Ventrolateral Midbrain Research Articles

The ventrolateral periaqueductal gray projects to caudal brainstem depressor regions: a functional-anatomical and physiological study

The reaction of shock, a precipitous, life-threatening fall in arterial pressure and heart rate, is evoked often by the combination of deep pain and blood loss following traumatic injury. A similar “shock-like” pattern of response can be evoked by excitation of the ventrolateral midbrain periaqueductal gray. Further, ventrolateral periaqueductal gray neurons are selectively activated by deep somatic or visceral pain and haemorrhage. The pathways mediating ventrolateral periaqueductal gray evoked hypotension and bradycardia are not known. In this study, the projections from the ventrolateral periaqueductal gray to “cardiovascular” regions in the caudal medulla of the rat were examined. Injections of the anterograde tracer, biotinylated dextran amine at physiologically-defined, ventrolateral periaqueductal gray depressor sites, revealed strong projections to the caudal midline medulla and to the depressor region of the caudal ventrolateral medulla. Injections of excitatory amino acids established that substantial falls in arterial pressure could be evoked from the ventrolateral periaqueductal gray-recipient parts of the caudal midline medulla. Injections of the retrograde tracer, cholera toxin subunit B at physiologically-defined, depressor sites in the caudal midline medulla and the caudal ventrolateral medulla confirmed the existence of substantial projections from the ventrolateral periaqueductal gray. Although previous studies have emphasized the importance of projections from the ventrolateral periaqueductal gray to the pressor region of the rostral ventrolateral medulla, this study has revealed the existence of strong ventrolateral periaqueductal gray projections to depressor regions within the caudal medulla (caudal midline medulla and caudal ventrolateral medulla) which likely contribute to ventrolateral periaqueductal gray-mediated hypotension and bradycardia.

Cardiovascular effects of microinjections of opioid agonists into the `Depressor Region' of the ventrolateral periaqueductal gray region

Microinjections of excitatory amino acids made into the ventrolateral midbrain periaqueductal gray of the rat have revealed that neurons in this region integrate a reaction characterised by quiescence, hyporeactivity, hypotension and bradycardia. Microinjections of both excitatory amino acids and opioids into the ventrolateral periaqueductal gray have shown also that it is a key central site mediating analgesia. The effects of injections of opioids into the ventrolateral periaqueductal gray on arterial pressure and heart rate or behaviour are unknown. In this study we first mapped in the rat the extent of the ventrolateral periaqueductal gray hypotensive region as revealed by microinjections of excitatory amino acids. We found that ventrolateral periaqueductal gray depressor region extended more rostrally than previously thought into the tegmentum ventrolateral to the periaqueductal gray. Subsequently we studied for the first time, the effects of microinjections of μ-, δ-, and κ-opioid agonists made into the ventrolateral periaqueductal grey depressor region. In contrast to the effects of excitatory amino acid injections, microinjections of the μ-opioid agonist ([ d-Ala 2, N-Me-Phe 4,Gly-ol 5]enkephalin) evoked hypertension and tachycardia at approximately 50% of sites. Similar to excitatory amino acid injections, microinjections of both the δ-opioid agonist ([ d-Pen 2, d-Pen 5]enkephalin), and the κ-opioid agonist ((5,7,8)-(+)- N-Methyl- N-[7-(1-pyrrolidinyl)-1-oxaspiro[4.5]dec-8-yl]-benzeneacetamide) evoked either a hypotension and bradycardia, or had no effect. These results indicate that different opiate receptor subtypes are present on a distinct population of ventrolateral periaqueductal gray neurons, or at different ventrolateral periaqueductal gray synaptic locations (pre- or post-synaptic).

Convergence of deep somatic and visceral nociceptive information onto a discrete ventrolateral midbrain periaqueductal gray region

Pain arising from deep structures (muscles, joints, viscera) is the type of pain of most clinical relevance and also the type of pain about whose central representation we have the least knowledge. In contrast to cutaneous pain which evokes defensive behaviours, hypertension and tachycardia, the physiological reactions to most deep pain (especially if persistent) usually include quiescence, hypotension, bradycardia and decreased reactivity to the environment. Excitation of neurons within a discrete ventrolateral midbrain periaqueductal gray region evokes a reaction seemingly identical to that evoked by pain arising from deep structures. We report here, using the technique of the noxious stimulus-evoked expression of the immediateearly gene, c-fos, that neurons within this same ventrolateral periaqneductal gray region are selectively activated by a range of deep somatic and visceral nociceptive manipulations. Thus we have identified a specific brain region that both receives convergent, deep somatic and visceral nociceptive input, and which mediates the behavioural and physiological reactions characteristic of most deep pain.

