning electrical stimulation of the vagus nerve revealed facilitatory reflexes which co-exist with inspiratory inhibitory reflexes. (4) The "evoked post-inspiratory phrenic activity" during TE-locked muscle nerve electrical stimulation, which was attenuated or abolished after vagotomy, was restored after vagal T1-locked conditioning stimuli combined with TE-locked muscle nerve electrical stimulation. The results suggest that vagal facilitatory reflexes augment the respiratory reflex facilitation during muscle nociceptive stimulation.

An associative process maintains reflex facilitation of the unconditioned nictitating membrane response during the early stages of training.

The presentation of a neutral or conditioned stimulus (CS) at an appropriate interval prior to the presentation of a corneal airpuff, or a paraorbital shock (unconditioned stimulus, US) can facilitate the amplitude of the unconditioned nictitating membrane (NM) response in rabbit. In two experiments, it was demonstrated that an associative process mediates the maintenance of that facilitation during repeated CS-US pairings. Although CS-alone presentations produced a substantial decrease in the amount of reflex facilitation in animals not pretrained with the CS, pretraining that consisted of paired CS-US presentations prevented that decrease when CS-alone presentations were subsequently given. Conditioned facilitation of the unconditioned response occurred very rapidly (within 5-12 trials in these experiments) and long before the appearance of overt conditioned responses to the CS. In addition, it was demonstrated that conditioned facilitation can be relatively specific to the tonal frequency of the CS. These results indicate the first sign of conditioning of the NM response is exhibited in the amplitude of the unconditioned response.

Facilitation and inhibition of the human startle blink reflexes by stimulus anticipation.

Facilitation and inhibition of the human startle blink reflexes by stimulus anticipation.

Facilitation and inhibition of the human startle blink reflexes by stimulus anticipation.

The cutaneous eyeblink has 2 electromyographic components, 1 unilateral and early (R1) and 1 bilateral and late (R2), which are served by different neural pathways. These 2 reactions were measured when the eliciting stimulus was expected or relatively surprising. Forewarning was varied in 3 ways: Subjects received notice that the stimulus was about to occur on some trials (Experiment 1); delivered the stimulus to themselves on some trials (Experiments 2 & 3); or experienced a series of trials in which a tone was paired with the eliciting stimulus, followed by tone-alone trials interspersed with test trials (Experiment 4). In each case, forewarning enhanced R1 amplitudes while depressing R2 but reduced the latency of both components. This mixed pattern of effects reveals that the preparatory state provoked by forewarning focuses excitatory and inhibitory processes simultaneously on different reflex pathways: inhibition central and excitation peripheral.

An associative process maintains reflex facilitation of the unconditioned nictitating membrane response during the early stages of training.

An associative process maintains reflex facilitation of the unconditioned nictitating membrane response during the early stages of training.

Reflex facilitation of the rabbit nictitating membrane response by an auditory stimulus as a function of interstimulus interval.

The ability of an auditory stimulus to facilitate the amplitude and latency of the unconditioned nictitating membrane (NM) response in rabbits was investigated over a wide range of interstimulus intervals (ISIs) for both delay (Experiments 1-4) and trace (Experiments 3 and 4) procedures. The auditory stimulus was a 1000-Hz tone (T) at either 85 or 95 dB, and the reflex-eliciting stimulus was a 2.0 psi (pounds per square inch) corneal air puff (AP). The results indicate that (a) robust facilitation of the NM response, as measured by an increased amplitude and a reduced latency, can be obtained at long ISIs (2,000-32,000 ms); (b) increasing the tone intensity can increase reflex facilitation of the peak amplitude; (c) at comparable ISIs, delay procedures produce more facilitation of both amplitude and latency than do trace procedures; and (d) when trace procedures are used, amplitude and latency facilitation by a 125-ms tone follows an inverted U-shaped ISI function in which facilitation peaks between 125 and 500 ms, rapidly decreases between 1,000 and 2,000 ms, and disappears by 4,000 ms.

Noradrenergic modulation of the masseteric reflex in behaving cats. II. Physiological studies

The masseteric (jaw closure) reflex was utilized as a model system for assessing functional changes in central norepinephrine (NE) neurotransmission. This monosynaptic reflex was chosen because of its simple and well-defined circuitry, and because its motor component receives a dense NE innervation. Previous experiments in our laboratory described NE modulation of this reflex in the anesthetized rat. The present experiments examine the effects of NE on this response in the unanesthetized, behaving cat. The masseteric reflex was elicited by electrical stimulation of the mesencephalic trigeminal nucleus, and the response was recorded via electrodes permanently implanted in the masseter muscle. The amplitude of the reflex response was measured before and at various intervals following microinfusion (0.5 microliters) of NE or of various NE agonists directly into the motor trigeminal nucleus (MoV). Microinfusions of NE (0.125-5.0 micrograms) produced dose-dependent increases in the amplitude of the elicited reflex response. These effects were evident within 1 min postinfusion and lasted up to 30 min; in all cases, the response amplitude returned to baseline levels. The increase seen in response to 0.5 micrograms NE was blocked by pretreatment with the alpha-1-adrenergic antagonist prazosin, but not by pretreatment with the serotonin (5-HT) antagonist methysergide. Methysergide did, however, completely block the increase in the amplitude seen in response to microinfusion of 5-HT. Infusion of the alpha-1-adrenergic agonist phenylephrine also increased the amplitude of the reflex response. By contrast, infusion of the beta-adrenergic agonist isoproterenol had no effect, whereas clonidine, a presynaptic alpha-2-adrenergic agonist, decreased its amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)