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L J Goldberg

Publications and source records attributed to L J Goldberg.

At least 19 recordsLinked to original sources
PubMed2001

Atypical pilar leiomyoma: cutaneous counterpart of uterine symplastic leiomyoma?

Four cases of cutaneous leiomyoma with cytologic atypia are reported. All four cases were adult men ranging in age from 33 to 92 years of age. Clinical diagnoses were diverse and included epidermal inclusion cyst, scar, nevus, dermatofibroma, squamous cell carcinoma, and basal cell carcinoma. Histological examination of all four lesions revealed a relatively circumscribed, mild to focally moderately cellular, dermal proliferation of large, irregularly shaped spindle cells in a fascicular arrangement. Some cells contained large irregular nuclei and abundant cytoplasm; others were multinucleate. Moderate to focal marked pleomorphism and rare mitotic figures were present, raising the possibility of leiomyosarcoma; however, the sparse mitotic activity and low cellularity did not warrant this diagnosis. This study suggests that cutaneous leiomyomas may exhibit bizarre or "symplastic" patterns analogous to their uterine counterparts.

Adult↗
PubMed2000

Gianotti-Crosti syndrome presenting as lichenoid dermatitis.

Papular acrodermatitis of childhood (Gianotti-Crosti syndrome) is an uncommon, self-limited disease characterized by an erythematous papular eruption symmetrically distributed on the face and limbs and mild lymphadenopathy, thought to be of viral origin. The histopathologic findings are nonspecific and include focal parakeratosis, mild spongiosis, superficial perivascular infiltrate, papillary dermal edema, and extravasated red blood cells. Interface changes with some basal vacuolization may be present, but are not a conspicuous feature. We present a 2 1/2-year-old boy with multiple papules and plaques on the face and extremities and cervical lymphadenopathy. Histopathologic analysis showed compact orthokeratosis, focal parakeratosis, hypergranulosis, psoriasiform epidermal hyperplasia, and a dense lichenoid lymphohistiocytic infiltrate with extensive exocytosis of mononuclear cells. Immunoperoxidase staining with CD 1 a revealed clusters of Langerhans cells in the epidermis and in the papillary dermis. In view of the clinical findings, a diagnosis of Gianotti-Crosti syndrome was made. Although there are a few reports describing a lichenoid pattern of infiltration in Gianotti-Crosti syndrome, this histologic pattern is not widely known. This case is presented to illustrate the fact that Gianotti-Crosti syndrome can present as lichenoid dermatitis, and, especially in children, should be added to the differential diagnoses of lichenoid infiltrates.

Acrodermatitis↗
PubMed1997

Is it lymphoma or lymphomatoid papulosis?

Distinguishing malignancy from premalignant conditions can be difficult. Controversy surrounds both the clinical and histologic criteria used to distinguish lymphomatoid papulosis, a benign disorder, from CD30+ anaplastic large-cell lymphoma. Three case histories illustrate important points in categorizing different lymphoproliferative disorders as benign or malignant. We emphasize a multidisciplinary approach to improve diagnosis and patient management.

Aged↗
PubMed1994

Giant cell lichenoid dermatitis: a possible manifestation of sarcoidosis.

Giant cell lichenoid dermatitis is a recently described dermatosis thought to be an unusual lichenoid drug eruption. It is characterized by a generalized, pruritic, papulosquamous eruption sparing palms, soles, face and mucous membranes. Histopathologic findings include areas of epidermal hyperplasia and atrophy with focal vacuolar alteration of the basal layer, exocytosis and cytoid body formation. The dermis contains a band-like, mononuclear cell infiltrate at the dermoepidermal junction with admixed eosinophils, plasma cells and large multinucleate cells. The histologic differential diagnosis includes infectious processes, sarcoidosis, lichen nitidus, lupus erythematosus and lichen planus. We report 3 patients with giant cell lichenoid dermatitis, one of whom was subsequently diagnosed as having sarcoidosis. Because giant cell lichenoid dermatitis may resemble sarcoidosis both clinically and histologically, and because cutaneous sarcoid is often associated with systemic involvement, the diagnosis of sarcoid should be strongly considered in patients with giant cell lichenoid dermatitis.

Aged↗
PubMed1994

Electrophysiological properties of guinea pig trigeminal motoneurons recorded in vitro.