Quiescence and hyporeactivity evoked by activation of cell bodies in the ventrolateral midbrain periaqueductal gray of the rat.

Much evidence suggests that the midbrain periaqueductal gray region (PAG) plays a pivotal role in mediating an animal's responses to threatening, stressful, or painful stimuli. Active defensive reactions, hypertension, tachycardia and tachypnea are coordinated by a longitudinally oriented column of cells, found lateral to the midbrain aqueduct, in the caudal two-thirds of the PAG. In contrast, microinjections of excitatory amino acid (EAA) made in the ventrolateral region of the PAG in anesthetized or isolated animals evoke hypotension, bradycardia, and behavioral arrest. The aim of the present study was to examine further the effects of activation of neurons in the ventrolateral PAG. By injecting into this region low doses (40 pmol) of kainic acid (KA), a long-acting EAA, it was possible to observe a freely moving rat's behavior in a social situation (i.e., paired with a weight-matched, untreated partner). Such injected rats become quiescent, i.e., there was a cessation of all ongoing spontaneous activity. These rats were also hyporeactive: the investigative approaches of the partner failed to evoke orientation, startle reactions, or vocalization. Electroencephalographic measurements indicated that the effects of injections of KA in the ventrolateral PAG were not secondary to seizure activity. In addition to the quiescence and hyporeactivity reported here, and the hypotension and bradycardia reported previously, the ventrolateral PAG is a part of the brain from which analgesia has been readily evoked by electrical stimulation, or microinjections of either EAA or morphine. As a reaction to "deep" or "inescapable" pain, chronic injury, or defeat, animals often reduce their somatomotor activity, become more solitary, and are generally much less responsive to their environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala efferents mediating electrically evoked startle-like responses and fear potentiation of acoustic startle.

One-pulse stimulation of the ventral amygdalofugal pathway (VAF), ventrolateral midbrain, or medial medulla evoked startle-like responses. Refractory periods tested by 2-pulse stimulation ranged from 0.2 to 0.5 ms in both midbrain and medulla sites and from 0.4 to 0.8 ms in VAF sites. Symmetric collision effects between midbrain and medulla sites suggest that fast-conducting axons between the sites mediate the response. Asymmetric collision effects between VAF and midbrain suggest that strong synapses between these sites mediate the response, with a transmission time of 1 ms. No collision was observed between contralateral sites. Bilateral lesions of midbrain sites blocked VAF responses and fear-conditioned startle, but failed to block acoustic startle, and partially blocked medulla responses. A new neural model of fear-potentiated startle is proposed.

Peptide immunoreactive neurons in the amygdala and the bed nucleus of the stria terminalis project to the midbrain central gray in the rat

The central nucleus of the amygdala, bed nucleus of the stria terminalis, and central gray are important components of the neural circuitry responsible for autonomic and behavioral responses to threatening or stressful stimuli. Neurons of the amygdala and bed nucleus of the stria terminalis that project to the midbrain central gray were tested for the presence of peptide immunoreactivity. To accomplish this aim, a combined immunohistochemical and retrograde tracing technique was used. Maximal retrograde labeling was observed in the amygdala and bed nucleus of the stria terminalis after injections of retrograde tracer into the caudal ventrolateral midbrain central gray. The majority of the retrogradely labeled neurons in the amygdala were located in the medial central nucleus, although many neurons were also observed in the lateral subdividion of the central nucleus. Most of the retrogradely labeled neurons in the BST were located in the ventral and posterior lateral subdivisions, although cells were also observed in most other subdivisions. Retrogradely labeled neurotensin, corticotropin releasing factor (CRF), and somatostatin neurons were mainly observed in the lateral central nucleus and the dorsal lateral BST. Retrogradely labeled substance P-immunoreactive cells were found in the medial central nucleus and the posterior and ventral lateral BST. Enkephalin-immunoreactive retrogradely labeled cells were not observed in the amygdala or bed nucleus of the stria terminalis. A few cells in the hypothalamus (paraventricular and lateral hypothalamic nuclei) that project to the central gray also contained CRF and neurotensin immunoreactivity. The results suggest the amygdala and the bed nucleus of the stria terminalis are a major forebrain source of CRF, neurotensin, somatostatin, and substance P terminals in the midbrain central gray.

