Rostral Lesions Research Articles

Lesions of the periaqueductal gray and rostral ventromedial medulla disrupt antinociceptive but not cardiovascular aversive conditional responses

The presentation of an auditory stimulus that signals a noxious event such as foot shock results in the simultaneous expression of multiple aversive conditional responses (CRs), which include a transient elevation of arterial blood pressure (ABP) and an opioid-mediated form of hypoalgesia. Recent evidence suggests that the neural circuits responsible for the expression of these two aversive responses may overlap. In the present study, rats were trained using a Pavlovian fear conditioning paradigm in which white noise was repeatedly paired with shock. After training, groups of animals received electrolytic lesions centered in the dorsal or ventral periaqueductal gray (PAG) or in the medial or lateral rostral medulla. In sham-lesioned animals that were given paired presentations of noise and shock, subsequent presentation of the auditory stimulus caused a significant transient elevation of ABP and time-dependent inhibition of the tail flick reflex evoked by radiant heat. Lesions of either the dorsal or the ventral PAG blocked the antinociceptive CR but did not significantly affect ABP responses. Lesions of the ventromedial, but not the lateral, rostral medulla blocked hypoalgesia. Rostral medullary lesions did not reliably affect stimulus-evoked cardiovascular responses or baseline ABP. These results indicate that antinociceptive and cardiovascular conditional responses are anatomically dissociable and support our proposal that conditional hypoalgesia is mediated by a serial neural circuit that includes the amygdala, PAG, and rostral ventromedial medulla.

Pathophysiology of saccadic contrapulsion in unilateral rostral cerebellar lesions

Saccadic lateropulsion is a typical sign in Wallenberg's syndrome and midline lesions of the caudal cerebellum (oculomotor vermis, nucl. fastigii). There are only two reports on saccadic contrapulsion (contraversive to the side of the lesion) after a rostral cerebellar lesion. The authors describe a patient with an infarction in the area of the right medial branch of the superior cerebellar artery affecting the medio-lateral rostral cerebellum which showed a saccadic contrapulsion with hypermetric saccades to the left and hypermetric saccades to the right. Based on recent experimental neuro-physiological, anatomical and lesion studies, which demonstrate that the caudal fastigial nucleus is essential for accurate saccades, it is proposed that a lesion of the efferent pathways from the caudal fastigial nucleus to the direct premotor structures for saccades in the brainstem which cross within the cerebellum, causes the contrapulsion seen in the patient.

Skew deviation with ocular torsion: a vestibular brainstem sign of topographic diagnostic value.

Fifty-six patients with unilateral brainstem infarctions presenting with skew deviation of the eyes were analyzed for static vestibular function in the roll plane. Ischemic lesions were allocated to the level and side of the brainstem by the clinical syndrome and neuroimaging. Two findings of clinical relevance were obtained: (1) All skew deviations were ipsiversive (ipsilateral eye was undermost) with caudal pontomedullary lesions and contraversive (contralateral eye was lowermost) with rostral pontomesencephalic lesions. (2) All skew deviations were associated with concomitant ocular torsion and tilts of subjective visual vertical toward the undermost eye. Thus, skew deviation or more correctly, ocular skew torsion is a sensitive brainstem sign of localizing and lateralizing value. Evidence is presented that the ocular skew torsion sign indicates a vestibular tone imbalance in the roll plane secondary to graviceptive pathway lesions.

ワレンベルグ症候群における延髄病変部位と自発眼振との関連

Spontaneous nystagmus was examined in 38 patients with lateral medullary infarct syndrome. Although horizontal nystagmus is commonly observed in this syndrome, the direction of nystagmus is not always consistent with the side of the lesion. Horizontal nystagmus beats away from the side of infarction in 79% of patients. Meanwhile, torsional nystagmus which is characteristic of this syndrome beats away from the side of infarction (ipsilateral slow phase beats) in all cases. In an investigation of the mechanism of torsional nystagmus, patients were assigned to one of two groups: typical form (lesions of the descending root of the trigeminal nerve) and ventral form (no or incomplete involvement of the root of the trigeminal nerve). Although horizontal nystagmus occurred in both the typical and the ventral form, torsional nystagmus was observed only in the typical form. Furthermore, cerebellar signs were more common within patients with torsional nystagmus than in those of horizontal nystagmus. There-fore, it is suspected that torsional nystagmus in the lateral medullary infarct syndrome may originate not in ventral but in rostral and dorsal lesions of the medulla, including the vestibular nucleus, which is related to torsional and vertical eye movements.