1. Intracellular recording and stimulation were made from guinea pig trigeminal motoneurons (TMNs) in brain stem slices. Electrophysiological properties were examined and the underlying currents responsible for motoneuron excitability were investigated by the use of current clamp and single electrode voltage clamp (SEVC) techniques. 2. The voltage responses to subthreshold hyperpolarizing or depolarizing current pulses showed voltage- and time-dependent inward rectification. SEVC analysis demonstrated that the hyperpolarizing inward rectification resulted from the development of a slowly occurring voltage-dependent inward current activated at hyperpolarized membrane potentials. This current persisted in solutions containing low Ca2+/Mn2+, tetraethylammonium (TEA), and Ba2+, whereas it was reduced by 1-3 mM cesium. The depolarizing inward rectification was mediated by a persistent sodium current (INa-P) that was completely abolished by bath application of tetrodotoxin (TTX). 3. Action potential characteristics were studied by intracellular stimulation with brief current pulses (< 3 ms) in combination with ionic substitutions or application of specific ionic conductance blocking agents. Bath application of TTX abolished the action potential, whereas 1-10 mM TEA or 0.5-2 mM 4-aminopyridine (4-AP) increased, significantly, the spike duration, suggesting participation of the delayed rectifier and A-current type conductances in spike repolarization. SEVC analysis revealed a TEA-sensitive sustained outward current and a fast, voltage-dependent, transient current with properties consistent with their roles in spike repolarization. 4. TMN afterhyperpolarizing potentials (AHPs) that followed a single spike consisted of fast and slow components usually separated by a depolarizing hump [afterdepolarization (ADP)]. The fast component was abolished by TEA or 4-AP but not by Mn2+, Co2+, or the bee venom apamin. In contrast, the slow AHP was readily reduced by Mn2+, Co2+, or apamin, suggesting participation of an apamin-sensitive, calcium-dependent K+ conductance in the production of the slow AHP. SEVC analysis and ionic substitutions demonstrated a slowly activating and deactivating calcium-dependent K+ current with properties that could account for the slow AHP observed in these neurons. 5. Repetitive discharge was examined with long depolarizing current pulses (1 s) and analysis of frequency-current plots. When evoked from resting potential (about -55 mV), spike onset from rheobase occurred rapidly and was maintained throughout the current pulse. At higher current intensities, early and late adaptations in spike discharge were observed. Frequency-current plots exhibited a bilinear relationship for the first interspike interval (ISI) in approximately 50% of the neurons tested and in most neurons tested during steady-state discharge (SS).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1994

Neuropharmacological mechanisms underlying rhythmical discharge in trigeminal interneurons during fictive mastication.

1. We have examined the effects of iontophoretic application of antagonists to excitatory amino acid (EAA) receptors, as well as glycine and gamma-aminobutyric acid (GABA), on rhythmically active (RA) brain stem neurons during cortically induced masticatory activity (RMA) in the anesthetized guinea pig. Ten of these neurons were antidromically activated at latencies of 0.3-0.9 ms by stimulation of the trigeminal motor nucleus (MoV). 2. RA neurons were divided into closer and opener type according to the phase of activation during RMA. Iontophoretic application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a specific non-N-methyl-D-aspartate (NMDA) receptor antagonist, suppressed discharge of both closer and opener type RA neurons during RMA. In contrast, iontophoretic application of 3-((1)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), a specific NMDA receptor antagonist, was not effective in suppressing discharge of most opener type RA neurons but did reduce activity of closer type RA neurons. 3. Spike discharge of most RA neurons was time locked to each cortical stimulus during RMA. Some of the RA neurons were activated at a short latency to short pulse train stimulation of the cortex in the absence of RMA. In most cases CNQX reduced such time-locked responses during RMA and greatly reduced discharge evoked by short pulse stimulation of the cortex in all cases. In contrast, CPP was not as effective in suppressing either the time-locked responses during RMA or the discharge evoked by short pulse train stimulation of the cortex. 4. D,L-Homocysteic acid (HCA) application produced low level maintained discharge in RA neurons before RMA induction. When RMA was evoked in combination with HCA, rhythmical burst discharges with distinct interburst periods during the opening phase of RMA were observed in most closer type RA neurons. In contrast, during RMA in combination with HCA application, opener type RA neurons showed burst discharges that were modulated during the RMA cycle but lacked distinct interburst periods during the closer phase of the cycle. 5. During application of strychnine (STR), a glycine antagonist, discharge of closer type RA neurons increased in the opener phase of RMA during continuous HCA application. In contrast, bicuculline methiodide (BIC), a GABA antagonist, did not increase unit discharge of closer type RA neurons in the opener phase of RMA. 6. It is concluded that closer type RA neurons receive, alternatively, EAA-mediated excitatory and glycine-mediated inhibitory masticatory synaptic drive signals during RMA.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

Hanlester Laboratories decision: how is it affected by new sanctions and penalties regulations?