The organization of descending tectofugal pathways underlying orienting in the frog, Rana pipiens

In the frog, identical orienting deficits, involving a failure to turn toward stimuli in the ipsilateral hemifield, can be produced by small white matter lesions either in the caudal mesencephalon (Kostyk and Grobstein, 1987a) or in the caudal medulla (Masino and Grobstein, 1989). These findings suggest that descending turn signals may run uninterrupted from the midbrain to the spinal cord, and that something other than tectospinal axons may carry such signals. We here report studies to determine whether there is a tecto-recipient structure whose axons pass through the known critical lesion sites in the caudal mesencephalon and medulla, and whether damage to such a structure, sparing tectospinal pathways, produces an orienting deficit. Horseradish peroxidase (HRP) was applied to behaviorally effective lesions in the caudal medulla and the resulting labelling patterns compared with those resulting from application of HRP to nearby but behaviorally ineffective lesions at the same rostrocaudal level. A column of large cells in the ventrolateral midbrain tegmentum (including nMLF as well as parts of AV and PV) was robustly labelled in all effective lesion cases, and less frequently labelled in ineffective cases. A quantitative analysis showed labelling in this region to be more highly correlated with the existence of a behavioral deficit than that in any other brain region. Reconstructions of single retrogradely labelled cells in the rostral part of the column (nMLF) showed that they have dendrites in a position to receive tectal input and axons which pass through the critical lesion sites in both the caudal mesencephalon and the caudal medulla. Tegmental lesions, sparing the tectospinal tracts, produced ipsilateral turning deficits in cases where the large cell column was completely removed but did not when the column was spared. The findings support the hypothesis that tectofugal signals involved in orienting turns descend uninterrupted to the spinal cord on something other than tectospinal axons, and suggest that the critical projections derive from the large cell column of the ventral tegmentum.

Galanin-like immunoreactivity within amygdaloid and hypothalamic neurons that project to the midbrain central grey in rat

The possibility that galanin-immunoreactive cells within the central nucleus of the amygdala (Ce) and the lateral part of the bed nucleus of the stria terminalis (BSTL) project to the midbrain central grey in the rat was investigated using the combined immunofluorescence-retrograde tracing technique. Injections of Fluoro-Gold tracer were made into the ventrolateral midbrain central grey and the brain tissue was processed for galanin-like immunoreactivity using the avidin-biotin Texas red immunofluorescence technique. Cells containing both galanin-like immunoreactivity and fluorescent retrograde tracer were identified within the medial Ce and in the ventral part of the BSTL. Retrogradely labeled galanin-like immunoreactive cells were also observed within the medial preoptic area and to a lesser extent within the dorsomedial and paraventricular hypothalamic nuclei. The results of this study demonstrate the presence of long descending pathways containing galanin-like immunoreactivity that originate from discrete regions of the amygdala and hypothalamus and terminate within the midbrain central grey.

Descending projections from the superior colliculus in rat: a study using orthograde transport of wheatgerm-agglutinin conjugated horseradish peroxidase.

Despite extensive behavioural work on the rat superior colliculus, its descending efferent pathways have not been fully characterised with modern anatomical tract-tracing techniques. To investigate these pathways, wheatgerm-agglutinin conjugated with horseradish peroxidase (1%) was injected at various locations within the superior colliculus of hooded rats. Label judged to be transported orthogradely was plotted on coronal sections modified from the atlas of Paxinos and Watson (1982). Two major descending pathways were identified. (i) The bulk of the fibres in the ipsilateral descending pathway leave the superior colliculus ventrolaterally, and course around the lateral margin of the midbrain reticular formation. Caudally, projecting fibres leave the main bundle to innervate the cuneiform nucleus, and parts of the pontomedullary reticular formation. Terminal fields associated with the major bundle of fibres are found in an area medial to the brachium of the inferior colliculus; the parabigeminal nucleus and adjacent tegmentum; the ventrolateral midbrain reticular formation; and the lateral pontine nuclei. (ii) The fibres of the main contralateral descending pathway leave the superior colliculus ventromedially, to cross midline in the dorsal tegmental decussation. They immediately turn caudally to join the predorsal bundle, in which they run the length of the brainstem to reach the cervical spinal cord. Major terminal fields occur in nucleus reticularis tegmenti pontis; the pedunculopontine/parabrachial area; paramedian pontomedullary reticular formation; and inferior olive. In addition there is lighter labelling in many areas of the pontomedullary reticular formation and in the cervical spinal cord. There was also a much sparser contralateral descending projection that crossed midline in the tectal commissure, and sent terminals to the contralateral cuneiform area and adjoining regions. These results suggest that the distribution of the descending efferent pathways from the superior colliculus in rats is similar to those described in other species. The fact that the two major pathways project to quite different terminal areas, together with previous findings that they have separate cells of origin within the tectum, suggests that they may also be functionally distinct.

