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PubMed2005

GABA(A) receptor activation in the lateral parabrachial nucleus induces water and hypertonic NaCl intake.

Inhibitory serotonergic and cholecystokinergic mechanisms in the lateral parabrachial nucleus and central GABAergic mechanisms are involved in the regulation of water and NaCl intake. In the present study we investigated if the GABA(A) receptors in the lateral parabrachial nucleus are involved in the control of water, NaCl and food intake in rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the lateral parabrachial nucleus were used. Bilateral injections of muscimol (0.2 nmol/0.2 microl) into the lateral parabrachial nucleus strongly increased 0.3 M NaCl (20.3+/-7.2 vs. saline: 2.6+/-0.9 ml/180 min) without changing water intake induced by the treatment with the diuretic furosemide combined with low dose of the angiotensin converting enzyme inhibitor captopril s.c. In euhydrated and satiated rats, bilateral lateral parabrachial nucleus injections of muscimol (0.2 and 0.5 nmol/0.2 microl) induced 0.3 M NaCl intake (12.1+/-6.5 and 32.5+/-7.3 ml/180 min, respectively, vs. saline: 0.4+/-0.2 ml/180 min) and water intake (5.2+/-2.0 and 7.6+/-2.8 ml/180 min, respectively, vs. saline: 0.8+/-0.4 ml/180 min), but no food intake (2+/-0.4 g/240 min vs. saline: 1+/-0.3 g/240 min). Bilateral lateral parabrachial nucleus injections of the GABA(A) antagonist bicuculline (1.6 nmol/0.2 microl) abolished the effects of muscimol (0.5 nmol/0.2 microl) on 0.3 M NaCl and water intake. Muscimol (0.5 nmol/0.2 microl) into the lateral parabrachial nucleus also induced a slight ingestion of water (4.2+/-1.6 ml/240 min vs. saline: 1.1+/-0.3 ml/240 min) when only water was available, a long lasting (for at least 2 h) increase on mean arterial pressure (14+/-4 mm Hg, vs. saline: -1+/-1 mm Hg) and only a tendency to increase urinary volume and Na+ and K+ renal excretion. Therefore the activation of GABA(A) receptors in the lateral parabrachial nucleus induces strong NaCl intake, a small ingestion of water and pressor responses, without changes on food intake.

Analysis of Variance↗
PubMed2006

Cardiovascular effects produced by activation of GABA receptors in the rostral ventrolateral medulla of conscious rats.

The rostral ventrolateral medulla (RVLM) has been proposed as a region playing a major role in the tonic and reflex control of sympathetic vasomotor activity and blood pressure. Pharmacological activation of GABA(A) receptors with muscimol in the RVLM of anesthetized rats results in a large fall in mean arterial pressure (MAP), heart rate (HR) and sympathetic activity. In this study we evaluated the effects of activation of GABA receptors in the RVLM of conscious, freely moving rats. Bilateral microinjections of muscimol into the RVLM of conscious rats produced a large fall in MAP (-38+/-4 mm Hg, n=7) when compared with saline injections (NaCl 0.9%, 7+/-1 mm Hg, n=4). The decrease in MAP evoked by muscimol was accompanied by a significant increase in HR (muscimol 69+/-13 bpm vs. vehicle -33+/-12 bpm, P<0.05), an effect that was completely abolished by beta1 adrenergic receptor blockade. Conversely, bilateral microinjections of GABA(B) agonist, baclofen, evoked a pressor response, but in this case, the increase was not significantly different from that evoked by vehicle injections. These results 1) indicate that GABA(A) receptors have a powerful influence on the resting activity of RVLM neurons in conscious rats; 2) indicate that a compensatory sympathetic-mediated tachycardia is present after inhibition of RVLM neurons in conscious rats; 3) confirm and extend previous findings showing that RVLM neurons are critical for blood pressure maintenance even in normal non-anesthetized conditions.

Adrenergic beta-1 Receptor Antagonists↗
PubMed2005

The involvement of the orbitofrontal cortex in learning under changing task contingencies.