Stimulation of corticospinal pathways at the level of the pyramidal decussation in neurological disorders.

A newly developed technique of brainstem stimulation was applied in 14 normal subjects and 23 patients with various neurological disorders. The electromyographic (EMG) responses of limb muscles following cortical, brainstem and cervical stimulation were recorded. The cortical-brainstem conduction time and brainstem-cervical conduction time were then calculated from the difference in latency between the two sites of stimulation. From the regression lines of the relationship between the normal conduction times in the first dorsal interosseous muscle and the length of the descending tracts, the site of activation by brainstem stimulation was estimated to lie near the cervical-medullary junction. The most distal lesion causing prolongation of cortical-brainstem conduction time was a small cerebral infarction in the lower pons. Herniation of the third cervical spinal disc was the most rostral lesion resulting in delayed brainstem-cervical conduction time and normal cortical-brainstem conduction time. These observations suggest that activation occurs at the level of the cervical-medullary junction where the pyramidal decussation lies. The conduction velocities of the activated tracts estimated from the regression lines for normal individuals were 57-92 m/s. In patients with supratentorial lesions, the threshold for brainstem stimulation was abnormally high. The abnormal findings in this test were correlated significantly with the clinical pyramidal signs. This suggests that the EMG responses elicited by brainstem stimulation are mediated mainly by the corticospinal tract. We conclude that the brainstem stimulation technique would be clinically useful for localization of lesions in the corticospinal tract; the primary lesion can be localized whether above or below the pyramidal decussation.

Funicular organization of avian brainstem‐spinal projections

The purpose of this study was to determine which reticulospinal projections need to be preserved to allow voluntary walking and to differentiate between those pathways descending within the ventrolateral funiculus versus the ventromedial funiculus. Retrogradely transported tracers (True Blue, Fast Blue, Diamidino Yellow dihydrochloride, fluorescein-conjugated dextran-amines) were used alone as discrete funicular injections (4-5 microliters) into the lumbar cord (L1), or in conjunction with a more rostral subtotal lesion of the low thoracic cord, to determine the trajectories of brainstem-spinal projections in adult ducks and geese. No difference was found between the species. The major components of the ventromedial funiculus include projections from the medullary reticular formation, pontine reticular formation, raphe obscurus and pallidus, lateral vestibular nucleus, and interstitial nucleus, and to a minor extent from the locus coeruleus, lateral hypothalamus, and nucleus periventricularis hypothalami. The components of the ventrolateral funiculus (VLF) include projections from the nucleus of the solitary tract, nucleus alatus, pontomedullary reticular formation, raphe pallidus, raphe magnus, locus coeruleus, subcoeruleus, lateral vestibular, and descending vestibular nuclei. The principal descending projections within the dorsolateral funiculus (DLF) arose from the red nucleus, the paraventricular nucleus, locus coeruleus, subcoeruleus, dorsal division of the caudal medullary reticular formation, and raphe magnus. The functional implications of the distribution of these descending pathways are discussed with regard to locomotion. Since birds were able to walk despite bilateral lesion of the DLF or VMF but were unable to walk following a bilateral lesion of the VLF, this suggests that medullary reticulospinal pathways coursing within the VLF are essential for the provision of locomotor drive.

Neuro‐ophthalmologic signs of AIDS

In 50 hospitalized patients with acquired immunodeficiency syndrome, signs of central eye movement limitation (28 cases) were most common. Peripheral eye movement limitations (18), abnormalities of vision (18), and abnormal spontaneous eye movements (15) occurred with about equal frequency. Meningitis (17), usually due to lymphoma (8) or Cryptococcus (8), was the usual cause of peripheral nervous system involvement, while toxoplasmosis (18) was more common than lymphoma (4) or presumed viral causes (8) in producing CNS dysfunction. The midbrain and pretectal (8) were affected about as often as the pontine tegmentum (9), but rostral brainstem lesions appeared to be the result of toxoplasmosis (4) or lymphoma (3), whereas a viral etiology was the presumed cause of most caudal stem involvement.