The effects of brainstem lesions on vocalization in the squirrel monkey

The present study is an attempt to find out the brain areas involved in the motor coordination of species-specific vocalization. For this purpose, high-frequency coagulations were placed in a systematic manner throughout the brainstem and posterior diencephalon in altogether 43 squirrel monkeys ( Saimiri sciureus). The effect of these lesions on different call types elicited by electrical brain stimulation was studied spectrographically. It was found that bilateral destruction of the ventrolateral, ventroposterior and intralaminar thalamus, periventricular and rostral periaqueductal gray, ventral tegmental area of Tsai, nucl. interpeduncularis, nucl. ruber, anterodorsolateral midbrain tegmentum, superior and inferior colliculi, pontine gray, cerebral peduncles, medial pontine reticular formation, raphe and vestibular nuclei did not affect the acoustic structure of the calls tested. On the other hand, lesions in the ventrolateral midbrain involving the substantia nigra and overlying reticular formation, in the midbrain tegmentum just below the inferior colliculus, in the lateral pons and almost the whole medulla (minimal lesion size: 2.5 mm 3) changed vocalization significantly. It is suggested that the latter areas are more or less directly involved in the motor coordination of vocalization, while the first are not.

Evidence for peripeduncular neurons having a role in the control of feminine sexual behavior in the rat

In order to test the hypothesis that peripeduncular nucleus (PPN) cells are essential for normal sexual behavior, synaptic blockade in the chronically implanted awake animal was attempted by means of the local injection of pentobarbital (PB) at a concentration which may interfere with synaptic transmission without affecting conduction in fibers. Ovariectomized, female rats were chronically implanted with cannulae directed to the PPN or the dorsal midbrain. After adequate estrogen priming, rats were injected with 22 mM pentobarbital (PB) or artificial cerebrospinal fluid (ACSF). Seven min after PB injection in PPN lordosis quotient was significantly lowered, whereas PB in dorsal midbrain or ACSF in PPN had no effect. It is concluded that PPN neurons themselves may have a functional role in the control of lordosis and loss of PPN neurons may account for impairment of reproductive behavior observed after lesions in the ventrolateral midbrain.

Determination of the course of brainstem catecholamine fibers mediating amphetamine anorexia

Previous studies suggest that brainstem catecholamine (CA) fibers which mediate amphetamine (AMPH)-induced anorexia ascend through the midlateral medial forebrain bundle and perifornical region and terminate in the perifornical hypothalamic region (PFH) at the level of the hypothalamic ventromedial nucleus 43. Through studies of wire-knife cuts (KCs) placed in the lower brainstem, the present paper further delineates the course of fibers mediating AMPH feeding suppression, as they ascend through the medullary, pontine and midbrain tegmentum. The results indicate that the crucial CA fibers ascend through the ventrolateral medulla just dorsal to the nucleus of the seventh cranial nerve, 1.1–1.9 mm lateral to midline. In their rostral course, these fibers apparently maintain a relatively straight position in the ventral pons and then enter the ventrolateral midbrain just dorsal to the medial lemniscus, between 0.7 and 1.1 mm lateral to midline. These medullary fibers, possibly originating from the norepinephrine/epinephrine-containing ventrolateral cell group (A1/C1), then appear to join additional fibers from the scattered dopamine-containing neurons positioned in the caudal midbrain (A8 CA cell group). Together, these dopamine, epinephrine and norepinephrine systems are believed to ascend into the medial aspect of the medial forebrain bundle on their way to the PFH at the level of the ventromedial nucleus.