Previous investigations examining the rat prefrontal cortex subregions in attentional-set shifting have commonly employed two-choice discriminations. To better understand how varying levels of difficulty influence the contribution of the prefrontal cortex to learning, the present studies examined the effects of orbitofrontal cortex inactivation in a two- or four-choice odor reversal learning test. Long-Evans rats were trained to dig in cups that contained distinct odors. In the two-choice odor discrimination, one odor cup was always associated with a cereal reinforcement in acquisition while the opposite odor cup was associated with a cereal reinforcement in reversal learning. In the four-choice odor discrimination, an additional two cups containing distinct odors were used that were never associated with reinforcement in acquisition or reversal learning. Bilateral infusions of the GABA-A agonist, muscimol (0.5 microg) into the orbitofrontal cortex did not impair acquisition of either the two- or four-choice discrimination task. However, muscimol infusions into the orbitofrontal cortex impaired two- and four-choice reversal learning. In the two-choice odor reversal, muscimol treatment selectively increased perseverative errors. In the four-choice odor reversal, muscimol treatment increased perseverative, regressive, as well as irrelevant errors. These findings suggest that the orbital prefrontal cortex not only enables task switching by supporting the initial inhibition of a previously relevant choice pattern, but under increasing task demands also enables the reliable execution of a new choice pattern and reduction of interference to irrelevant stimuli.

Animals↗
PubMed2005

The enhancing effects of hippocampal infusions of glucose are not restricted to spatial working memory.

Extensive evidence shows that hippocampal infusions of glucose enhance spontaneous alternation (SA) performance or reverse deficits in this task. The current experiments determined whether the enhancing effects of hippocampal infusions of glucose are restricted to spatial working memory. Specifically we tested whether hippocampal infusions of glucose would reverse deficits in an emotional reference memory task (continuous multiple trial inhibitory avoidance [CMIA]) produced by septal infusions of the gamma-aminobutyric acid agonist muscimol. Male Sprague-Dawley rats were given septal infusions of vehicle or muscimol (0.15 nmol: SA; 5 nmol: CMIA) combined with hippocampal infusions of vehicle or glucose (50 nmol) 15 min prior to assessing SA or CMIA training. CMIA retention was tested 48 h later. Muscimol infusions decreased percent alternation scores and avoidance retention latencies. Importantly, hippocampal infusions of glucose reversed the deficits produced by the septal muscimol infusions on both tasks. These findings show for the first time that hippocampal glucose infusions also influence emotional memory, indicating that the enhancing effects of glucose generalize to memory tasks that vary in motivational and cognitive demand.

Animals↗
PubMed2005

GABA receptor agonists in the medial preoptic area and maternal behavior in lactating rats.

We studied the effects of injecting agonists of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) muscimol (GABA-A receptor agonist) and baclofen (GABA-B receptor agonist) in the medial preoptic area (MPOA) and neighboring brain regions, the bed nucleus of the stria terminalis (BNST), and lateral preoptic area (LPO) on maternal behavior. Lactating female rats were implanted with bilateral cannulae in the MPOA/BNST on day 1 postpartum. On day 5, a maternal behavior test was conducted in the home cage after females received injections of muscimol or baclofen (0, 12.5, 50 or 200 ng per side). On day 7, after MPOA/BNST injections, a second maternal behavior test was conducted with pups placed at the end of a T-runway projecting from the home cage. Finally, after injections on day 9 maternal aggression, olfaction, and locomotor behavior were tested. The GABA receptor agonists injected in the MPOA/BNST produced dose-dependent deficits in all components of maternal behavior, including maternal aggression, except licking. Muscimol produced deficits in the active component, nest building at lower doses than baclofen, both agonists produced deficits in retrieving, while baclofen produced deficits in passive components (hovering and crouching over pups) at lower doses than muscimol. Both GABA receptor agonists increased locomotor activity and reduced olfactory responsiveness but these were only correlated with deficits in retrieving and crouching in baclofen-treated females.

Analysis of Variance↗
PubMed2002

Tonic sympathoinhibition arising from the hypothalamic PVN in the conscious rabbit.

In the conscious rabbit muscimol (1-10 nmol/side) was microinjected into the hypothalamic paraventricular nucleus to inhibit neuronal function and the acute changes in mean arterial pressure (MAP), heart rate and renal sympathetic nerve activity (RSNA) were monitored. Muscimol (1 nmol) had no effect on the cardiovascular variables, as was the case with vehicle. However, muscimol (10 nmol) elicited a significant increase in RSNA of 184+/-40% and a reduction in heart rate of 49+/-12 beats/min but no change in MAP. The effect of blocking endogenous glutamatergic inputs with the glutamate antagonist, kynurenate (25 nmol), into the PVN was also examined. Kynurenate elicited an increase in RSNA of 35+/-9% with no significant change in MAP or HR. The results suggest that muscimol inhibits a tonically active inhibitory influence on RSNA arising from the PVN in the conscious rabbit. A glutamatergic input into the PVN appears to contribute to the tonic activation of this inhibitory influence.