Induction of somatic sensory inputs to the lateral geniculate nucleus in congenitally blind mice and in phenotypically normal mice

The incidence of aberrant innervation of the lateral geniculate nucleus by ascending somatic sensory axons was examined following injections of wheat germ agglutinin conjugated with horseradish peroxidase into the dorsal column nuclei of adult mice which were: (1) normal; (2) normal, but bilaterally enucleated on the day of birth; (3) normal, but received a large unilateral lesion of the rostral cortex on the day of birth; (4) normal, bilaterally enucleated, as well as unilaterally lesioned in the rostral cortex on the day of birth; (5) homozygous for an ocular retardation mutation (or j/or j); or (6) homozygous for the or j mutation and received a large unilateral lesion of the rostral cerebral cortex on the day of birth. In the phenotypically normal animals which were untreated, no somatic sensory inputs enter into the dorsal lateral geniculate nucleus. A few labeled axons enter into and arborize within the dorsal lateral geniculate nucleus in normal animals which received bilateral enucleations or unilateral rostral cortical lesions on the day of birth. However, in congenitally blind animals and in phenotypically normal animals which received bilateral enucleations as well as unilateral rostral cortical lesions on the day of birth, a significant number of labeled axons enter into and arborize within the dorsal lateral geniculate nucleus. Among all these experimental groups, the densest innervation of the lateral geniculate nucleus occurred in congenitally blind animals which received rostral cortical lesions on the day of birth. In these, robust arborizations of labeled somatic sensory axons occupy a substantial extent of the lateral geniculate nucleus. These results not only demonstrate that ascending somatic sensory axons can be rerouted to the lateral geniculate nucleus, but also indicate that the ability of a thalamic afferent pathway to undergo extensive reorganization and to innervate inappropriate thalamic targets following early perturbations is not unique to the retinal projection (in which this has previously been demonstrated), and may be a more general characteristic of the major thalamic afferent systems.

Facial dystonia: clinical features, prognosis and pharmacology in 31 patients

The natural history and response to different treatments were assessed in 31 consecutive patients with blepharospasm (BS) and/or oromandibular dystonia (OMD). The mean age at onset was 52.4 years and there was a female preponderance of 2.5 to 1. Ocular symptoms preceded the onset of blepharospasm in more than 50% of the affected patients, whereas psychiatric and dental problems prior to the onset of focal dystonia were found in 10% and 13% of the cases respectively. Dystonia elsewhere, mainly in the craniocervical area, was found in 23% of patients and appeared to follow a somatotopic progression. The first 2-3 years of history were crucial for the spread of dystonia to other face and body parts. When OMD was the first symptom, a lower tendency of dystonia to progress elsewhere was observed. A putative cause was found in 14% of patients who showed clinical and radiographic evidence of basal ganglia or rostral brainstem-diencephalon lesions. The response to different drugs was inconsistent although transient improvement was induced by haloperidol in 6 patients, by L-Dopa plus deprenyl in 3 patients, by trihexyphenidyl in 2 patients and by clonazepam in 2 patients. One, apparently spontaneous, remission was observed. Botulinum A toxin was injected in the orbicularis oculi of 8 patients affected by BS: moderate to marked improvement lasting 5 to 30 weeks (mean 14.5 weeks) was achieved in all cases; transient ptosis, lasting 1 to 3 weeks, occurred in 3 cases.

Localization by kainic acid lesions of neurones transmitting the carotid chemoreceptor stimulus for respiration in rat.

1. An attempt has been made to test the hypothesis that in the nucleus of the tractus solitarius (NTS) in the rat, the most caudal region of synaptic terminals of the carotid sinus nerve, just caudal to the obex, represents mainly the site of synapse of chemoreceptor fibres from the carotid body. 2. Under halothane anaesthesia, the neurotoxin kainic acid was used to lesion this region and a second region, immediately rostral to obex, where terminals are thought to arise mainly from baroreceptor fibres of the carotid sinus nerve. 3. Measurements based on the distribution of fluorescent dye co-injected with the kainic acid showed that the two groups of 100 nl microinjections were centered 0.82 mm apart and that the injectate spread through mean distances of 0.57 mm (caudal microinjections) and 0.52 mm (rostral microinjections). Nissl staining was used to determine cellular degeneration. The caudal lesions mostly involved ventrolateral and commissural subnuclei of NTS and the rostral lesions involved lateral and dorsolateral subnuclei. 4. Ventilatory sensitivity to hypoxia was tested under light halothane anaesthesia, 1 day after lesioning. To enhance the responses, the contralateral carotid sinus nerve was sectioned prior to experiments. Caudal lesions reduced the ventilatory response to inspired oxygen (20.9-9.6% O2) by a mean of 67% and rostral lesions by 18% of the effect produced by carotid sinus nerve section on that side. Subsequent section of the carotid sinus nerve on the side of the NTS lesion confirmed that caudal lesions produced effects comparable to those of carotid body denervation; rostral lesions did not. 5. These results strongly support the hypothesis that chemoreceptor and baroreceptor afferent fibres in the carotid sinus nerve synapse at substantially separable sites in the nucleus of the tractus solitarius. The identification of the site in NTS caudal to the obex as the principal site of carotid chemoreceptor synapses places them close to but not upon respiratory premotor neurones of the same nucleus.