Does naloxone suppress self-stimulation by decreasing reward or by increasing aversion?

Fifty-eight rats were implanted with electrodes in the ventrolateral midbrain central gray from which both self-stimulation reward and/or stimulation-produced analgesia can be obtained. Thirty-nine cases were positive for self-stimulation; of these, 24 also displayed significant stimulation-produced analgesia and 15 did not. Injections of the opiate receptor blocker, naloxone, suppressed self-stimulation by approximately 40% at both analgesic and non-analgesic reward sites. Since naloxone failed to act preferentially at analgesic reward sites, the hypothesis that naloxone suppresses self-stimulation primarily by antagonizing endorphin-mediated analgesia, and thereby increasing the aversive properties of the brain stimulation, was not supported. Rather, the data are consistent with the hypothesis that naloxone suppresses self-stimulation by antagonizing endorphin-mediated reward.

Midbrain LHRH infusions enhance lordotic behavior in ovariectomized estrogen-primed rats independently of a hypothalamic responsiveness to LHRH

Lordotic behavior of ovariectomized estrone-primed rats was measured after infusions of luteinizing hormone-releasing hormone (LHRH), thyrotropin (TRH) or saline into the ventrolateral midbrain central gray (VL-MCG), or after LHRH or saline infusions into a lateral control site, the dorsolateral reticular formation (DL-RF). Infusion of LHRH, but not TRH, into the VL-MCG increased lordotic behavior. LHRH had no effect in the DL-RF. In a second experiment, rats were fitted with cannulae in the VL-MCG and in the arcuate-ventromedial nucleus area (ARC-VM). Serotonin was infused into the ARC-VM, and LHRH was infused into either the ARC-VM or the VL-MCG. Serotonin blocked the behavioral effect of LHRH infusion into the ARC-VM, but did not prevent enhancement of lordosis by LHRH infusions into the VL-MCG. These results suggest that LHRH infusions into the midbrain do not require hypothalamic responsiveness to LHRH for their effect, and are therefore unlikely to act by diffusion of LHRH rostrally. The effect of LHRH in the midbrain is site-specific, since lateral infusions (1.75 mm away) were ineffective.

Long descending projections of the hypothalamus in the pigeon, Columba livia.

An autoradiographic analysis was performed on the descending projections of nucleus periventricularis magnocellularis (PVM) of the hypothalamus in the pigeon. A PVM-medullospinal pathway was observed coursing posteriorly through the lateral hypothalamus, ventrolateral midbrain tegmentum, and into the spinal lemniscus (ls) in the ventrolateral pons and medulla. In the pons, some fibers course dorsomedially from ls and terminate at the lateral border of the locus coeruleus. At medullary levels, fibers from ls sweep dorsomedially in the plexus of Horsley and project to certain regions of the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (NX). Specifically, PVM fibers project heavily into NTS subnuclei medialis superficialis, medialis ventralis, and lateralis (sulcalis) dorsalis as well as into the ventral parvocellular subnucleus of NX. Fibers in ls were traced caudally into the lateral funiculus as far as upper cervical levels of the spinal cord. Although autoradiographs of lower cervical or thoracic spinal cord sections were not available, PVM fibers do descend to thoracic spinal cord levels, as evidenced by the retrograde transport of horseradish peroxidase. In addition to the medullospinal pathway, the autoradiographs demonstrated PVM projections to septum, diencephalon, and midbrain. Labeled PVM fibers are found in the lateral septal nucleus, nucleus of the anterior pallial commisure, dorsomedial thalamic nucleus, dorsolateral anterior thalamic nucleus (pars ventralis), median eminence, medial and lateral hypothalamus, medial mammillary area, and nucleus intercollicularis and central gray of the midbrain. The projection of fibers to medullospinal regions and median eminence suggests that PVM is homologous to the mammalian paraventricular nucleus. These projections to specific subnuclei of NTS and NX denote hypothalamic control over certain autonomic functions.

Participation of the lateral midbrain tegmentum in the neuroendocrine control of sexual behavior and lactation in the rat

Electrolytic lesions were placed in the ventrolateral midbrain and their effects on lactational performance and sexual behavior were assessed. The neuronal injury, situated just above the lateral tip of the substantia nigra in the lateral tegmentum, caused an immediate impairment in lactational performance as measured by the weight gain of the offspring, and interfered also with the hormonal induction of sexual receptivity and proceptivity. In similarly lesioned male rats, mounting behavior was virtually absent, but nociceptive thresholds and locomotor activity in the open-field remained unaltered. It seems likely that some, but not all, of these effects were due to disruption of a pathway carrying somatosensory information relevant for lactation and sexual behavior.