Anesthesia↗
PubMed2002

GABAergic regulation of the central nucleus of the amygdala: implications for sleep control.

It is becoming established that the amygdala has a strong influence on arousal state, with most evidence indicating a role in the regulation of rapid eye movement sleep (REM). Electrically activating the central nucleus of the amygdala (CNA) can increase subsequent REM and enhance REM-related phenomena. However, drugs that may be inhibitory to CNA have been typically reported to reduce REM. This suggests that enhancing activity in CNA could promote REM, and that inhibiting activity in CNA could suppress REM. We reversibly inactivated CNA using the GABA(A) agonist, muscimol, or blocked GABAergic inhibition with the GABA(A) antagonist, bicuculline, and examined the effects on sleep and wakefulness. Rats (90-day-old male Sprague-Dawley) were implanted with electrodes for recording EEG and EMG. Cannulae were aimed into CNA for microinjecting muscimol (0.001, 0.3 and 1.0 microM/0.2 microl saline) or bicuculline (56 and 333 pM/0.2 microl saline). Each animal received bilateral microinjections of muscimol, bicuculine or saline alone followed by 6-h sleep recordings. Microinjections of low concentrations of muscimol into CNA produced relatively selective decreases in total REM and number of REM episodes that lasted up to 6 h. In contrast, microinjections of bicuculline into CNA produced significant increases in REM. There were no significant reductions in NREM or wakefulness. These findings demonstrate that inactivating CNA can produce a relatively selective suppression of REM. The possible role that spontaneous activity in CNA may play in REM initiation and/or maintenance is discussed.

Amygdala↗
PubMed2003

A5 region modulation of the cardiorespiratory responses evoked from parabrachial cell bodies in the anaesthetised rat.

We have examined the importance of the A5 region modulating cardiorespiratory responses evoked from the parabrachial complex (PB) in spontaneously breathing rats. Cardiorespiratory changes were analyzed in response to electrical stimulation and glutamate microinjections into the PB (10-20 nl, 1-2 nmol) before and after ipsilateral microinjection of muscimol (50 nl, 0.25 nmol) or lidocaine (50 nl, 0.5 nmol) within the A5 region. Stimulation of medial parabrachial and Kölliker-Fuse nuclei (mPB-KF) evoked a decrease in respiratory rate (P<0.001) with a rise in blood pressure (P<0.001) and heart rate (P<0.05). After muscimol or lidocaine microinjections within the A5 region, the pressor and heart rate responses to mPB-KF stimulation were reduced (P<0.05, both cases). Muscimol within the A5 region altered the respiratory response to glutamate stimulation of mPB-KF, evoking an increase in respiratory rate (P<0.05). Lidocaine abolished the respiratory response to mPB-KF stimulation. Stimulation of the lateral parabrachial nuclei (lPB) caused an increase in respiratory rate (P<0.001) with a rise in blood pressure (P<0.001) and heart rate (P<0.05). Muscimol or lidocaine microinjections within A5 region decreased heart rate (P<0.05) and pressor responses (P<0.05) evoked from lPB. The increase of respiratory rate persisted unchanged. To confirm functional interactions between A5 and PB, extracellular recordings of putative A5 neurones were obtained during PB stimulation. Eighty-three A5 cells were recorded, 35 were activated from the mPB-KF (42%). The results indicate that neurones of the A5 region participate in the cardiorespiratory response evoked from the different regions of the PB complex. The possible mechanisms involved in these interactions are discussed.