The following excerpts from the briefs recently submitted to Administrative Law Judge (ALJ) Stephen Kessel in the Hanlester Laboratories administrative proceeding, deal with the applicability of a January 29, 1992 final rule on fraud and abuse sanctions and civil money penalties (57 Fed. Reg. 3,298 (January 29, 1992) to the case. Counsel for Hanlester Laboratories, Patric Hooper and W. Bradley Tully of Hooper, Lundy & Bookman, Inc. in Los Angeles, argue that the Office of the Inspector General (OIG-HHS) is trying to change the rules "well after the game has been played," and that this "is obviously being done for the sole purpose of negating the rights" of the Hanlester respondents. The Office of the General Counsel (OGC), in a brief prepared by OGC attorney Larry J. Goldberg, contends that ALJ Kessel "must apply these regulations in rendering his decision," arguing that the "regulations at issue do not even involve a change in policy, but merely a clarification." The Hanlester case (The Inspector General v. Hanlester Network et al., No. C-448 (Department of Health and Human Services, Departmental Appeals Board, Civil Remedies Division) was remanded by the Departmental Appeals Board to ALJ Kessel on September 18, 1991. It is the first case to consider the application of the antikickback statute to a joint venture, and is the first HHS civil exclusion case to be brought as the result of allegations of violations of the antikickback statute (see HealthSpan, November 1991, p. 8).

Fees and Charges↗
PubMed1991

Genioglossus EMG activity during rhythmic jaw movements in the anesthetized guinea pig.

The electromyograph (EMG) activity of the left anterior digastric and the genioglossus muscles was studied in ketamine-anesthetized guinea pigs under 3 separate jaw movement paradigms. The first paradigm has been previously named spontaneous rhythmic jaw movements. These jaw movements occur 1-2 h after the onset of ketamine anesthesia. After spontaneous rhythmic jaw movements began, a single dose of apomorphine caused a new, second jaw movement paradigm to occur, apomorphine-induced rhythmic jaw movements. The final paradigm, cortically-evoked rhythmic jaw movements, was elicited by electrical stimulation of the masticatory area of the cerebral cortex. Genioglossus EMG activity was complex and highly variable in spontaneous rhythmic jaw movements; however, apomorphine-induced jaw movements were characterized by simultaneously occurring rhythmic EMG bursts of approximately 230 ms duration in both the digastric and genioglossus muscles. In 4 of 5 animals, genioglossus muscle activity onset preceded digastric muscle activity onset by approximately 20 ms. These results support the hypothesis that apomorphine-induced rhythmic jaw movements are an analog of lapping in the awake animal. In cortically-evoked rhythmic jaw movements, both digastric and genioglossus EMG activity were time-locked to the cortical electrical stimulation, with an onset latency of approximately 11 ms for the digastric EMG activity and of 16 ms for the genioglossus EMG activity. These results support the hypothesis that both trigeminal and hypoglossal motoneuron pools are closely coupled in certain coordinative movement patterns.

Anesthesia, General↗
PubMed1991

Effect of Herpes simplex virus infection on the trigeminal jaw-opening reflex in guinea pigs.

Herpes simplex virus (HSV) infection induces numerous electrophysiological and microscopic changes in neurons in vitro. To investigate the effect of HSV infection on in vivo neuronal activity, we induced an acute, latent and reactivated HSV infection of the trigeminal ganglia of guinea pigs through orofacial HSV inoculation and studied its effect on the trigeminal jaw-opening reflex of anesthetized guinea pigs. During the acute viral infection period both the threshold for elicitation of the reflex, and the latency to the onset of the reflex response were increased. During the latent viral infection in the trigeminal ganglia, the jaw-opening reflexes in the viral infected animals were not different from those of non-infected control animals. However, reactivation of the latent viral infection in these animals resulted in increases in both the threshold and latency of the jaw-opening reflex. These changes were similar to those found in animals with the acute viral infection. These results indicate that acute or reactivated latent HSV infection of the nervous system results in functional changes in the reflex pathways involving the trigeminal gasserian ganglia and brainstem neurons harboring infectious HSV-1.