Angiotensin acts at the subfornical organ to increase plasma oxytocin concentrations in the rat

We have examined the effects of systemic angiotensin II (AII) on plasma oxytocin (OXY) concentrations in freely moving male Sprague-Dawley rats. We have also examined the role of the subfornical organ (SFO) as a CNS site at which circulating AII acts to influence secretion of this neurohypophysial peptide. OXY concentrations were measured by radioimmunoassay in plasma samples obtained by drawing blood samples through indwelling atrial catheters. In SFO intact animals ( n = 8) AII infusion (1.0 μg/kg/min) resulted in increases in plasma OXY concentrations from baseline values of 6.8 ± 2.5 pg/ml to postinfusion concentrations of 44.9 ± 11.9 pg/ml. In a second series of experiments electrolytic lesions were placed in the region of the SFO prior to testing the effects of AII infusion on OXY concentrations. Two further experimental groups were thus established according to the histologically verified location of lesions in either the rostral or caudal SFO. In the caudal SFO lesioned group AII infusion resulted in increases in plasma OXY concentrations from control values of 6.9 ± 1.4 pg/ml to postinfusion levels of 45.1 ± 9.8 pg/ml. These changes were not significantly different from the SFO intact group. In contrast rostral SFO lesions resulted in significantly elevated basal concentrations of OXY (17.4 ± 3.4 pg/ml, n = 6) while postinfusion concentrations were found to be 22.8 ± 4.9 pg/ml indicating that AII infusion was without effect following such lesions. These data are in accordance with the hypothesis that circulating AII acts at the SFO to influence SFO efferents which in turn activate OXY secreting neurons in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei. These neuroendocrine cells then release this peptide into the systemic circulation from the posterior pituitary.

‘Cat P300’ disappears after septal lesions

Endogenous responses were recorded from 9 awake cats with loud and soft clicks randomly presented as rare ( P = 0.15) or frequent ( P = 0.80) stimuli; a reinforced tone CS ( P = 0.05) resulted in a conditioned eye blink response and focused the cat's attention on the auditory stimuli. Subsequent to 12 preoperative recording sessions the medial septal area was lesioned in 7 cats and similar but more rostral lesions were placed in 2 cats. Thereafter, 12 postoperative recording sessions were carried out, the animals were terminated, and the brains processed for AChE histochemistry and histology of the lesioned areas. Destruction of the medial septum and vertical limb of the diagonal band of Broca resulted in a transient postoperative ‘cat P300’ followed by reduction and disappearance of the response. The hippocampus of these animals was characterized by marked AChE depletion. In contrast, the animals with lesions rostral to the medial septal area showed no postoperative change in the P300 response and no depletion of hippocampal AChE. These data indicate an important role for the medial septal area as a modulator of ‘cat P300’ generation possibly through the cholinergic component of the septohippocampal projection system.

Central control of gastric acid secretion by extralateralhypothalamic nuclei

Whether secretion of gastric acid (GAS) is in response to peripheral and/or central administration of chemical or electrical stimuli can be differentiated by vagotomy. GAS has been shown to be controlled by specific lateral hypothalamic (LHA) neurons. Application of 2-deoxy-D-glucose (2-DG) or insulin to the LHA by microinjection or iontophoresis has experimentally induced GAS. The paraventricular nucleus (PVN) has now been found to also affect GAS. GAS was produced more copiously and more quickly by rostral PVN lesion than by lesion of the ventromedial (VMH) or dorsomedial (DMH) nucleus, and nearly as much by caudal PVN lesion. Microinjection of 2-DG into the LHA induced GAS more potently in animals with rostral PVN lesions than in those with caudal PVN, VMH or DMH lesions, or in intact animals. Results indicate that the PVN may be an additional central site from which GAS is affected.