Afferent projections related to attack sites in the ventral midbrain tegmentum of the cat

Quiet attack was elicited by electrical stimulation of the ventrolateral midbrain tegmentum of the cat. The paw was not used other than to position or hold the rat during the bite. Bites were directed toward the head and neck region and were not accompanied by autonomic responses other than pupillary dilation and sometimes slight piloerection on the back. Horseradish peroxidase was deposited at the attack sites. Cells labeled with the peroxidase reaction product were located in gyrus proreus, gyrus genualis, nucleus accumbens, bed nucleus of the stria terminalis, bed nucleus of the anterior commissure, nucleus of the diagonal band, substantia innominata, anterior amygdaloid area, ventromedial hypothalamic area, paraventricular nucleus, perifornical hypothalamic area, lateral hypothalamic area, dorsal hypothalamic area, fields of Forel, midbrain reticular formation, superior colliculus, ventral central grey, lateral central gray, locus coeruleus, parabrachial nuclei, nucleus of the lateral lemniscus, oral pontine reticular nucleus, and the dorsal raphe. Other regions were less prominently labeled. Previous studies have shown most of these sites to have some involvement in attack.

Role of the periaqueductal grey in vocal expression of emotion

In 32 squirrel monkeys (Saimiri sciureus) the role of the periaqueductal grey has been investigated by combined stimulation/lesioning and by neuroanatomical experiments. The results are as follows. Firstly, periaqueductal lesions invading the laterally adjacent tegmentum abolish species-specific calls elicitable by electrical brain stimulation. This holds for stimulation sites rostral as well as caudal to this area. The only vocalizations which survive are phonations of an artificial character which can be evoked from the lateral medulla. Spontaneous vocalizations also seem to be abolished. Secondly, vocalizations elicited from the periaqueductal grey are not affected by bilateral lesions in vocalization-eliciting areas rostral to it, but are abolished by lesions in the dorsolateral pons and ventrolateral medulla. Thirdly, the periaqueductal grey receives direct projections from all vocalization-eliciting areas tested, viz. the precallosal cingulate gyrus, gyrus rectus, medial amygdata, central amygdaloid nucleus/substantia innominata, nucleus striae terminalis, dorsal hypothalamus, midline thalamus, periventricular grey, dorsolateral and ventrolateral midbrain tegmentum. Fourthly, the periaqueductal grey projects directly to the nucleus ambiguus, the site of the laryngeal motoneurones. The course of the main bulk of fibres corresponds to the lesion sites effective in abolishing periaqueductally elicited vocalizations. From these results, it was concluded that the caudal periaqueductal-lateral tegmental area is a necessary relay station for all external and internal stimuli capable of inducing species-specific calls. Its position within the stimulus-response loop seems to be on the output side, immediately above the level of motor-corrdination but below that of stimulus recognition.

Midbrain central gray: LHRH infusion enhances lordotic behavior in estrogen-primed ovariectomized rats

Ovariectomized rats were implanted with 23 gauge stainless steel cannulae in the ventrolateral midbrain central gray. Twelve sexually active rats were estrone-primed and infused with saline and 50 ng luteinizing hormone-releasing hormone (LHRH) in counterbalanced order. Infusion of luteinizing hormone-releasing hormone significantly enhanced the lordotic response to coital stimulation compared to saline infusion. These results support the role of hypothalamo-mesencephalic LHRH-containing pathways in modulating lordotic behavior in estrogen-primed Ovariectomized rats.

Mesencephalic participation in the control of sexual behavior in the female rat.

Electric stimuli applied to both pudendal nerves evoked field potentials, unit responses, and multiunit responses in the ventrolateral midbrain, in and around the peripeduncular nucleus. Bilateral lesions placed in this region suppressed sexual behavioral responses (lordosis and courting behavior) of ovariectomized rats primed with 5, 10, 100, and 1,000 microgram of estradiol benzoate and 2 mg of progesterone per kilogram of body weight. It is proposed that the region in question represents a relay station for the integration of sensory and endocrine information concerned in the control of receptive sexual behavior in the female rat.