Animals↗
PubMed1991

Porokeratosis arising in a burn scar.

A histologically verified porokeratosis arose in a burn scar on the back of a 47-year-old man. This phenomenon has not been previously reported. We discuss the literature on porokeratosis, the relation between epidermal and dermal injury, and the genesis of this lesion.

Burns↗
PubMed1990

The effects of nanoliter ejections of lidocaine into the pontomedullary reticular formation on cortically induced rhythmical jaw movements in the guinea pig.

In the ketamine/urethane anesthetized guinea pig, electromyographic (EMG) responses of the anterior digastric muscle were studied when loci within the lower brainstem were microejected with lidocaine (2%) during rhythmical jaw movements (RJMs) evoked by repetitive electrical stimulation of the masticatory area of the cortex. The area investigated was between the trigeminal motor nucleus (Mot V) and the rostral pole of the inferior olive. Microejections of lidocaine, contralateral to the cortical stimulus site, into the ventral-medial portion of Mot V where digastric motoneurons are known to be located, resulted in reduction or complete abolishment of the digastric EMG activity ipsilateral to the ejection with no effective change in mean cycle duration (CD) or mean percent normalized integrated amplitude of the contralateral digastric EMG. Microejections of lidocaine, contralateral to the cortical stimulus site, into the ponto-medullary reticular formation in areas that included portions of the caudal nucleus pontis caudalis (PnC), nucleus gigantocellularis (GC), medial nucleus parvocellularis (PCRt), and dorsal paragigantocellularis (dPGC), in most cases produced a bilateral reduction in the mean normalized integrated amplitude and a bilateral increase in the mean cycle duration. In these sites, the bilateral increase in mean cycle duration of digastric EMG bursts was also associated with a significant increase of coefficient of variation in CD. In many cases, microejection of lidocaine completely abolished rhythmical digastric activity, bilaterally. HRP injections into Mot V were performed to determine the locations of trigeminal premotoneurons and their relationship to effective lidocaine sites for rhythmical jaw movement suppression. Retrogradely labeled cells were found mainly in the mesencephalic nucleus of V; trigeminal principal and spinal V sensory nuclei, bilaterally; and within the intermediate and lateral regions of reticular formation, bilaterally. No labeling was found in the medial reticular formation, including the nucleus gigantocellularis and dorsal paragigantocellularis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

An analysis of mandibular movement trajectories and masticatory muscle EMG activity during drinking in the guinea pig.

Electromyographic (EMG) activity of the anterior digastric, lateral pterygoid, and deep masseter muscles as well as the associated jaw movements during drinking were studied in the awake guinea pig. Drinking was characterized by rhythmic, vertically directed jaw movements with little or no associated lateral movements. The jaw opening phase of each cycle was associated with bilaterally synchronized EMG activity in the digastric and lateral pterygoid muscles, and the jaw closing phase with bilaterally synchronized activity in the masseter muscles. The mean EMG burst durations (+/- 1 S.E.) in the digastric and masseter muscles were 164.2 +/- 14.93 ms and 94.3 +/- 26.44 ms, respectively. The digastric muscle EMG burst duration was significantly correlated with drinking cycle time and with masseter muscle EMG onset; on the other hand, masseter muscle EMG burst duration was not correlated with cycle time. These patterns of EMG activity and jaw movement trajectories are similar to those induced by apomorphine in the ketamine-anesthetized guinea pig.

Animals↗
PubMed1989

Angiotensin II-induced rhythmic jaw movements in the ketamine-anesthetized guinea pig.

The EMG activity of the left anterior digastric muscle as well as associated jaw movements were studied in ketamine-anesthetized guinea pigs that had received i.v. infusions of angiotensin II (ANG-II). Rhythmic jaw movements with two distinct movement profiles were associated with ANG-II infusion. One movement profile was typified by vertical jaw opening and closing movements with little or no associated horizontal movement. The second rhythmical jaw movement profile was unlike the first in that jaw closing was accompanied by a significant horizontal deflection of the jaw. Both jaw movement profiles were similar in that little or no horizontal movement occurred during jaw opening. Tongue protrusions were also observed during jaw opening in both cases. The results show that ANG-II induces rhythmic jaw movements in anesthetized guinea pigs. ANG-II-induced jaw movement profiles and digastric muscle EMG activity are similar to those seen after an i.v. injection of apomorphine in the anesthetized guinea pig, and to those associated with lapping in the awake animal.