Interlimb coordination during stepping in the cat: The role of the dorsal spinocerebellar tract

The role of the dorsal spinocerebellar tract (DSCT) in the neural control of normal interlimb coordination during overground stepping in adult cats was investigated using select spinal cord lesions. Previously, it had been shown that lesions of the caudal thoracic dorsal columns (DCs) which might involve the DSCT or its afferent fibers resulted in a marked change in the patterns of forelimb-hind limb coupling during locomotion. In the present study, more rostral DC lesions, which probably included the DSCT or its afferent fibers considerably less, resulted in nearly identical changes in the patterns of interlimb coordination during stepping. Lesions of the dorsolateral funniculus (DLF) at similar spinal levels resulted in no significant changes in interlimb coordination. These lesions did destroy the DSCT, since retrograde transport of horseradish peroxidase (HRP) from the anterior cerebellar vermis to the nucleus dorsalis was blocked caudal to the lesion. These results are consistent with the notion that the DSCT plays little if any role in the precise timing of step cycles of the different limbs.

Pathways for orofacial pain sensation in the trigeminal brain-stem nuclear complex of the Macaque monkey.

Eleven Macaque monkeys underwent a variety of lesions in the trigeminal afferent system; namely, tractotomy, rhizotomy, and radiofrequency destruction of various components of the bulbospinal trigeminal nuclear complex. Behavioral responses were evaluated before and after the lesions using a quantitative paradigm which measured lever-pressing in response to electrical stimulation of the dental pulp or facial skin, and by assessing adversive responses to facial cutaneous and intraoral pin-scratch. Thresholds for lever-pressing in response to cutaneous facial stimulation were elevated by tractotomy, elevated further by a combination of tractotomy and rhizotomy of the seventh, ninth, and 10th cranial nerves and cervical dorsal roots C1-3, and maximally elevated by complete radiofrequency destruction of the trigeminal nucleus caudalis. These lesions also abolished adversive responses to cutaneous facial pin-scratch. None of these lesion combinations, however, altered lever-pressing responses to dental pulp stimulation. Radiofrequency destruction of the trigeminal nuclei principalis, oralis, and interpolaris caused elevations of lever-pressing thresholds in response to dental pulp stimulation, and also smaller but statistically significant elevations on cutaneous electrical stimulation. Mild reductions in adversive responses to cutaneous pin-scratch were also produced by these rostral nuclear lesions, suggesting analgesia. The experiments suggest that primary afferent fibers for dental pain perception travel only in the trigeminal nerve and that these fibers relay via the trigeminal brain-stem nuclei principalis, oralis, and interpolaris. Primary afferent fibers for cutaneous facial pain perception travel in the trigeminal, facial, glossopharyngeal, and vagus nerves, and the upper cervical dorsal and ventral roots, and these afferents relay mainly in the trigeminal nucleus caudalis.

Modulation of cardiovascular response to dynamic exercise by fastigial nucleus.

Mongrel dogs (n = 34) were used to record the cardiovascular responses during submaximal exercise-tolerance tests (ETT) before and after the placement of lesions in rostral portions of the cerebellar fastigial nucleus (FN). Sterile surgical procedures were used to implant solid-state pressure transducers into the left ventricle or descending aorta (anesthesia 1% halothane in O2) and multipolar stainless steel electrodes into FN (anesthesia alpha-chloralose 115 mg/kg iv). Heart rate (HR), maximal left ventricular systolic pressure ( LVPmax ) and its first derivative ( dLVP /dt), and mean arterial blood pressure (MAP) were recorded during a motorized treadmill ETT. Electrolytic direct-current or radio-frequency lesions were made through the indwelling FN electrodes, and the ETT was repeated following 10-14 days recovery. Two-way analysis of variance (ANOVA), with repeated measures on one, and one-way ANOVA for simple effects indicated a significant reduction in HR and MAP (P less than 0.01) but not LVPmax and dLVP /dt occurred during exercise as a result of rostral FN lesions. Although the trend for reduced LVPmax and dLVP /dt was also evident, a relatively greater decrease in blood pressure occurred in the peripheral vasculature during exercise. It was concluded that FN acts as a modulator of HR and MAP during dynamic exercise because of the observed deficits, and because FN is known to both send efferent projections to medullary vasomotor areas and receive projections from motor cortex and muscle and joint afferents.

Experimental gaze palsies in monkeys and their relation to human pathology.