Animals↗
PubMed1998

Modulation of GABAergic receptor binding by activation of calcium and calmodulin-dependent kinase II membrane phosphorylation.

gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system (CNS). Because of the important role that GABA plays in the CNS, alteration of GABAA receptor function would significantly affect neuronal excitability. Protein phosphorylation is a major mechanism for regulating receptor function in the brain and has been implicated in modulating GABAA receptor function. Therefore, this study was initiated to determine the role of calmodulin-dependent kinase II (CaM kinase II) membrane phosphorylation on GABAA receptor binding. Synaptosomal membrane fractions were tested for CaM kinase II activity towards endogenous substrates. In addition, muscimol binding was evaluated under equilibrium conditions in synaptosomal membrane fractions subjected to either basal (Mg2+ alone) or maximal CaM kinase II-dependent phosphorylation. Activation of endogenous CaM kinase II-dependent phosphorylation resulted in a significant enhancement of the apparent Bmax for muscimol binding without significantly altering the apparent binding affinity. The enhanced muscimol binding could be increased further by the addition of exogenous CaM kinase II to synaptosomal membrane fractions. Co-incubation with inhibitors of kinase activity during the phosphorylation reactions blocked the CaM kinase II-dependent increase in muscimol binding. The data support the hypothesis that activation of CaM kinase II-dependent phosphorylation caused an increased GABAA receptor binding and may play an important role in modulating the function of this inhibitory receptor/chloride ion channel complex.

Animals↗
PubMed1999

Activation of protein kinase C by phorbol dibutyrate modulates GABAA receptor binding in rat brain slices.

Effects of protein kinase C (PKC) activation on the function of the GABA/benzodiazepine receptor-chloride complex were analyzed by quantitative autoradiography using [3H]muscimol, [3H]flunitrazepam and [35S]TBPS in rat brain slices. The density of [3H]muscimol binding was highest in cerebellar granular layers and high in both the frontal cortex and thalamus, but binding levels in the hippocampus were low. After activation of PKC by 100 nM phorbol-12,13-dibutyrate (PDBu), [3H]muscimol binding was decreased in the frontal cortex, striatum and thalamus, but binding levels were not changed in the hippocampus or cerebellum. The density of [3H]flunitrazepam binding was high in the cortex, hippocampus and molecular layers of cerebellum but was low in thalamus. PDBu increased the [3H]flunitrazepam binding only in the striatum and in part of the cortex and thalamus after activation of PKC. After activation of PKC by PDBu [35S]TBPS binding was increased in most areas, but binding levels were not changed in the brainstem or cerebellum. The receptor binding was markedly decreased in almost all areas by the addition of 2.5 mM Mg2+. Elevated [35S]TBPS binding produced by PDBu was significantly inhibited by the addition of Mg2+. These results suggest that the activation of PKC potentiates benzodiazepine and TBPS binding, but decreases muscimol binding in a region-specific manner in the rat brain.

Animals↗
PubMedDate not supplied

Effects of superior colliculus inhibition on three-dimensional visual motion processing in the lateral suprasylvian visual area of the cat.

PURPOSE: To determine whether visual inputs from the tectothalamocortical pathway influence three-dimensional motion processing within the lateral suprasylvian (LS) area of the cat. METHODS: Tungsten microelectrodes were used for recording visual-evoked potentials (VEPs) from the LS area of 4 cats. Random dot stereograms were used as visual stimuli. Three-dimensional, motion-triggered VEPs were recorded from the LS area. Each motion sequence consisted of an abrupt onset of motion disparity with a 2 degrees amplitude followed by an abrupt offset and a stationary phase of 900 ms. The velocity of the motion disparity was varied in eight steps from 10 degrees to 400 degrees per second. The onset of motion disparity was used as the trigger for recording the VEPs. Single or multiple injections (two to three) of muscimol were made mainly into the rostral superior colliculus (SC). The amplitudes of the VEPs before and after the muscimol injection were compared. RESULTS: A large negative wave ( N1) with an implicit time of 92.7 +/- 13.5 ms (mean +/- SD, n = 98) was recorded consistently. The amplitude of N1 was significantly larger on stereovision of motion disparity than on either binocular vision of two-dimensional lateral motion or monocular vision, indicating that N1 contains neurons sensitive to motion disparity. The amplitude of N1 was not altered by muscimol injection into the SC at velocities < or =50 degrees/s. On the other hand, the amplitude of N1 was reduced to 66-71% of that observed before muscimol injection at velocities > or =75 degrees/s. CONCLUSIONS: These findings suggest that the LS area processes three-dimensional motion inputs via two parallel pathways, the geniculostriate pathway and the tectothalamocortical pathway, at velocities of motion disparity > or =75 degrees/s, while the three-dimensional motion inputs project to the LS area only via the geniculostriate pathway at velocities of motion disparity < or = 50 degrees/s.

Animals↗
PubMed2000

Differential potentiative effects of GABA receptor agonists in the production of antinociception induced by morphine and beta-endorphin administered intrathecally in the mouse.