Anesthesia↗
PubMed1989

Intracellular analysis of trigeminal motoneuron rhythmical activity during stimulation of pontomedullary reticular formation in anesthetized guinea pig.

1. The effects of repetitive stimulation of the nucleus pontis caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation on jaw opener and closer motoneurons were examined. The PnC-Gi was stimulated at 75 Hz at current intensities less than 90 microA. 2. Rhythmically occurring, long-duration, depolarizing membrane potentials in jaw opener motoneurons [excitatory masticatory drive potential (E-MDP)] and long-duration hyperpolarizing membrane potentials [inhibitory masticatory drive potentials (I-MDP)] in jaw closer motoneurons were evoked by 40-Hz repetitive masticatory cortex stimulation. These potentials were completely suppressed by PnC-Gi stimulation. PnC-Gi stimulation also suppressed the short-duration, stimulus-locked depolarizations [excitatory postsynaptic potentials (EPSPs)] in jaw opener motoneurons and short-duration, stimulus-locked hyperpolarizations [inhibitory postsynaptic potentials (IPSPs)] in jaw closer motoneurons, evoked by the same repetitive cortical stimulation. 3. Short pulse train (3 pulses; 500 Hz) stimulation of the masticatory area of the cortex in the absence of rhythmical jaw movements activated the short-latency paucisynaptic corticotrigeminal pathways and evoked short-duration EPSPs and IPSPs in jaw opener and closer motoneurons, respectively. The same PnC-Gi stimulation that completely suppressed rhythmical MDPs, and stimulus-locked PSPs evoked by repetitive stimulation to the masticatory area of the cortex, produced an average reduction in PSP amplitude of 22 and 17% in jaw closer and opener motoneurons, respectively. 4. PnC-Gi stimulation produced minimal effects on the amplitude of the antidromic digastric field potential or on the intracellularly recorded antidromic digastric action potential. Moreover, PnC-Gi stimulation had little effect on jaw opener or jaw closer motoneuron membrane resting potentials in the absence of rhythmical jaw movements (RJMs). PnC-Gi stimulation produced variable effects on conductance pulses elicited in jaw opener and closer motoneurons in the absence of RJMs. 5. These results indicate that the powerful suppression of cortically evoked MDPs in opener and closer motoneurons during PnC-Gi stimulation is most likely not a result of postsynaptic inhibition of trigeminal motoneurons. It is proposed that this suppression is a result of suppression of activity in neurons responsible for masticatory rhythm generation.

Action Potentials↗
PubMed1988

Effects of pontomedullary reticular formation stimulation on the neuronal networks responsible for rhythmical jaw movements in the guinea pig.

1. In the ketamine-anesthetized guinea pig, electromyographic (EMG) responses of the digastric muscle and vertical and horizontal movements of the mandible were studied when loci within the caudal pontine and rostral medullary reticular formation were stimulated during rhythmic jaw movements (RJMs) evoked by stimulation of the masticatory area of the cortex. 2. Within these regions electrical brain stem stimulation of the pontis nucleus caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation completely blocked RJMs at stimulus intensities as low as 10 microA while suppressing the short-latency digastric EMG response that was time locked to each cortical stimulus in the train. PnC-Gi stimulation did not, however, reduce the excitability of the short-latency corticotrigeminal excitatory pathway to digastric motoneurons when tested by short pulse train stimulation at 2 Hz (3 pulses, 500 Hz, 0.3 ms) in the absence of RJMs. 3. Short trains (80 ms) of PnC-Gi stimuli delivered at various phases of the RJM cycle produced a permanent phase shift of the RJM rhythm. If the stimulus train was delivered at an early phase of the cycle (8-40%) the next cycle onset was advanced; if the train was delivered later in the cycle (60-80%) the next cycle onset was delayed. Long trains of PnC-Gi stimuli (100, 200, 300, and 400 ms) increased the time of onset of the next cycle by an amount directly proportional to the duration of the stimulus train. 4. Digastric EMG activity occurring during cortically evoked RJMs occupied nearly 50% of the cycle. If a short train of PnC-Gi stimuli was delivered between approximately 5 and 125 ms after the onset of the burst, the duration of the burst was significantly shortened. 5. These results demonstrate that the suppression of cortically evoked RJMs resulting from PnC-Gi stimulation is due to direct effects on central circuits responsible for the production of the RJM behavior and not on the motoneurons themselves. The evidence presented is consistent with our previously presented hypothesis that the neurons involved in mediating the short-latency corticotrigeminal pathway to digastric motoneurons are separate and distinct from those neurons comprising the central networks responsible for the production of the fundamental jaw oscillation during RJMs.