Lesions were placed in the paramedian pontine reticular formation ( PPRF ) of monkeys and the resulting gaze palsies studied. Brainstem regions were identified by single cell recordings before kainic acid was injected to selectively destroy neuronal cell bodies in the vicinity. Unilateral PPRF lesions led to a loss of all rapid eye movements towards the ipsilateral side. Deficits were identical to those after experimental electrolytic lesions in monkeys, or structural lesions in humans. Bilateral PPRF lesions produced two different syndromes. Rostral PPRF lesions led to a selective loss of horizontal rapid eye movements leaving vertical movements intact. Caudal PPRF lesions led in addition to a severe disruption of vertical rapid eye movements.

The effect of forebrain lesions in the neonatal rat: survival of midbrain dopaminergic neurons and the crossed nigrostriatal projection.

Lesions were placed in the striatum and the olfactory tubercle of 1-day-old rat pups. Control and experimental animals were raised to adulthood. Efferent projections of mesencephalic neurons were examined by injecting the retrograde tracers horseradish peroxidase or Fast Blue into the undamaged striata of some experimental animals. The survival of the mesencephalic dopaminergic neurons was monitored by using immunocytochemical localization of tyrosine hydroxylase. Small lesions in the caudate-putamen had no appreciable effect on the survival of tyrosine hydroxylase-containing neurons in the mesencephalon, but the density of dopaminergic terminals adjacent to the lesion increased in the remaining caudate-putamen. Striatal lesions that involved an estimated area of more than one-third resulted in loss of dopamine neurons of the substantia nigra compacta. Rostral lesions in the striatum affected mostly rostrally positioned neurons in the substantia nigra. Dorsal lesions of the caudate-putamen resulted in disappearance of dorsal A9 neurons. Reduction of the A10 and A8 dopamine neuron groups occurred if the neonatal lesions involved the olfactory tubercle and nucleus accumbens. Some tyrosine hydroxylase-containing neurons persisted even after the largest lesions. These dopaminergic neurons formed a crossed nigrostriatal pathway which was confirmed by retrogradely transported tracers. The density of this crossed projection in the adult appeared unaffected by the neonatal lesion. We concluded that dopaminergic neurons form topographically ordered projections with their targets in the newborn rat. Rearrangement of these fibers appeared limited, but compensatory increase of axon terminal density was evident in partially lesioned target areas.

Characteristics of aggressive behavior induced by nucleus accumbens septi lesions in rats

The effect of selective caudal and/or rostral nucleus accumbens septi lesions on emotional behavior were studied in male Wistar King A rats. The caudal, rostral, and both areas of the accumbens nuclei were lesioned each in separate animal groups. The rats of all groups exhibited hyperirritability and muricide after accumbens lesions. Muricide was highest in incidence in the group of both caudal and rostral accumbens lesions and remained unchanged throughout the experimental period of 15 days. Moreover, accumbens-lesioned rats also showed mouse-eating behavior. These results suggest that the accumbens plays an important role in modulating aggression, and the characteristics of aggressive behavior induced by accumbens lesions resemble that of raphe-lesioned rats.

Vomeronasal and olfactory pathways to the amygdala controlling male hamster sexual behavior: Autoradiographic and behavioral analyses

Previous studies suggest that the rostral corticomedial amygdala (CMA), particularly the medial nucleus, is an important site where vomeronasal and olfactory stimuli critical to male hamster copulatory behavior are processed. To test the possibility that mating deficits seen after lesions of the rostrally-placed medial nucleus may be due to the interruption of chemosensory afferents to more caudal areas, we injected tritiated amino acids into the accessory and main olfactory bulbs of male hamsters in which we had first produced bilateral electrolytic lesions or sham lesions in either the rostral CMA or basolateral amygdala, and then observed mating behavior. Autoradiographic analysis of ‘vomeronasal’ projections from the accessory olfactory bulb and ‘olfactory’ projections from the main bulb, revealed that rostral CMA lesions which damaged the medial nucleus and extended to the ventral surface of the brain (ventral lesions) interrupted vomeronasal input to the more caudally-placed posteromedial cortical nucleus, but spared olfactory inputs to adjacent caidal areas of the amygdala and piriform lobe. In contrast, lesions which damaged a major portion of the medial nucleus but left its ventral surface intact (dorsal lesions) spared both vomeronasal and olfactory inputs to more caudal areas. Animals with both dorsal and ventral lesions failed to mate posteperatively, whereas animals bearing sham lesions of basolateral amygdaloid lesions, which, like dorsal lesions, spared caudally-directed chemosensory afferents, continued to mate normally. We conclude that mating deficits seen after rostral CMA lesions are due primarily to destruction of the medial nucleus.