The effect of muscimol or baclofen injected intrathecally (i.t.) on the inhibition of the tail-flick response induced by morphine and beta-endorphin administered i.t. was studied in ICR mice. The i.t. injection of muscimol (100 ng) or baclofen (10 ng) alone did not affect the basal inhibition of the tail-flick response. Morphine (0.2 microg) and beta-endorphin (0.1 microg) caused only slight inhibition of the tail-flick response. Baclofen, but not muscimol, injected i.t. enhanced the inhibition of the tail-flick response induced by i.t. administered morphine. Both muscimol and baclofen injected i.t. significantly enhanced i.t. injected beta-endorphin-induced inhibition of the tail-flick response. Our results suggest that the GABA(B), but not GABA(A), receptors located in the spinal cord appear to be involved in enhancing the inhibition of the tail-flick response induced by morphine administered spinally. In addition, both GABA(A) and GABA(B) receptors are involved in enhancing the inhibition of the tail-flick response induced by beta-endorphin administered i.t.

Amino Acids↗
PubMed1997

Action of delta-9-tetrahydrocannabinol on GABA(A) receptor-mediated responses in a grease-gap recording preparation of the rat hippocampal slice.

We have investigated the effects of delta-9-tetrahydrocannabinol (delta-9-THC) on gamma-aminobutyric acid (GABA) receptor-mediated responses in a grease-gap recording preparation of the rat hippocampus. GABA, and the selective GABA(A) receptor agonist muscimol, evoked depolarizing responses with EC50 values of 8.5 mM and 17.0 microM, respectively. Responses to both of these agonists were selectively reduced by the non-competitive GABA(A) antagonist picrotoxin (5 microM), but were unaffected by the GABA(B) antagonist 2-hydroxysaclofen (500 microM). Responses evoked by the selective GABA(B) receptor agonist baclofen were not sufficiently large to analyse. The GABA uptake inhibitor, nipecotic acid (500 microM), potentiated responses to GABA, but not to muscimol. Similarly, 10-1000 nM delta-9-THC had no significant effect on the response to muscimol, whereas 1000 nM delta-9-THC significantly increased the response to GABA. Since GABA is the substrate of an avid uptake system, but muscimol is not, the results are consistent with the suggestion that delta-9-THC inhibits the uptake of GABA in the hippocampus.

Animals↗
PubMed1998

Receptor subtype specific effects of GABA agonists on neurons receiving aortic depressor nerve inputs within the nucleus of the solitary tract.

The inhibitory amino acid gamma amino butyrate (GABA) has been shown to profoundly alter the integration of arterial baroreceptor inputs within the nucleus of the solitary tract (NTS). However, the relative roles of the major GABA receptor subtypes, the GABA(A) and the GABA(B) receptors, in the modulation of monosynaptic compared to polysynaptic afferent transmission within the NTS remain uncharacterized. In anesthetized rats, three types of NTS neuron were identified by their responses to aortic depressor nerve (ADN) stimulation; monosynaptic neurons (MSNs), polysynaptic neurons (PSNs) and ADN non-evoked neurons (NENs). Selective GABA(A) and GABA(B) agonists were applied to these neurons using iontophoretic techniques. The endogenous ligand GABA (2 mM), the selective GABA(A) agonist muscimol (0.04 and 0.02 mM) and the GABA(B) agonist baclofen (10 mM) all inhibited the spontaneous discharge of MSNs, PSNs and NENs (P < 0.01 for each group). In addition, GABA, muscimol and baclofen also inhibited ADN evoked discharge in both MSNs and PSNs (P < 0.05 for each group). Both GABA and baclofen significantly inhibited ADN evoked discharge in PSNs to a greater extent than in MSNs (P < 0.05 for each comparison). Muscimol at both doses, however, similarly inhibited ADN evoked discharge in both MSNs and PSNs. Examination of action potential amplitude and co-iontophoretic application of glutamate and GABA agonists suggested that GABA and muscimol induced inhibition were likely to be post-synaptic in origin, while baclofen produced both pre-synaptic and post-synaptic inhibition, depending upon the cell. In conclusion, GABA can influence baroreceptor afferent integration through both pre-synaptic and post-synaptic mechanisms. Furthermore, the effects of GABA(B) agonists are variable depending upon the level of afferent integration, with MSNs being generally less sensitive than PSNs.