Animals↗
PubMed1986

Comparison of mandibular movement trajectories and associated patterns of oral muscle electromyographic activity during spontaneous and apomorphine-induced rhythmic jaw movements in the guinea pig.

Vertical and horizontal movements of the lower jaw (mandible) of ketamine-anesthetized guinea pigs were recorded in association with electromyographic (EMG) activity in the anterior digastric, lateral pterygoid, medial pterygoid, and deep masseter muscles during spontaneously occurring rhythmic jaw movements (SRJMs) and during rhythmical jaw movements induced by the intravenous administration of apomorphine (ARJMs). Both ARJMs and SRJMs were near periodic and occurred at frequencies in the 2- to 5-Hz range. However, the profiles of the mandibular movements and associated patterns of jaw muscle EMG activity differed dramatically for SRJMs versus ARJMs. SRJMs were characterized by prominent lateral excursions of the mandible that occurred in association with both the jaw opening and closing movements. The lateral excursions were directed to the left side on some SRJM cycles and to the right side on others. The direction of the lateral component alternated irregularly, but no more than three consecutive cycles with horizontal movements to the same side were observed at any time. Each SRJM cycle was generated by the occurrence of one of two coordinated sequences of EMG activity. One sequence produced right-sided cycles, the other produced left-sided cycles. Each sequence was initiated by an EMG burst in the digastric muscle ipsilateral to the direction of the horizontal excursion of the mandible, followed by EMG bursts in the contralateral digastric, lateral pterygoid, and medial pterygoid muscles. The EMG bursts in the digastrics and contralateral lateral pterygoid muscles were associated with jaw opening and the initial stage of lateral movement. EMG activity in the contralateral medial pterygoid muscle was associated with the onset of closing and a second stage of lateral movement. Masseter muscle activity was also observed during SRJMs, but only in a subset of the animals tested (3 of 12). When present, the masseter activity began well after the onset of jaw closing. No significant horizontal mandibular movements were observed during ARJMs. The mandibular trajectories during opening and closing always remained close to the midline. The opening phase of ARJM cycles was associated with bilaterally synchronized activity in the digastric and lateral pterygoid muscles. The closing phase was associated with bilaterally symmetric activity in the masseter muscles. The medial pterygoid muscles displayed little or no EMG activity during ARJMs. The durations of the EMG bursts recorded in the masseter muscle were correlated with cycle time during SRJMs, as were the burst durations of the digastric and lateral pterygoid muscles during ARJMs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Effects of a serotonin agonist and antagonist on cortically induced rhythmical jaw movements in the anesthetized guinea pig.

The effects of systemic injections of a serotonin agonist (quipazine), and antagonist (methysergide), on rhythmical jaw movements (RJMs) in the ketamine anesthetized guinea pig were examined. It was observed that quipazine, (1) significantly elevated the electrical threshold for inducing RJMs by repetitive stimulation of the masticatory cortex and (2) reduced the amplitude of the digastric and masseter EMG activity during RJMs. In contrast, the excitability of the short latency pathway from masticatory cortex to digastric motoneurons, and the excitability of the digastric reflex evoked by electrical stimulation of the mucosa of the tongue were not significantly affected by quipazine administration. Methysergide administration had little effect on the threshold for evoking RJMs, and on the excitability of the digastric reflex and short latency pathway from cortex to digastric motoneurons. These data suggest that the central pattern generator (CPG) for RJMs is not critically dependent upon serotonin receptor activation since RJMs can be induced after methysergide administration. On the other hand, excitation of the CPG by repetitive cortical stimulation can be inhibited by serotonin receptor activation. These results are interpreted as supporting our previously described model of RJM production by repetitive cortical stimulation.

Animals↗