Animals↗
PubMed1997

Dynamics of GABA(A) receptor binding in the ventromedial hypothalamus during postnatal development in the rat.

In vitro quantitative autoradiography of [3H]muscimol binding was used to examine the developmental pattern of GABA(A) receptor expression in the ventromedial hypothalamus (VMN) of Long-Evans rats. Peak levels of [3H]muscimol binding were observed in the VMN on postnatal day 14 (PN14), binding levels were significantly lower in the VMN at earlier (PN0 and PN7) and later (PN70) ages. The developmental pattern of [3H]muscimol binding observed in the VMN differed from that seen in the hippocampus where binding was found to increase progressively from PN0 to PN14 and was maintained at high levels in adulthood. Although the profile of GABA(A) receptor expression in the developing VMN undergoes considerable modification during the critical period for sexual differentiation, no significant differences in [3H]muscimol binding were observed between male and female animals at any developmental age.

Aging↗
PubMed1991

GABAergic control of basal forebrain cholinergic neurons and memory.

The involvement of the GABAergic innervation of basal forebrain neurons in the rats' conditional visual discrimination performance was examined. Performance in such a task is based on the subjects's ability to retrieve information about response rules, and previous experiments have demonstrated that basal forebrain lesions interfere with this ability. Following the acquisition of the task, chronic guide cannulae were stereotaxically implanted into the substantia innominata of both hemispheres, and the animals were retrained. Administration of the GABAA-agonist muscimol into the substantia innominata (0, 25, 50 ng/0.5 microliters/hemisphere) dose-dependently decreased the number of correct responses, increased the number of errors of omission, increased response latency, but did not affect side bias. Systemic co-administration of the cholinesterase inhibitor physostigmine (0, 0.1, 0.2 mg/kg; i.p.) exclusively interacted with the effects of muscimol on correct responding. Specifically, physostigmine dose-dependently intensified and attenuated the muscimol-induced reduction in correct responding. Although it cannot be excluded that alternative neuronal mechanisms were involved in the mediation of the effects of muscimol and their interaction with physostigmine, these findings support previous evidence indicating that the activity of basal forebrain cholinergic neurons is controlled by a GABAergic input, and that this neuronal link is involved in mnemonic processing.

Animals↗
PubMed2000

Activation of gamma-aminobutyric acid(A) receptors in the paraventricular nucleus of the hypothalamus reduces apomorphine-, N-methyl-D-aspartic acid- and oxytocin-induced penile erection and yawning in male rats.

The effect of muscimol and baclofen injected into the paraventricular nucleus of the hypothalamus on penile erection and yawning induced by apomorphine, oxytocin and N-methyl-D-aspartic acid (NMDA) was studied in male rats. Muscimol (20-200 ng), but not baclofen (200 ng), injected into the paraventricular nucleus of the hypothalamus 10 min before apomorphine (50 ng), oxytocin (10 ng) or NMDA (50 ng) reduced penile erection and yawning induced by the above compounds given into the paraventricular nucleus. Bicuculline (250 ng) injected into the paraventricular nucleus 5 min before muscimol (100 ng) prevented the inhibitory effect of muscimol on penile erection and yawning induced by apomorphine, oxytocin and NMDA. The present results show that gamma-aminobutyric acid (GABA) inhibits penile erection and yawning by acting on GABA(A) receptors in the paraventricular nucleus of the hypothalamus.

Animals↗
PubMed2001

The activation of gamma aminobutyric acid(A) receptors in the paraventricular nucleus of the hypothalamus reduces non-contact penile erections in male rats.

Male rats show 4-6 penile erection episodes when put in the presence of an inaccessible receptive female. These non-contact penile erections were reduced dose-dependently by muscimol, a gamma aminobutyric acid (GABA)(A) receptor agonist, when given into the paraventricular nucleus of the hypothalamus (0.1, 0.5, 1 and 2 microg). In contrast, baclofen, a GABA(B) receptor agonist (2 microg) was ineffective. Muscimol reduction of non-contact penile erections was not seen when male rats were pretreated with bicuculline methiodide (2 microg) given 5 min before muscimol into the paraventricular nucleus. Since muscimol injected into the paraventricular nucleus also prevents penile erection induced by drugs (e.g. apomorphine, oxytocin or N-methyl-D-aspartic acid), the present results show that an increased GABAergic activity in the paraventricular nucleus can impair the expression of penile erection induced not only by drugs but also by sexual physiological stimuli.

Animals↗